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1. The genomic and evolutionary landscapes of anaplastic thyroid carcinoma

Author: Zeng, Peter YF, Prokopec, Stephenie D, Lai, Stephen Y, Pinto, Nicole, Chan-Seng-Yue, Michelle A, Clifton-Bligh, Roderick, Williams, Michelle D, Howlett, Christopher J, Plantinga, Paul, Cecchini, Matthew J, Lam, Alfred K, Siddiqui, Iram, Wang, Jianxin, Sun, Ren X, Watson, John D, Korah, Reju, Carling, Tobias, Agrawal, Nishant, Cipriani, Nicole, Ball, Douglas, Nelkin, Barry, Rooper, Lisa M, Bishop, Justin A, Garnis, Cathie, Berean, Ken, Nicolson, Norman G, Weinberger, Paul, Henderson, Ying C, Lalansingh, Christopher M, Tian, Mao, Yamaguchi, Takafumi N, Livingstone, Julie, Salcedo, Adriana, Patel, Krupal, Vizeacoumar, Frederick, Datti, Alessandro, Xi, Liu, Nikiforov, Yuri E, Smallridge, Robert, Copland, John A, Marlow, Laura A, Hyrcza, Martin D, Delbridge, Leigh, Sidhu, Stan, Sywak, Mark, Robinson, Bruce, Fung, Kevin, Ghasemi, Farhad, Kwan, Keith, MacNeil, S Danielle, Mendez, Adrian, Palma, David A, Khan, Mohammed I, Shaikh, Mushfiq, Ruicci, Kara M, Wehrli, Bret, Winquist, Eric, Yoo, John, Mymryk, Joe S, Rocco, James W, Wheeler, David, Scherer, Steve, Giordano, Thomas J, Barrett, John W, Faquin, William C, Gill, Anthony J, Clayman, Gary, Boutros, Paul C, and Nichols, Anthony C
Subjects: Biological Sciences, Genetics, Human Genome, Cancer, Rare Diseases, Aetiology, 2.1 Biological and endogenous factors, Humans, Thyroid Carcinoma, Anaplastic, Thyroid Neoplasms, Mutation, Adenocarcinoma, Genomics, CP: Cancer, CP: Genomics, anaplastic thyroid cancer, cancer progression, genomics, tumour evolution, tumour heterogeneity, Biochemistry and Cell Biology, Medical Physiology, Biological sciences
Abstract: Anaplastic thyroid carcinoma is arguably the most lethal human malignancy. It often co-occurs with differentiated thyroid cancers, yet the molecular origins of its aggressivity are unknown. We sequenced tumor DNA from 329 regions of thyroid cancer, including 213 from patients with primary anaplastic thyroid carcinomas. We also whole genome sequenced 9 patients using multi-region sequencing of both differentiated and anaplastic thyroid cancer components. Using these data, we demonstrate thatanaplastic thyroid carcinomas have a higher burden of mutations than other thyroid cancers, with distinct mutational signatures and molecular subtypes. Further, different cancer driver genes are mutated in anaplastic and differentiated thyroid carcinomas, even those arising in a single patient. Finally, we unambiguously demonstrate that anaplastic thyroid carcinomas share a genomic origin with co-occurring differentiated carcinomas and emerge from a common malignant field through acquisition of characteristic clonal driver mutations.
Published: 2024

2. A polygenic two-hit hypothesis for prostate cancer

Author: Houlahan, Kathleen E, Livingstone, Julie, Fox, Natalie S, Kurganovs, Natalie, Zhu, Helen, Sietsma Penington, Jocelyn, Jung, Chol-Hee, Yamaguchi, Takafumi N, Heisler, Lawrence E, Jovelin, Richard, Costello, Anthony J, Pope, Bernard J, Kishan, Amar U, Corcoran, Niall M, Bristow, Robert G, Waszak, Sebastian M, Weischenfeldt, Joachim, He, Housheng H, Hung, Rayjean J, Hovens, Christopher M, and Boutros, Paul C
Subjects: Biomedical and Clinical Sciences, Clinical Sciences, Oncology and Carcinogenesis, Cancer, Genetics, Aging, Prostate Cancer, Urologic Diseases, Prevention, Genetic Testing, Human Genome, Good Health and Well Being, Male, Humans, Prostatic Neoplasms, Risk Factors, Prognosis, Genetic Predisposition to Disease, Oncology & Carcinogenesis, Oncology and carcinogenesis
Abstract: Prostate cancer is one of the most heritable cancers. Hundreds of germline polymorphisms have been linked to prostate cancer diagnosis and prognosis. Polygenic risk scores can predict genetic risk of a prostate cancer diagnosis. Although these scores inform the probability of developing a tumor, it remains unknown how germline risk influences the tumor molecular evolution. We cultivated a cohort of 1250 localized European-descent patients with germline and somatic DNA profiling. Men of European descent with higher genetic risk were diagnosed earlier and had less genomic instability and fewer driver genes mutated. Higher genetic risk was associated with better outcome. These data imply a polygenic "two-hit" model where germline risk reduces the number of somatic alterations required for tumorigenesis. These findings support further clinical studies of polygenic risk scores as inexpensive and minimally invasive adjuncts to standard risk stratification. Further studies are required to interrogate generalizability to more ancestrally and clinically diverse populations.
Published: 2023

3. The proteomic landscape of glioblastoma recurrence reveals novel and targetable immunoregulatory drivers

Author: Tatari, Nazanin, Khan, Shahbaz, Livingstone, Julie, Zhai, Kui, Mckenna, Dillon, Ignatchenko, Vladimir, Chokshi, Chirayu, Gwynne, William D, Singh, Manoj, Revill, Spencer, Mikolajewicz, Nicholas, Zhu, Chenghao, Chan, Jennifer, Hawkins, Cynthia, Lu, Jian-Qiang, Provias, John P, Ask, Kjetil, Morrissy, Sorana, Brown, Samuel, Weiss, Tobias, Weller, Michael, Han, Hong, Greenspoon, Jeffrey N, Moffat, Jason, Venugopal, Chitra, Boutros, Paul C, Singh, Sheila K, and Kislinger, Thomas
Subjects: Biomedical and Clinical Sciences, Neurosciences, Rare Diseases, Orphan Drug, Brain Cancer, Clinical Research, Brain Disorders, Biotechnology, Cancer, Genetics, 2.1 Biological and endogenous factors, Aetiology, Good Health and Well Being, Humans, Glioblastoma, Brain Neoplasms, Proteomics, Neoplasm Recurrence, Local, Transcriptome, Immunosuppression, OAS2, Clinical Sciences, Neurology & Neurosurgery
Abstract: Glioblastoma (GBM) is characterized by extensive cellular and genetic heterogeneity. Its initial presentation as primary disease (pGBM) has been subject to exhaustive molecular and cellular profiling. By contrast, our understanding of how GBM evolves to evade the selective pressure of therapy is starkly limited. The proteomic landscape of recurrent GBM (rGBM), which is refractory to most treatments used for pGBM, are poorly known. We, therefore, quantified the transcriptome and proteome of 134 patient-derived pGBM and rGBM samples, including 40 matched pGBM-rGBM pairs. GBM subtypes transition from pGBM to rGBM towards a preferentially mesenchymal state at recurrence, consistent with the increasingly invasive nature of rGBM. We identified immune regulatory/suppressive genes as important drivers of rGBM and in particular 2-5-oligoadenylate synthase 2 (OAS2) as an essential gene in recurrent disease. Our data identify a new class of therapeutic targets that emerge from the adaptive response of pGBM to therapy, emerging specifically in recurrent disease and may provide new therapeutic opportunities absent at pGBM diagnosis.
Published: 2022

4. Estimation of tumor cell total mRNA expression in 15 cancer types predicts disease progression

Author: Cao, Shaolong, Wang, Jennifer R, Ji, Shuangxi, Yang, Peng, Dai, Yaoyi, Guo, Shuai, Montierth, Matthew D, Shen, John Paul, Zhao, Xiao, Chen, Jingxiao, Lee, Jaewon James, Guerrero, Paola A, Spetsieris, Nicholas, Engedal, Nikolai, Taavitsainen, Sinja, Yu, Kaixian, Livingstone, Julie, Bhandari, Vinayak, Hubert, Shawna M, Daw, Najat C, Futreal, P Andrew, Efstathiou, Eleni, Lim, Bora, Viale, Andrea, Zhang, Jianjun, Nykter, Matti, Czerniak, Bogdan A, Brown, Powel H, Swanton, Charles, Msaouel, Pavlos, Maitra, Anirban, Kopetz, Scott, Campbell, Peter, Speed, Terence P, Boutros, Paul C, Zhu, Hongtu, Urbanucci, Alfonso, Demeulemeester, Jonas, Van Loo, Peter, and Wang, Wenyi
Subjects: Human Genome, Genetics, Cancer, 2.1 Biological and endogenous factors, Aetiology, Humans, Neoplasms, Genetic Heterogeneity, Genomics, RNA, Messenger, Disease Progression
Abstract: Single-cell RNA sequencing studies have suggested that total mRNA content correlates with tumor phenotypes. Technical and analytical challenges, however, have so far impeded at-scale pan-cancer examination of total mRNA content. Here we present a method to quantify tumor-specific total mRNA expression (TmS) from bulk sequencing data, taking into account tumor transcript proportion, purity and ploidy, which are estimated through transcriptomic/genomic deconvolution. We estimate and validate TmS in 6,590 patient tumors across 15 cancer types, identifying significant inter-tumor variability. Across cancers, high TmS is associated with increased risk of disease progression and death. TmS is influenced by cancer-specific patterns of gene alteration and intra-tumor genetic heterogeneity as well as by pan-cancer trends in metabolic dysregulation. Taken together, our results indicate that measuring cell-type-specific total mRNA expression in tumor cells predicts tumor phenotypes and clinical outcomes.
Published: 2022

5. Methylation Subtypes of Primary Prostate Cancer Predict Poor Prognosis

Author: Wang, Xiaoyu, Jordahl, Kristina M, Zhu, Chenghao, Livingstone, Julie, Rhie, Suhn K, Wright, Jonathan L, Grady, William M, Boutros, Paul C, Stanford, Janet L, and Dai, James Y
Subjects: Biomedical and Clinical Sciences, Clinical Sciences, Oncology and Carcinogenesis, Human Genome, Prostate Cancer, Genetic Testing, Urologic Diseases, Genetics, Clinical Research, Cancer, Aging, Good Health and Well Being, Biomarkers, Tumor, Canada, Cohort Studies, DNA Methylation, Humans, Male, Prognosis, Prostatectomy, Prostatic Neoplasms, Medical and Health Sciences, Epidemiology, Biomedical and clinical sciences, Health sciences
Abstract: BackgroundPatients with prostate cancer experience heterogeneous outcomes after radical prostatectomy. Genomic studies including The Cancer Genome Atlas (TCGA) have reported molecular signatures of prostate cancer, but few studies have assessed the prognostic effects of DNA methylation profiles.MethodsWe conducted the largest methylome subtyping analysis for primary prostate tumors to date, using methylome data from three patient populations: TCGA, a prostate cancer cohort study conducted at the Fred Hutchinson Cancer Research Center (FH; Seattle, WA), and the Canadian International Cancer Genome Consortium (ICGC) cohort. Four subtypes were detected in the TCGA dataset, then independently assigned to FH and ICGC cohort data. The identified methylation subtypes were assessed for association with cancer prognosis in the above three patient populations.ResultsUsing a set of hypermethylated CpG sites, four methylation subtypes were identified in TCGA. Compared with subtype 1, subtype 4 had an HR of 2.09 (P = 0.029) for biochemical recurrence (BCR) in TCGA patients. HRs of 2.76 (P = 0.002) for recurrence and 9.73 (P = 0.002) for metastatic-lethal (metastasis or prostate cancer-specific death) outcomes were observed in the FH cohort. A similar pattern of association was noted in the Canadian ICGC cohort, though HRs were not statistically significant.ConclusionsA hypermethylated subtype was associated with an increased hazard of recurrence and mortality in three studies with prostate tumor methylome data. Further molecular work is needed to understand the effect of methylation subtypes on cancer prognosis.ImpactThis study identified a DNA methylation subtype that was associated with worse prostate cancer prognosis after radical prostatectomy.
Published: 2022

6. Decreased ATM Protein Expression Is Substantiated with PTEN Loss in Defining Aggressive Phenotype of Prostate Cancer Associated with Lethal Disease

Author: Walker, Simon R, Abdelsalam, Ramy, Ghosh, Sunita, Livingstone, Julie, Palanisamy, Nallasivam, Boutros, Paul C, Yip, Steven M, Lees-Miller, Susan P, and Bismar, Tarek A
Subjects: Biomedical and Clinical Sciences, Clinical Sciences, Oncology and Carcinogenesis, Prostate Cancer, Aging, Urologic Diseases, Cancer, Ataxia Telangiectasia, Rare Diseases, Clinical Research, Neurodegenerative, 2.1 Biological and endogenous factors, Detection, screening and diagnosis, Aetiology, 4.1 Discovery and preclinical testing of markers and technologies, Good Health and Well Being, ATM, PTEN, ERG, Protein expression, Immunohistochemistry, Gleason score, Poly-ADP ribose polymerase and, ATR inhibitors, Androgen deprivation therapy, Cancer-specific mortality, Overall survival, Poly-ADP ribose polymerase and ATR inhibitors, Urology & Nephrology, Clinical sciences
Abstract: BackgroundAtaxia Telangiectasia Mutated (ATM) serine/threonine protein kinase is a known tumor suppressor, involved in DNA damage repair. It has prognostic and predictive therapeutic implications and is associated with aggressive prostate cancer (PCa).ObjectiveTo investigate the prognostic value of ATM protein expression in PCa patients and assessed the combined value of ATM, ERG, and PTEN status.Design setting and participantsThis study consisted of 303 patients with incidental, locally advanced, and castrate-resistant PCa by transurethral resection of the prostate (TURP).Outcome measurements and statistical analysisTURP samples from 303 PCa patients were assessed by immunohistochemistry (IHC for ATM, ERG, and PTEN. Individual and combined marker status were correlated with International Society of Urological Pathology Gleason grade group, overall survival (OS), and PCa-specific mortality (PCSM).Results and limitationsDecreased ATM expression (negative/weak intensity) occurred in 164/303 (54.1%) patients, and was associated with shorter OS and higher PCSM (p = 0.015 and p = 0.001, respectively). Negative/weak ATM expression was significantly associated with PCSM with a hazard ratio of 2.09 (95% confidence interval 1.34-3.27, p = 0.001). Assessment of Combined ATM/PTEN expression showed improved prognostic power to predict OS and PCSM, independent of Gleason grade groups.ConclusionsDecreased ATM protein expression is associated with poor outcomes in advanced PCa patients. Patients with combined low ATM/PTEN negative expression are at the highest risk for reduced OS and PCSM. Assessing the combined status of ATM/PTEN by IHC in PCa patients may aid in risk stratification relative to OS and PCSM. Moreover, since ATM plays an integral role in DNA damage response pathways, future studies will enhance our understanding of how outcomes of patients with altered ATM and PTEN expression can be improved further with poly-ADP ribose polymerase inhibitors (PARPi), combinations of PARPi and androgen receptor-targeted therapies, as well as platinum-based chemotherapies.Patient summaryLower ATM intensity is associated with increased cancer-specific mortality in prostate cancer patients. Patients with lower ATM and PTEN negative expression showed decreased overall survival and increased cancer mortality compared with controls.
Published: 2021

7. Copy Number Profiles of Prostate Cancer in Men of Middle Eastern Ancestry.

Author: Albawardi, Alia, Livingstone, Julie, Almarzooqi, Saeeda, Palanisamy, Nallasivam, Houlahan, Kathleen E, Awwad, Aktham Adnan Ahmad, Abdelsalam, Ramy A, Boutros, Paul C, and Bismar, Tarek A
Subjects: copy number aberrations, middle eastern ancestry, prostate cancer, Aging, Genetics, Human Genome, Prostate Cancer, Cancer, Urologic Diseases, Biotechnology, Oncology and Carcinogenesis
Abstract: Our knowledge of prostate cancer (PCa) genomics mainly reflects European (EUR) and Asian (ASN) populations. Our understanding of the influence of Middle Eastern (ME) and African (AFR) ancestry on the mutational profiles of prostate cancer is limited. To characterize genomic differences between ME, EUR, ASN, and AFR ancestry, fluorescent in situ hybridization (FISH) studies for NKX3-1 deletion and MYC amplification were carried out on 42 tumors arising in individuals of ME ancestry. These were supplemented by analysis of genome-wide copy number profiles of 401 tumors of all ancestries. FISH results of NKX3-1 and MYC were assessed in the ME cohort and compared to other ancestries. Gene level copy number aberrations (CNAs) for each sample were statistically compared between ancestry groups. NKX3-1 deletions by FISH were observed in 17/42 (17.5%) prostate tumors arising in men of ME ancestry, while MYC amplifications were only observed in 1/42 (2.3%). Using CNAs called from arrays, the incidence of NKX3-1 deletions was significantly lower in ME vs. other ancestries (20% vs. 52%; p = 2.3 × 10-3). Across the genome, tumors arising in men of ME ancestry had fewer CNAs than those in men of other ancestries (p = 0.014). Additionally, the somatic amplification of 21 specific genes was more frequent in tumors arising in men of ME vs. EUR ancestry (two-sided proportion test; Q < 0.05). Those included amplifications in the glutathione S-transferase family on chromosome 1 (GSTM1, GSTM2, GSTM5) and the IQ motif-containing family on chromosome 3 (IQCF1, IQCF2, IQCF13, IQCF4, IQCF5, IQCF6). Larger studies investigating ME populations are warranted to confirm these observations.
Published: 2021

8. Loss of CDCP1 triggers FAK activation in detached prostate cancer cells.

Author: Pollan, Sara G, Teng, Pai-Chi, Jan, Yu Jen, Livingstone, Julie, Huang, Cai, Kim, Minhyung, Mariscal, Javier, Rodriguez, Maria, Chen, Jie-Fu, You, Sungyong, DiVizio, Dolores, Boutros, Paul C, Chan, Keith Syson, Rasorenova, Olga, Cress, Anne, Spassov, Danislav, Moasser, Mark, Posadas, Edwin M, Freedland, Stephen J, Freeman, Michael R, Zheng, Jie J, and Knudsen, Beatrice S
Subjects: CDCP1, PIP5K1c, anoikis, focal adhesion kinase, prostate cancer metastasis, Urologic Diseases, Cancer, Prostate Cancer, Aetiology, 2.1 Biological and endogenous factors
Abstract: A major metastasis suppressing mechanism is the rapid apoptotic death of cancer cells upon detachment from extracellular matrix, a process called anoikis. Focal adhesion kinase (PTK2/FAK) is a key enzyme involved in evasion of anoikis. We show that loss of the Cub-domain containing protein-1 (CDCP1), paradoxically stimulates FAK activation in the detached state of prostate cancer cells. In CDCP1low DU145 and PC3 prostate cancer cells, detachment-activation of FAK occurs through local production of PI(4,5)P2. PI(4,5)P2 is generated by the PIP5K1c-201 splicing isoform of PIP5K1c, which contains a unique SRC phosphorylation site. In the detached state, reduced expression of CDCP1 and an alternative CDCP1-independent SRC activation mechanism triggers PIP5K1c-pY644 phosphorylation by SRC. This causes a switch of Talin binding from β1-integrin to PIP5K1c-pY644 and leads to activation of PIP5K1c-FAK. Reduced CDCP1 expression also inactivates CDK5, a negative regulator of PIP5K1c. Furthermore, immersion of prostate cancer cells in 10% human plasma or fetal bovine serum is required for activation of PIP5K1c-FAK. The PIP5K1c induced detachment-activation of FAK in preclinical models sensitizes CDCP1low prostate cancer cells to FAK inhibitors. In patients, CDCP1High versus CDCP1low circulating tumor cells differ in expression of AR-v7, ONECUT2 and HOXB13 oncogenes and TMPRSS2 and display intra-patient heterogeneity of FAK-pY397 expression. Taken together, CDCP1low and CDCP1high detached prostate cancer cells activate distinct cytoplasmic kinase complexes and targetable transcription factors, which has important therapeutic implications.
Published: 2021

9. The telomere length landscape of prostate cancer

Author: Livingstone, Julie, Shiah, Yu-Jia, Yamaguchi, Takafumi N, Heisler, Lawrence E, Huang, Vincent, Lesurf, Robert, Gebo, Tsumugi, Carlin, Benjamin, Eng, Stefan, Drysdale, Erik, Green, Jeffrey, van der Kwast, Theodorus, Bristow, Robert G, Fraser, Michael, and Boutros, Paul C
Subjects: Prostate Cancer, Genetics, Cancer, Biotechnology, Human Genome, Aging, Urologic Diseases, Aetiology, 2.1 Biological and endogenous factors, DNA Copy Number Variations, Epigenome, Gene Fusion, Genomics, Humans, Male, Prostatic Neoplasms, Proteome, Telomerase, Telomere, Transcriptome
Abstract: Replicative immortality is a hallmark of cancer, and can be achieved through telomere lengthening and maintenance. Although the role of telomere length in cancer has been well studied, its association to genomic features is less well known. Here, we report the telomere lengths of 392 localized prostate cancer tumours and characterize their relationship to genomic, transcriptomic and proteomic features. Shorter tumour telomere lengths are associated with elevated genomic instability, including single-nucleotide variants, indels and structural variants. Genes involved in cell proliferation and signaling are correlated with tumour telomere length at all levels of the central dogma. Telomere length is also associated with multiple clinical features of a tumour. Longer telomere lengths in non-tumour samples are associated with a lower rate of biochemical relapse. In summary, we describe the multi-level integration of telomere length, genomics, transcriptomics and proteomics in localized prostate cancer.
Published: 2021

10. Somatic driver mutation prevalence in 1844 prostate cancers identifies ZNRF3 loss as a predictor of metastatic relapse

Author: Fraser, Michael, Livingstone, Julie, Wrana, Jeffrey L, Finelli, Antonio, He, Housheng Hansen, van der Kwast, Theodorus, Zlotta, Alexandre R, Bristow, Robert G, and Boutros, Paul C
Subjects: Biomedical and Clinical Sciences, Oncology and Carcinogenesis, Prostate Cancer, Cancer, Genetics, Human Genome, Urologic Diseases, 2.1 Biological and endogenous factors, 4.1 Discovery and preclinical testing of markers and technologies, Detection, screening and diagnosis, Aetiology, Biomarkers, Tumor, Cell Cycle, Cell Cycle Proteins, Gene Expression Regulation, Neoplastic, Humans, Male, Mutation, Neoplasm Recurrence, Local, Prevalence, Prognosis, Prostatic Neoplasms, Ubiquitin-Protein Ligases
Abstract: Driver gene mutations that are more prevalent in metastatic, castration-resistant prostate cancer (mCRPC) than localized disease represent candidate prognostic biomarkers. We analyze 1,844 localized (1,289) or mCRPC (555) tumors and quantify the prevalence of 113 somatic driver single nucleotide variants (SNVs), copy number aberrations (CNAs), and structural variants (SVs) in each state. One-third are significantly more prevalent in mCRPC than expected while a quarter are less prevalent. Mutations in AR and its enhancer are more prevalent in mCRPC, as are those in TP53, MYC, ZNRF3 and PRKDC. ZNRF3 loss is associated with decreased ZNRF3 mRNA abundance, WNT, cell cycle & PRC1/2 activity, and genomic instability. ZNRF3 loss, RNA downregulation and hypermethylation are prognostic of metastasis and overall survival, independent of clinical and pathologic indices. These data demonstrate a strategy for identifying biomarkers of localized cancer aggression, with ZNRF3 loss as a predictor of metastasis in prostate cancer.
Published: 2021

11. Immune-focused multi-omics analysis of prostate cancer: leukocyte Ig-Like receptors are associated with disease progression.

Author: Vittrant, Benjamin, Bergeron, Alain, Molina, Oscar Eduardo, Leclercq, Mickael, Légaré, Xavier-Philippe, Hovington, Hélène, Picard, Valérie, Martin-Magniette, Marie-Laure, Livingstone, Julie, Boutros, Paul C, Collins, Colin, Fradet, Yves, and Droit, Arnaud
Subjects: Leukocytes, Humans, Prostatic Neoplasms, Neoplasm Recurrence, Local, Disease Progression, Immunoglobulins, Male, Prostate cancer, biochemical recurrence, immunotherapy, leukocyte Ig-Like Receptors, multi-omics analysis, Urologic Diseases, Prevention, Cancer, Aging, Prostate Cancer, Genetics, Immunization, Biotechnology, Human Genome, Immunology, Oncology and Carcinogenesis
Abstract: Prostate cancer (PCa) immunotherapy has shown limited efficacy so far, even in advanced-stage cancers. The success rate of PCa immunotherapy might be improved by approaches more adapted to the immunobiology of the disease. The objective of this study was to perform a multi-omics analysis to identify immune genes associated with PCa progression to better characterize PCa immunobiology and propose new immunotherapeutic targets. mRNA, miRNA, methylation, copy number aberration, and single nucleotide variant datasets from The Cancer Genome Atlas PRAD cohort were analyzed after filtering for genes associated with immunity. Sparse partial least squares-discriminant analyses were performed to identify features associated with biochemical recurrence (BCR) in each type of omics data. Selected features predicted BCR with a balanced error rate (BER) of 0.20 to 0.51 in single-omics and of 0.05 in multi-omics analyses. Amongst features associated with BCR were genes from the Immunoglobulin Ig-like Receptor (LILR) family which are immune checkpoints with immunotherapeutic potential. Using Multivariate INTegrative (MINT) analysis, the association of five LILR genes with BCR was quantified in a combination of three RNA-seq datasets and confirmed with Kaplan-Meier analysis in both these and in an independent RNA-seq dataset. Finally, immunohistochemistry showed that a high number of LILRB1 positive cells within the tumors predicted long-term adverse outcomes. Thus, tumors characterized by abnormal expression of LILR genes have an elevated risk of recurring after definitive local therapy. The immunotherapeutic potential of these regulators to stimulate the immune response against PCa should be evaluated in pre-clinical models.
Published: 2020

12. Transcriptomic Heterogeneity of Gleason Grade Group 5 Prostate Cancer

Author: Kishan, Amar U, Romero, Tahmineh, Alshalalfa, Mohammed, Liu, Yang, Tran, Phuoc T, Nickols, Nicholas G, Ye, Huihui, Sajed, Dipti, Rettig, Matthew B, Reiter, Robert E, Garraway, Isla P, Spratt, Daniel E, Freedland, Steven J, Zhao, Xin, Li, Ziwen, Deek, Matthew, Livingstone, Julie, Mahal, Brandon A, Nguyen, Paul L, Feng, Felix Y, Den, Robert B, Schaeffer, Edward M, Lotan, Tamara L, Karnes, R Jeffrey, Klein, Eric A, Ross, Ashley E, Grogan, Tristan, Davicioni, Elai, Elashoff, David, Boutros, Paul C, and Weidhaas, Joanne B
Subjects: Biomedical and Clinical Sciences, Clinical Sciences, Oncology and Carcinogenesis, Cancer, Prostate Cancer, Aging, Biotechnology, Clinical Trials and Supportive Activities, Genetics, Human Genome, Clinical Research, Urologic Diseases, Aetiology, 2.1 Biological and endogenous factors, Aged, Cohort Studies, Genetic Variation, Humans, Male, Middle Aged, Neoplasm Grading, Prostatic Neoplasms, Transcriptome, Gleason grade group 5, Gleason score 9, Gleason score 10, Biomarkers, Transcriptomics, Urology & Nephrology, Clinical sciences
Abstract: Gleason grade group (GG) 5 prostate cancer has been associated with an aggressive natural history, and retrospective data support a role for treatment intensification. However, clinical outcomes remain heterogeneous in this cohort, and intensified treatments carry an increased risk of adverse events. We sought to explore the transcriptomic heterogeneity of GG 5 tumors by querying transcriptomic data from the tumors of 2138 patients with GG 5 disease who underwent prostatectomy. Four distinct consensus clusters were identified with respect to differential transcriptional activation of hallmark pathways, with distinct molecular subtyping profiles and different average genomic risks (AGRs). One cluster, accounting for 325 tumors (15.2% of the population), was enriched for genes related to the cell cycle/proliferation, metabolic pathways, androgen response pathways, and DNA repair, and had a higher AGR than the other clusters (p
Published: 2020

13. Noncoding mutations target cis-regulatory elements of the FOXA1 plexus in prostate cancer.

Author: Zhou, Stanley, Hawley, James R, Soares, Fraser, Grillo, Giacomo, Teng, Mona, Madani Tonekaboni, Seyed Ali, Hua, Junjie Tony, Kron, Ken J, Mazrooei, Parisa, Ahmed, Musaddeque, Arlidge, Christopher, Yun, Hwa Young, Livingstone, Julie, Huang, Vincent, Yamaguchi, Takafumi N, Espiritu, Shadrielle MG, Zhu, Yanyun, Severson, Tesa M, Murison, Alex, Cameron, Sarina, Zwart, Wilbert, van der Kwast, Theodorus, Pugh, Trevor J, Fraser, Michael, Boutros, Paul C, Bristow, Robert G, He, Housheng Hansen, and Lupien, Mathieu
Subjects: Cell Line, Tumor, Humans, Prostatic Neoplasms, Transcription Factors, Cell Proliferation, Gene Expression Regulation, Neoplastic, Binding Sites, Regulatory Sequences, Nucleic Acid, Mutation, Male, Hepatocyte Nuclear Factor 3-alpha, Cell Line, Tumor, Gene Expression Regulation, Neoplastic, Regulatory Sequences, Nucleic Acid
Abstract: Prostate cancer is the second most commonly diagnosed malignancy among men worldwide. Recurrently mutated in primary and metastatic prostate tumors, FOXA1 encodes a pioneer transcription factor involved in disease onset and progression through both androgen receptor-dependent and androgen receptor-independent mechanisms. Despite its oncogenic properties however, the regulation of FOXA1 expression remains unknown. Here, we identify a set of six cis-regulatory elements in the FOXA1 regulatory plexus harboring somatic single-nucleotide variants in primary prostate tumors. We find that deletion and repression of these cis-regulatory elements significantly decreases FOXA1 expression and prostate cancer cell growth. Six of the ten single-nucleotide variants mapping to FOXA1 regulatory plexus significantly alter the transactivation potential of cis-regulatory elements by modulating the binding of transcription factors. Collectively, our results identify cis-regulatory elements within the FOXA1 plexus mutated in primary prostate tumors as potential targets for therapeutic intervention.
Published: 2020

14. The genomic landscape of metastatic castration-resistant prostate cancers reveals multiple distinct genotypes with potential clinical impact.

Author: van Dessel, Lisanne F, van Riet, Job, Smits, Minke, Zhu, Yanyun, Hamberg, Paul, van der Heijden, Michiel S, Bergman, Andries M, van Oort, Inge M, de Wit, Ronald, Voest, Emile E, Steeghs, Neeltje, Yamaguchi, Takafumi N, Livingstone, Julie, Boutros, Paul C, Martens, John WM, Sleijfer, Stefan, Cuppen, Edwin, Zwart, Wilbert, van de Werken, Harmen JG, Mehra, Niven, and Lolkema, Martijn P
Subjects: Lymph Nodes, Humans, Bone Neoplasms, Liver Neoplasms, Soft Tissue Neoplasms, Prostatic Neoplasms, Neoplasm Metastasis, Cyclin-Dependent Kinases, Oncogene Proteins, Fusion, BRCA2 Protein, Receptors, Androgen, Genotype, Male, Microsatellite Instability, Enhancer Elements, Genetic, DNA Copy Number Variations, Recombinational DNA Repair, Prostatic Neoplasms, Castration-Resistant, Whole Genome Sequencing, Chromatin Immunoprecipitation Sequencing, Oncogene Proteins, Fusion, Receptors, Androgen, Enhancer Elements, Genetic, Castration-Resistant, Biotechnology, Genetics, Cancer, Prostate Cancer, Urologic Diseases, Human Genome
Abstract: Metastatic castration-resistant prostate cancer (mCRPC) has a highly complex genomic landscape. With the recent development of novel treatments, accurate stratification strategies are needed. Here we present the whole-genome sequencing (WGS) analysis of fresh-frozen metastatic biopsies from 197 mCRPC patients. Using unsupervised clustering based on genomic features, we define eight distinct genomic clusters. We observe potentially clinically relevant genotypes, including microsatellite instability (MSI), homologous recombination deficiency (HRD) enriched with genomic deletions and BRCA2 aberrations, a tandem duplication genotype associated with CDK12-/- and a chromothripsis-enriched subgroup. Our data suggests that stratification on WGS characteristics may improve identification of MSI, CDK12-/- and HRD patients. From WGS and ChIP-seq data, we show the potential relevance of recurrent alterations in non-coding regions identified with WGS and highlight the central role of AR signaling in tumor progression. These data underline the potential value of using WGS to accurately stratify mCRPC patients into clinically actionable subgroups.
Published: 2019

15. Genome-wide germline correlates of the epigenetic landscape of prostate cancer

Author: Houlahan, Kathleen E, Shiah, Yu-Jia, Gusev, Alexander, Yuan, Jiapei, Ahmed, Musaddeque, Shetty, Anamay, Ramanand, Susmita G, Yao, Cindy Q, Bell, Connor, O’Connor, Edward, Huang, Vincent, Fraser, Michael, Heisler, Lawrence E, Livingstone, Julie, Yamaguchi, Takafumi N, Rouette, Alexandre, Foucal, Adrien, Espiritu, Shadrielle Melijah G, Sinha, Ankit, Sam, Michelle, Timms, Lee, Johns, Jeremy, Wong, Ada, Murison, Alex, Orain, Michèle, Picard, Valérie, Hovington, Hélène, Bergeron, Alain, Lacombe, Louis, Lupien, Mathieu, Fradet, Yves, Têtu, Bernard, McPherson, John D, Pasaniuc, Bogdan, Kislinger, Thomas, Chua, Melvin LK, Pomerantz, Mark M, van der Kwast, Theodorus, Freedman, Matthew L, Mani, Ram S, He, Housheng H, Bristow, Robert G, and Boutros, Paul C
Subjects: Biomedical and Clinical Sciences, Oncology and Carcinogenesis, Prostate Cancer, Urologic Diseases, Genetics, Aging, Cancer, Human Genome, Aetiology, 2.1 Biological and endogenous factors, DNA Methylation, Epigenome, Gene Expression Profiling, Gene Expression Regulation, Neoplastic, Genetic Predisposition to Disease, Genome, Human, Germ-Line Mutation, Humans, Male, Neoplasm Recurrence, Local, Prostatic Neoplasms, Proto-Oncogene Proteins c-akt, Quantitative Trait Loci, Medical and Health Sciences, Immunology, Biomedical and clinical sciences, Health sciences
Abstract: Oncogenesis is driven by germline, environmental and stochastic factors. It is unknown how these interact to produce the molecular phenotypes of tumors. We therefore quantified the influence of germline polymorphisms on the somatic epigenome of 589 localized prostate tumors. Predisposition risk loci influence a tumor's epigenome, uncovering a mechanism for cancer susceptibility. We identified and validated 1,178 loci associated with altered methylation in tumoral but not nonmalignant tissue. These tumor methylation quantitative trait loci influence chromatin structure, as well as RNA and protein abundance. One prominent tumor methylation quantitative trait locus is associated with AKT1 expression and is predictive of relapse after definitive local therapy in both discovery and validation cohorts. These data reveal intricate crosstalk between the germ line and the epigenome of primary tumors, which may help identify germline biomarkers of aggressive disease to aid patient triage and optimize the use of more invasive or expensive diagnostic assays.
Published: 2019

16. Molecular Hallmarks of Multiparametric Magnetic Resonance Imaging Visibility in Prostate Cancer

Author: Houlahan, Kathleen E, Salmasi, Amirali, Sadun, Taylor Y, Pooli, Aydin, Felker, Ely R, Livingstone, Julie, Huang, Vincent, Raman, Steven S, Ahuja, Preeti, Sisk, Anthony E, Boutros, Paul C, and Reiter, Robert E
Subjects: Biomedical and Clinical Sciences, Clinical Sciences, Oncology and Carcinogenesis, Prostate Cancer, Aging, Urologic Diseases, Cancer, Biomedical Imaging, 4.1 Discovery and preclinical testing of markers and technologies, Detection, screening and diagnosis, Aged, Gene Dosage, Gene Expression Profiling, Genome, Humans, Male, Middle Aged, Multiparametric Magnetic Resonance Imaging, Prostatic Neoplasms, RNA, Long Noncoding, RNA, Messenger, RNA, Small Nuclear, Transcriptome, Tumor Burden, Tumor Microenvironment, Prostate cancer, Multiparametric magnetic resonance imaging visibility, Radiogenomics, Nimbosus, Transcriptomics, Urology & Nephrology, Clinical sciences
Abstract: Multiparametric magnetic resonance imaging (mpMRI) has transformed the management of localized prostate cancer by improving identification of clinically significant disease at diagnosis. Approximately 20% of primary prostate tumors are invisible to mpMRI, and we hypothesize that this invisibility reflects fundamental molecular properties of the tumor. We therefore profiled the genomes and transcriptomes of 40 International Society of Urological Pathology grade 2 tumors: 20 mpMRI-invisible (Prostate Imaging-Reporting and Data System [PI-RADS] v2
Published: 2019

17. The Proteogenomic Landscape of Curable Prostate Cancer

Author: Sinha, Ankit, Huang, Vincent, Livingstone, Julie, Wang, Jenny, Fox, Natalie S, Kurganovs, Natalie, Ignatchenko, Vladimir, Fritsch, Katharina, Donmez, Nilgun, Heisler, Lawrence E, Shiah, Yu-Jia, Yao, Cindy Q, Alfaro, Javier A, Volik, Stas, Lapuk, Anna, Fraser, Michael, Kron, Ken, Murison, Alex, Lupien, Mathieu, Sahinalp, Cenk, Collins, Colin C, Tetu, Bernard, Masoomian, Mehdi, Berman, David M, van der Kwast, Theodorus, Bristow, Robert G, Kislinger, Thomas, and Boutros, Paul C
Subjects: Biological Sciences, Biomedical and Clinical Sciences, Bioinformatics and Computational Biology, Genetics, Oncology and Carcinogenesis, Aging, Biotechnology, Prostate Cancer, Cancer, Urologic Diseases, Human Genome, Aetiology, 2.1 Biological and endogenous factors, Adult, Aged, Aged, 80 and over, Biomarkers, Tumor, Cell Line, Tumor, Epigenomics, Gene Expression Profiling, Humans, Male, Middle Aged, Prognosis, Prostatic Neoplasms, Proteogenomics, Proto-Oncogene Proteins c-ets, Translocation, Genetic, Whole Genome Sequencing, biomarker, epigenome, genome, multi-omic features, prostate cancer, proteome, transcriptome, Neurosciences, Oncology & Carcinogenesis, Biochemistry and cell biology, Oncology and carcinogenesis
Abstract: DNA sequencing has identified recurrent mutations that drive the aggressiveness of prostate cancers. Surprisingly, the influence of genomic, epigenomic, and transcriptomic dysregulation on the tumor proteome remains poorly understood. We profiled the genomes, epigenomes, transcriptomes, and proteomes of 76 localized, intermediate-risk prostate cancers. We discovered that the genomic subtypes of prostate cancer converge on five proteomic subtypes, with distinct clinical trajectories. ETS fusions, the most common alteration in prostate tumors, affect different genes and pathways in the proteome and transcriptome. Globally, mRNA abundance changes explain only ∼10% of protein abundance variability. As a result, prognostic biomarkers combining genomic or epigenomic features with proteomic ones significantly outperform biomarkers comprised of a single data type.
Published: 2019

18. Cribriform and intraductal prostate cancer are associated with increased genomic instability and distinct genomic alterations

Author: Böttcher, René, Kweldam, Charlotte F, Livingstone, Julie, Lalonde, Emilie, Yamaguchi, Takafumi N, Huang, Vincent, Yousif, Fouad, Fraser, Michael, Bristow, Robert G, van der Kwast, Theodorus, Boutros, Paul C, Jenster, Guido, and van Leenders, Geert JLH
Subjects: Human Genome, Genetics, Cancer, Prostate Cancer, Urologic Diseases, Adenocarcinoma, Aged, Biomarkers, Tumor, Carcinoma, Intraductal, Noninfiltrating, DNA Copy Number Variations, Follow-Up Studies, Genomic Instability, Genomics, Humans, Male, Middle Aged, Prognosis, Prostatic Neoplasms, Cribriform, Intraductal carcinoma, Prostate cancer, Copy number alteration, Aggressive disease, Genomic instability, Oncology and Carcinogenesis, Public Health and Health Services, Oncology & Carcinogenesis
Abstract: BackgroundInvasive cribriform and intraductal carcinoma (CR/IDC) is associated with adverse outcome of prostate cancer patients. The aim of this study was to determine the molecular aberrations associated with CR/IDC in primary prostate cancer, focusing on genomic instability and somatic copy number alterations (CNA).MethodsWhole-slide images of The Cancer Genome Atlas Project (TCGA, N = 260) and the Canadian Prostate Cancer Genome Network (CPC-GENE, N = 199) radical prostatectomy datasets were reviewed for Gleason score (GS) and presence of CR/IDC. Genomic instability was assessed by calculating the percentage of genome altered (PGA). Somatic copy number alterations (CNA) were determined using Fisher-Boschloo tests and logistic regression. Primary analysis were performed on TCGA (N = 260) as discovery and CPC-GENE (N = 199) as validation set.ResultsCR/IDC growth was present in 80/260 (31%) TCGA and 76/199 (38%) CPC-GENE cases. Patients with CR/IDC and ≥ GS 7 had significantly higher PGA than men without this pattern in both TCGA (2.2 fold; p = 0.0003) and CPC-GENE (1.7 fold; p = 0.004) cohorts. CR/IDC growth was associated with deletions of 8p, 16q, 10q23, 13q22, 17p13, 21q22, and amplification of 8q24. CNAs comprised a total of 1299 gene deletions and 369 amplifications in the TCGA dataset, of which 474 and 328 events were independently validated, respectively. Several of the affected genes were known to be associated with aggressive prostate cancer such as loss of PTEN, CDH1, BCAR1 and gain of MYC. Point mutations in TP53, SPOP and FOXA1were also associated with CR/IDC, but occurred less frequently than CNAs.ConclusionsCR/IDC growth is associated with increased genomic instability clustering to genetic regions involved in aggressive prostate cancer. Therefore, CR/IDC is a pathologic substrate for progressive molecular tumour derangement.
Published: 2018

19. Mammary molecular portraits reveal lineage-specific features and progenitor cell vulnerabilities

Author: Casey, Alison E, Sinha, Ankit, Singhania, Rajat, Livingstone, Julie, Waterhouse, Paul, Tharmapalan, Pirashaanthy, Cruickshank, Jennifer, Shehata, Mona, Drysdale, Erik, Fang, Hui, Kim, Hyeyeon, Isserlin, Ruth, Bailey, Swneke, Medina, Tiago, Deblois, Genevieve, Shiah, Yu-Jia, Barsyte-Lovejoy, Dalia, Hofer, Stefan, Bader, Gary, Lupien, Mathieu, Arrowsmith, Cheryl, Knapp, Stefan, De Carvalho, Daniel, Berman, Hal, Boutros, Paul C, Kislinger, Thomas, and Khokha, Rama
Subjects: Prevention, Stem Cell Research - Nonembryonic - Non-Human, Cancer, Biotechnology, Human Genome, Stem Cell Research - Nonembryonic - Human, Breast Cancer, Stem Cell Research, Regenerative Medicine, Genetics, 1.1 Normal biological development and functioning, Underpinning research, Generic health relevance, Animals, Breast Neoplasms, Cell Line, Tumor, Cell Lineage, DNA Methylation, DNA, Neoplasm, Epigenesis, Genetic, Epigenomics, Humans, Mice, Mice, Transgenic, Neoplastic Stem Cells, Progesterone, Proteome, RNA, Neoplasm, Risk Factors, Transcriptome, Tumor Suppressor Protein p53, Up-Regulation, Biological Sciences, Medical and Health Sciences, Developmental Biology
Abstract: The mammary epithelium depends on specific lineages and their stem and progenitor function to accommodate hormone-triggered physiological demands in the adult female. Perturbations of these lineages underpin breast cancer risk, yet our understanding of normal mammary cell composition is incomplete. Here, we build a multimodal resource for the adult gland through comprehensive profiling of primary cell epigenomes, transcriptomes, and proteomes. We define systems-level relationships between chromatin-DNA-RNA-protein states, identify lineage-specific DNA methylation of transcription factor binding sites, and pinpoint proteins underlying progesterone responsiveness. Comparative proteomics of estrogen and progesterone receptor-positive and -negative cell populations, extensive target validation, and drug testing lead to discovery of stem and progenitor cell vulnerabilities. Top epigenetic drugs exert cytostatic effects; prevent adult mammary cell expansion, clonogenicity, and mammopoiesis; and deplete stem cell frequency. Select drugs also abrogate human breast progenitor cell activity in normal and high-risk patient samples. This integrative computational and functional study provides fundamental insight into mammary lineage and stem cell biology.
Published: 2018

20. moPepGen: Rapid and Comprehensive Proteoform Identification

Author: Zhu, Chenghao, primary, Liu, Lydia Y., additional, Yamaguchi, Takafumi N., additional, Zhu, Helen, additional, Hugh-White, Rupert, additional, Livingstone, Julie, additional, Patel, Yash, additional, Kislinger, Thomas, additional, and Boutros, Paul C., additional
Published: 2024
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21. Decreased ATM Protein Expression Is Substantiated with PTEN Loss in Defining Aggressive Phenotype of Prostate Cancer Associated with Lethal Disease

Author: Walker, Simon R., Abdelsalam, Ramy, Ghosh, Sunita, Livingstone, Julie, Palanisamy, Nallasivam, Boutros, Paul C., Yip, Steven M., Lees-Miller, Susan P., and Bismar, Tarek A.
Published: 2021
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22. Germline BRCA2 mutations drive prostate cancers with distinct evolutionary trajectories.

Author: Taylor, Renea A, Fraser, Michael, Livingstone, Julie, Espiritu, Shadrielle Melijah G, Thorne, Heather, Huang, Vincent, Lo, Winnie, Shiah, Yu-Jia, Yamaguchi, Takafumi N, Sliwinski, Ania, Horsburgh, Sheri, Meng, Alice, Heisler, Lawrence E, Yu, Nancy, Yousif, Fouad, Papargiris, Melissa, Lawrence, Mitchell G, Timms, Lee, Murphy, Declan G, Frydenberg, Mark, Hopkins, Julia F, Bolton, Damien, Clouston, David, McPherson, John D, van der Kwast, Theodorus, Boutros, Paul C, Risbridger, Gail P, and Bristow, Robert G
Subjects: Prostate, Humans, Carcinoma, Ductal, Prostatic Neoplasms, Neoplasm Invasiveness, Genetic Predisposition to Disease, Genomic Instability, BRCA2 Protein, Protein Isoforms, Prostatectomy, Retrospective Studies, Gene Expression Profiling, DNA Mutational Analysis, Evolution, Molecular, Epigenesis, Genetic, Gene Expression Regulation, Neoplastic, Heterozygote, Germ-Line Mutation, Aged, Middle Aged, Male, Mediator Complex, Whole Genome Sequencing, Carcinoma, Ductal, Evolution, Molecular, Epigenesis, Genetic, Gene Expression Regulation, Neoplastic
Abstract: Germline mutations in the BRCA2 tumour suppressor are associated with both an increased lifetime risk of developing prostate cancer (PCa) and increased risk of aggressive disease. To understand this aggression, here we profile the genomes and methylomes of localized PCa from 14 carriers of deleterious germline BRCA2 mutations (BRCA2-mutant PCa). We show that BRCA2-mutant PCa harbour increased genomic instability and a mutational profile that more closely resembles metastastic than localized disease. BRCA2-mutant PCa shows genomic and epigenomic dysregulation of the MED12L/MED12 axis, which is frequently dysregulated in metastatic castration-resistant prostate cancer (mCRPC). This dysregulation is enriched in BRCA2-mutant PCa harbouring intraductal carcinoma (IDC). Microdissection and sequencing of IDC and juxtaposed adjacent non-IDC invasive carcinoma in 10 patients demonstrates a common ancestor to both histopathologies. Overall we show that localized castration-sensitive BRCA2-mutant tumours are uniquely aggressive, due to de novo aberration in genes usually associated with metastatic disease, justifying aggressive initial treatment.
Published: 2017

23. Crowdsourced estimation of cognitive decline and resilience in Alzheimer's disease

Author: Allen, Genevera I, Amoroso, Nicola, Anghel, Catalina, Balagurusamy, Venkat, Bare, Christopher J, Beaton, Derek, Bellotti, Roberto, Bennett, David A, Boehme, Kevin L, Boutros, Paul C, Caberlotto, Laura, Caloian, Cristian, Campbell, Frederick, Neto, Elias Chaibub, Chang, Yu‐Chuan, Chen, Beibei, Chen, Chien‐Yu, Chien, Ting‐Ying, Clark, Tim, Das, Sudeshna, Davatzikos, Christos, Deng, Jieyao, Dillenberger, Donna, Dobson, Richard JB, Dong, Qilin, Doshi, Jimit, Duma, Denise, Errico, Rosangela, Erus, Guray, Everett, Evan, Fardo, David W, Friend, Stephen H, Fröhlich, Holger, Gan, Jessica, St George‐Hyslop, Peter, Ghosh, Satrajit S, Glaab, Enrico, Green, Robert C, Guan, Yuanfang, Hong, Ming‐Yi, Huang, Chao, Hwang, Jinseub, Ibrahim, Joseph, Inglese, Paolo, Iyappan, Anandhi, Jiang, Qijia, Katsumata, Yuriko, Kauwe, John SK, Klein, Arno, Kong, Dehan, Krause, Roland, Lalonde, Emilie, Lauria, Mario, Lee, Eunjee, Lin, Xihui, Liu, Zhandong, Livingstone, Julie, Logsdon, Benjamin A, Lovestone, Simon, Ma, Tsung‐wei, Malhotra, Ashutosh, Mangravite, Lara M, Maxwell, Taylor J, Merrill, Emily, Nagorski, John, Namasivayam, Aishwarya, Narayan, Manjari, Naz, Mufassra, Newhouse, Stephen J, Norman, Thea C, Nurtdinov, Ramil N, Oyang, Yen‐Jen, Pawitan, Yudi, Peng, Shengwen, Peters, Mette A, Piccolo, Stephen R, Praveen, Paurush, Priami, Corrado, Sabelnykova, Veronica Y, Senger, Philipp, Shen, Xia, Simmons, Andrew, Sotiras, Aristeidis, Stolovitzky, Gustavo, Tangaro, Sabina, Tateo, Andrea, Tung, Yi‐An, Tustison, Nicholas J, Varol, Erdem, Vradenburg, George, Weiner, Michael W, Xiao, Guanghua, Xie, Lei, Xie, Yang, Xu, Jia, Yang, Hojin, Zhan, Xiaowei, Zhou, Yunyun, Zhu, Fan, and Zhu, Hongtu
Subjects: Biomedical and Clinical Sciences, Biological Psychology, Clinical Sciences, Neurosciences, Psychology, Acquired Cognitive Impairment, Prevention, Neurodegenerative, Alzheimer's Disease including Alzheimer's Disease Related Dementias (AD/ADRD), Dementia, Alzheimer's Disease, Aging, Brain Disorders, Neurological, Alzheimer Disease, Apolipoproteins E, Biomarkers, Cognition Disorders, Computational Biology, Databases, Bibliographic, Humans, Predictive Value of Tests, Azheimer's disease, Crowdsource, Big data, Bioinformatics, Cognitive decline, Imaging, Genetics, Alzheimer's Disease Neuroimaging Initiative, Geriatrics, Clinical sciences, Biological psychology
Abstract: Identifying accurate biomarkers of cognitive decline is essential for advancing early diagnosis and prevention therapies in Alzheimer's disease. The Alzheimer's disease DREAM Challenge was designed as a computational crowdsourced project to benchmark the current state-of-the-art in predicting cognitive outcomes in Alzheimer's disease based on high dimensional, publicly available genetic and structural imaging data. This meta-analysis failed to identify a meaningful predictor developed from either data modality, suggesting that alternate approaches should be considered for prediction of cognitive performance.
Published: 2016

24. Molecular landmarks of tumor hypoxia across cancer types

Author: Bhandari, Vinayak, Hoey, Christianne, Liu, Lydia Y., Lalonde, Emilie, Ray, Jessica, Livingstone, Julie, Lesurf, Robert, Shiah, Yu-Jia, Vujcic, Tina, Huang, Xiaoyong, Espiritu, Shadrielle M. G., Heisler, Lawrence E., Yousif, Fouad, Huang, Vincent, Yamaguchi, Takafumi N., Yao, Cindy Q., Sabelnykova, Veronica Y., Fraser, Michael, Chua, Melvin L. K., van der Kwast, Theodorus, Liu, Stanley K., Boutros, Paul C., and Bristow, Robert G.
Published: 2019
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25. The genomic and evolutionary landscapes of anaplastic thyroid carcinoma

Author: Zeng, Peter YF, primary, Prokopec, Stephenie D., additional, Lai, Stephen Y., additional, Pinto, Nicole, additional, Chan-Seng-Yue, Michelle A., additional, Clifton-Bligh, Roderick, additional, Williams, Michelle D., additional, Howlett, Christopher J., additional, Plantinga, Paul, additional, Cecchini, Matthew, additional, Lam, Alfred K., additional, Siddiqui, Iram, additional, Wang, Jianxin, additional, Sun, Ren, additional, Watson, John, additional, Korah, Reju, additional, Carling, Tobias, additional, Agrawal, Nishant, additional, Cipriani, Nicole, additional, Ball, Douglas, additional, Nelkin, Barry, additional, Rooper, Lisa M., additional, Bishop, Justin A., additional, Garnis, Cathie, additional, Berean, Ken, additional, Nicolson, Norman, additional, Weinberger, Paul, additional, Henderson, Ying C., additional, Lalansingh, Christopher M., additional, Tian, Mao, additional, Yamaguchi, Takafumi, additional, Livingstone, Julie, additional, Salcedo, Adriana, additional, Patel, Krupal, additional, Vizeacoumar, Frederick, additional, Datti, Alessandro, additional, Xi, Liu, additional, Nikiforov, Yuri, additional, Smallridge, Robert, additional, Copland, John A., additional, Marlow, Laura A., additional, Hyrcza, Martin D., additional, Delbridge, Leigh, additional, Sidhu, Stan, additional, Sywak, Mark, additional, Robinson, Bruce, additional, Fung, Kevin, additional, Ghasemi, Farhad, additional, Kwan, Keith, additional, MacNeil, Danielle, additional, Mendez, Adrian, additional, Palma, David A., additional, Khan, Mohammed I., additional, Shaikh, Mushfiq, additional, Ruicci, Kara M., additional, Wehrli, Bret, additional, Winquist, Eric, additional, Yoo, John, additional, Mymryk, Joe, additional, Rocco, James W., additional, Wheeler, David, additional, Scherer, Steve, additional, Giordano, Thomas J., additional, Barrett, John W., additional, Faquin, William C., additional, Gill, Anthony J., additional, Clayman, Gary, additional, Boutros, Paul C., additional, and Nichols, Anthony C., additional
Published: 2023
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26. Abstract 4305: Germline structural variants shape prostate cancer clinical and molecular evolution

Author: Wang, Nicholas K., primary, Rouette, Alexandre, additional, Houlahan, Kathleen E., additional, Yamaguchi, Takafumi N., additional, Livingstone, Julie, additional, Jung, Chol-Hee, additional, Georgeson, Peter, additional, Fraser, Michael, additional, Shiah, Yu-Jia, additional, Yao, Cindy Q., additional, Huang, Vincent, additional, Fox, Natalie S., additional, Kurganovs, Natalie, additional, Kasaian, Katayoon, additional, Sabelnykova, Veronica Y., additional, Jayalath, Jay, additional, Weke, Kenneth, additional, Zhu, Helen, additional, van der Kwast, Theodorus, additional, Papenfuss, Tony, additional, He, Housheng H., additional, Corcoran, Niall M., additional, Bristow, Robert G., additional, Zlotta, Alexandre R., additional, Hovens, Christopher, additional, and Boutros, Paul C., additional
Published: 2023
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27. Data from Rab11-FIP1C Is a Critical Negative Regulator in ErbB2-Mediated Mammary Tumor Progression

Author: Boulay, Pierre-Luc, primary, Mitchell, Louise, primary, Turpin, Jason, primary, Huot-Marchand, Julie-Émilie, primary, Lavoie, Cynthia, primary, Sanguin-Gendreau, Virginie, primary, Jones, Laura, primary, Mitra, Shreya, primary, Livingstone, Julie M., primary, Campbell, Shirley, primary, Hallett, Michael, primary, Mills, Gordon B., primary, Park, Morag, primary, Chodosh, Lewis, primary, Strathdee, Douglas, primary, Norman, Jim C., primary, and Muller, William J., primary
Published: 2023
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28. Supplemental Figure 2 In vitro role of FIP1C in regulating cell proliferation in ErbB2/neuNDL primary cells from Rab11-FIP1C Is a Critical Negative Regulator in ErbB2-Mediated Mammary Tumor Progression

Author: Boulay, Pierre-Luc, primary, Mitchell, Louise, primary, Turpin, Jason, primary, Huot-Marchand, Julie-Émilie, primary, Lavoie, Cynthia, primary, Sanguin-Gendreau, Virginie, primary, Jones, Laura, primary, Mitra, Shreya, primary, Livingstone, Julie M., primary, Campbell, Shirley, primary, Hallett, Michael, primary, Mills, Gordon B., primary, Park, Morag, primary, Chodosh, Lewis, primary, Strathdee, Douglas, primary, Norman, Jim C., primary, and Muller, William J., primary
Published: 2023
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29. Supplemental Figure 3 Characterization of FIP1C/ErbB2/neuNDL cell lines in regulating tumor growth using athymic NCr mice from Rab11-FIP1C Is a Critical Negative Regulator in ErbB2-Mediated Mammary Tumor Progression

Author: Boulay, Pierre-Luc, primary, Mitchell, Louise, primary, Turpin, Jason, primary, Huot-Marchand, Julie-Émilie, primary, Lavoie, Cynthia, primary, Sanguin-Gendreau, Virginie, primary, Jones, Laura, primary, Mitra, Shreya, primary, Livingstone, Julie M., primary, Campbell, Shirley, primary, Hallett, Michael, primary, Mills, Gordon B., primary, Park, Morag, primary, Chodosh, Lewis, primary, Strathdee, Douglas, primary, Norman, Jim C., primary, and Muller, William J., primary
Published: 2023
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30. Supplemental Materials and Methods from Rab11-FIP1C Is a Critical Negative Regulator in ErbB2-Mediated Mammary Tumor Progression

Author: Boulay, Pierre-Luc, primary, Mitchell, Louise, primary, Turpin, Jason, primary, Huot-Marchand, Julie-Émilie, primary, Lavoie, Cynthia, primary, Sanguin-Gendreau, Virginie, primary, Jones, Laura, primary, Mitra, Shreya, primary, Livingstone, Julie M., primary, Campbell, Shirley, primary, Hallett, Michael, primary, Mills, Gordon B., primary, Park, Morag, primary, Chodosh, Lewis, primary, Strathdee, Douglas, primary, Norman, Jim C., primary, and Muller, William J., primary
Published: 2023
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31. Supplemental Figure Legends from Rab11-FIP1C Is a Critical Negative Regulator in ErbB2-Mediated Mammary Tumor Progression

Author: Boulay, Pierre-Luc, primary, Mitchell, Louise, primary, Turpin, Jason, primary, Huot-Marchand, Julie-Émilie, primary, Lavoie, Cynthia, primary, Sanguin-Gendreau, Virginie, primary, Jones, Laura, primary, Mitra, Shreya, primary, Livingstone, Julie M., primary, Campbell, Shirley, primary, Hallett, Michael, primary, Mills, Gordon B., primary, Park, Morag, primary, Chodosh, Lewis, primary, Strathdee, Douglas, primary, Norman, Jim C., primary, and Muller, William J., primary
Published: 2023
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32. Supplemental Figure 1 Schematics of the tetracycline inducible-FIP1C-MTB and inducible knock-out FIP1C mouse models from Rab11-FIP1C Is a Critical Negative Regulator in ErbB2-Mediated Mammary Tumor Progression

Author: Boulay, Pierre-Luc, primary, Mitchell, Louise, primary, Turpin, Jason, primary, Huot-Marchand, Julie-Émilie, primary, Lavoie, Cynthia, primary, Sanguin-Gendreau, Virginie, primary, Jones, Laura, primary, Mitra, Shreya, primary, Livingstone, Julie M., primary, Campbell, Shirley, primary, Hallett, Michael, primary, Mills, Gordon B., primary, Park, Morag, primary, Chodosh, Lewis, primary, Strathdee, Douglas, primary, Norman, Jim C., primary, and Muller, William J., primary
Published: 2023
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33. Supplemental Figure 5 FIP1C is not distribute at adjacent junctional complexes. Clinical relevance of FIP1C in Her2-positive breast cancer patients from Rab11-FIP1C Is a Critical Negative Regulator in ErbB2-Mediated Mammary Tumor Progression

Author: Boulay, Pierre-Luc, primary, Mitchell, Louise, primary, Turpin, Jason, primary, Huot-Marchand, Julie-Émilie, primary, Lavoie, Cynthia, primary, Sanguin-Gendreau, Virginie, primary, Jones, Laura, primary, Mitra, Shreya, primary, Livingstone, Julie M., primary, Campbell, Shirley, primary, Hallett, Michael, primary, Mills, Gordon B., primary, Park, Morag, primary, Chodosh, Lewis, primary, Strathdee, Douglas, primary, Norman, Jim C., primary, and Muller, William J., primary
Published: 2023
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34. Supplemental Figure 4 FIP1C is a negative modulator of Akt and MAPK activation in an ErbB2-driven model from Rab11-FIP1C Is a Critical Negative Regulator in ErbB2-Mediated Mammary Tumor Progression

Author: Boulay, Pierre-Luc, primary, Mitchell, Louise, primary, Turpin, Jason, primary, Huot-Marchand, Julie-Émilie, primary, Lavoie, Cynthia, primary, Sanguin-Gendreau, Virginie, primary, Jones, Laura, primary, Mitra, Shreya, primary, Livingstone, Julie M., primary, Campbell, Shirley, primary, Hallett, Michael, primary, Mills, Gordon B., primary, Park, Morag, primary, Chodosh, Lewis, primary, Strathdee, Douglas, primary, Norman, Jim C., primary, and Muller, William J., primary
Published: 2023
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35. A polygenic two-hit hypothesis for prostate cancer

Author: Houlahan, Kathleen E, primary, Livingstone, Julie, additional, Fox, Natalie S, additional, Kurganovs, Natalie, additional, Zhu, Helen, additional, Sietsma Penington, Jocelyn, additional, Jung, Chol-Hee, additional, Yamaguchi, Takafumi N, additional, Heisler, Lawrence E, additional, Jovelin, Richard, additional, Costello, Anthony J, additional, Pope, Bernard J, additional, Kishan, Amar U, additional, Corcoran, Niall M, additional, Bristow, Robert G, additional, Waszak, Sebastian M, additional, Weischenfeldt, Joachim, additional, He, Housheng H, additional, Hung, Rayjean J, additional, Hovens, Christopher M, additional, and Boutros, Paul C, additional
Published: 2023
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36. Germline determinants of the prostate tumor genome

Author: Houlahan, Kathleen E., primary, Yuan, Jiapei, additional, Schwarz, Tommer, additional, Livingstone, Julie, additional, Fox, Natalie S., additional, Jaratlerdsiri, Weerachai, additional, van Riet, Job, additional, Taraszka, Kodi, additional, Kurganovs, Natalie, additional, Zhu, Helen, additional, Sietsma Penington, Jocelyn, additional, Jung, Chol-Hee, additional, Yamaguchi, Takafumi N, additional, Jiang, Jue, additional, Heisler, Lawrence E, additional, Jovelin, Richard, additional, Ramanand, Susmita G, additional, Bell, Connor, additional, O’Connor, Edward, additional, Mutambirwa, Shingai B.A., additional, Seo, Ji-Heui, additional, Costello, Anthony J., additional, Pomerantz, Mark M., additional, Pope, Bernard J., additional, Zaitlen, Noah, additional, Kishan, Amar U., additional, Corcoran, Niall M., additional, Bristow, Robert G., additional, Waszak, Sebastian M., additional, Bornman, Riana M.S., additional, Gusev, Alexander, additional, Lolkema, Martijn P., additional, Weischenfeldt, Joachim, additional, Hung, Rayjean J., additional, He, Housheng H., additional, Hayes, Vanessa M., additional, Pasaniuc, Bogdan, additional, Freedman, Matthew L., additional, Hovens, Christopher M., additional, Mani, Ram S., additional, and Boutros, Paul C., additional
Published: 2022
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37. A deep learning system accurately classifies primary and metastatic cancers using passenger mutation patterns

Author: Jiao, Wei, Atwal, Gurnit, Polak, Paz, Karlic, Rosa, Cuppen, Edwin, Al-Shahrour, Fatima, Bailey, Peter J, Biankin, Andrew V, Boutros, Paul C, Campbell, Peter J, Chang, David K, Cooke, Susanna L, Deshpande, Vikram, Faltas, Bishoy M, Faquin, William C, Garraway, Levi, Getz, Gad, Grimmond, Sean M, Haider, Syed, Hoadley, Katherine A, Kaiser, Vera B, Kato, Mamoru, Kübler, Kirsten, Lazar, Alexander J, Li, Constance H, Louis, David N, Margolin, Adam, Martin, Sancha, Nahal-Bose, Hardeep K, Nielsen, G Petur, Nik-Zainal, Serena, Omberg, Larsson, P’ng, Christine, Perry, Marc D, Rheinbay, Esther, Rubin, Mark A, Semple, Colin A, Sgroi, Dennis C, Shibata, Tatsuhiro, Siebert, Reiner, Smith, Jaclyn, Stein, Lincoln D, Stobbe, Miranda D, Sun, Ren X, Thai, Kevin, Wright, Derek W, Wu, Chin-Lee, Yuan, Ke, Zhang, Junjun, Danyi, Alexandra, de Ridder, Jeroen, van Herpen, Carla, Lolkema, Martijn P, Steeghs, Neeltje, Morris, Quaid D, Aaltonen, Lauri A, Abascal, Federico, Abeshouse, Adam, Aburatani, Hiroyuki, Adams, David J, Agrawal, Nishant, Ahn, Keun Soo, Ahn, Sung-Min, Aikata, Hiroshi, Akbani, Rehan, Akdemir, Kadir C, Al-Ahmadie, Hikmat, Al-Sedairy, Sultan T, Alawi, Malik, Albert, Monique, Aldape, Kenneth, Alexandrov, Ludmil B, Ally, Adrian, Alsop, Kathryn, Alvarez, Eva G, Amary, Fernanda, Amin, Samirkumar B, Aminou, Brice, Ammerpohl, Ole, Anderson, Matthew J, Ang, Yeng, Antonello, Davide, Anur, Pavana, Aparicio, Samuel, Appelbaum, Elizabeth L, Arai, Yasuhito, Aretz, Axel, Arihiro, Koji, Ariizumi, Shun-ichi, Armenia, Joshua, Arnould, Laurent, Asa, Sylvia, Assenov, Yassen, Aukema, Sietse, Auman, J Todd, Aure, Miriam RR, Awadalla, Philip, Aymerich, Marta, Bader, Gary D, Baez-Ortega, Adrian, Bailey, Matthew H, Balasundaram, Miruna, Balu, Saianand, Bandopadhayay, Pratiti, Banks, Rosamonde E, Barbi, Stefano, Barbour, Andrew P, Barenboim, Jonathan, Barnholtz-Sloan, Jill, Barr, Hugh, Barrera, Elisabet, Bartlett, John, Bartolome, Javier, Bassi, Claudio, Bathe, Oliver F, Baumhoer, 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Xiao, Xiao, Xing, Rui, Xiong, Heng, Xu, Qinying, Xu, Yanxun, Xue, Hong, Yachida, Shinichi, Yakneen, Sergei, Yamaguchi, Rui, Yamaguchi, Takafumi N, Yamamoto, Masakazu, Yamamoto, Shogo, Yamaue, Hiroki, Yang, Fan, Yang, Huanming, Yang, Jean Y, Yang, Liming, Yang, Lixing, Yang, Shanlin, Yang, Tsun-Po, Yang, Yang, Yao, Xiaotong, Yaspo, Marie-Laure, Yates, Lucy, Yau, Christina, Ye, Chen, Ye, Kai, Yellapantula, Venkata D, Yoon, Christopher J, Yoon, Sung-Soo, Yousif, Fouad, Yu, Jun, Yu, Kaixian, Yu, Willie, Yu, Yingyan, Yuan, Yuan, Yuen, Denis, Yung, Christina K, Zaikova, Olga, Zamora, Jorge, Zapatka, Marc, Zenklusen, Jean C, Zenz, Thorsten, Zeps, Nikolajs, Zhang, Cheng-Zhong, Zhang, Fan, Zhang, Hailei, Zhang, Hongwei, Zhang, Hongxin, Zhang, Jiashan, Zhang, Jing, Zhang, Xiuqing, Zhang, Xuanping, Zhang, Yan, Zhang, Zemin, Zhao, Zhongming, Zheng, Liangtao, Zheng, Xiuqing, Zhou, Wanding, Zhou, Yong, Zhu, Bin, Zhu, Hongtu, Zhu, Jingchun, Zhu, Shida, Zou, Lihua, Zou, Xueqing, deFazio, Anna, van As, Nicholas, van Deurzen, Carolien HM, van de Vijver, Marc J, Veer, L van’t, and von Mering, Christian
Subjects: Human Biology & Physiology, Ecology,Evolution & Ethology, Tumour Biology, Genetics & Genomics, Structural Biology & Biophysics, Computational & Systems Biology
Abstract: In cancer, the primary tumour’s organ of origin and histopathology are the strongest determinants of its clinical behaviour, but in 3% of cases a patient presents with a metastatic tumour and no obvious primary. Here, as part of the ICGC/TCGA Pan-Cancer Analysis of Whole Genomes (PCAWG) Consortium, we train a deep learning classifier to predict cancer type based on patterns of somatic passenger mutations detected in whole genome sequencing (WGS) of 2606 tumours representing 24 common cancer types produced by the PCAWG Consortium. Our classifier achieves an accuracy of 91% on held-out tumor samples and 88% and 83% respectively on independent primary and metastatic samples, roughly double the accuracy of trained pathologists when presented with a metastatic tumour without knowledge of the primary. Surprisingly, adding information on driver mutations reduced accuracy. Our results have clinical applicability, underscore how patterns of somatic passenger mutations encode the state of the cell of origin, and can inform future strategies to detect the source of circulating tumour DNA.
Published: 2023
Full Text: View/download PDF

38. Combined burden and functional impact tests for cancer driver discovery using DriverPower

Author: Shuai, Shimin, Abascal, Federico, Amin, Samirkumar B, Bader, Gary D, Bandopadhayay, Pratiti, Barenboim, Jonathan, Beroukhim, Rameen, Bertl, Johanna, Boroevich, Keith A, Brunak, Søren, Campbell, Peter J, Carlevaro-Fita, Joana, Chakravarty, Dimple, Chan, Calvin Wing Yiu, Chen, Ken, Choi, Jung Kyoon, Deu-Pons, Jordi, Dhingra, Priyanka, Diamanti, Klev, Feuerbach, Lars, Fink, J Lynn, Fonseca, Nuno A, Frigola, Joan, Gambacorti-Passerini, Carlo, Garsed, Dale W, Gerstein, Mark, Getz, Gad, Guo, Qianyun, Gut, Ivo G, Haan, David, Hamilton, Mark P, Haradhvala, Nicholas J, Harmanci, Arif O, Helmy, Mohamed, Herrmann, Carl, Hess, Julian M, Hobolth, Asger, Hodzic, Ermin, Hong, Chen, Hornshøj, Henrik, Isaev, Keren, Izarzugaza, Jose MG, Johnson, Rory, Johnson, Todd A, Juul, Malene, Juul, Randi Istrup, Kahles, Andre, Kahraman, Abdullah, Kellis, Manolis, Khurana, Ekta, Kim, Jaegil, Kim, Jong K, Kim, Youngwook, Komorowski, Jan, Korbel, Jan O, Kumar, Sushant, Lanzós, Andrés, Larsson, Erik, Lawrence, Michael S, Lee, Donghoon, Lehmann, Kjong-Van, Li, Shantao, Li, Xiaotong, Lin, Ziao, Liu, Eric Minwei, Lochovsky, Lucas, Lou, Shaoke, Madsen, Tobias, Marchal, Kathleen, Martincorena, Iñigo, Martinez-Fundichely, Alexander, Maruvka, Yosef E, McGillivray, Patrick D, Meyerson, William, Muiños, Ferran, Mularoni, Loris, Nakagawa, Hidewaki, Nielsen, Morten Muhlig, Paczkowska, Marta, Park, Keunchil, Park, Kiejung, Pedersen, Jakob Skou, Pons, Tirso, Pulido-Tamayo, Sergio, Raphael, Benjamin J, Reimand, Jüri, Reyes-Salazar, Iker, Reyna, Matthew A, Rheinbay, Esther, Rubin, Mark A, Rubio-Perez, Carlota, Sahinalp, S Cenk, Saksena, Gordon, Salichos, Leonidas, Sander, Chris, Schumacher, Steven E, Shackleton, Mark, Shapira, Ofer, Shen, Ciyue, Shrestha, Raunak, Sidiropoulos, Nikos, Sieverling, Lina, Sinnott-Armstrong, Nasa, Stein, Lincoln D, Stuart, Joshua M, Tamborero, David, Tiao, Grace, Tsunoda, Tatsuhiko, Umer, Husen M, Uusküla-Reimand, Liis, Valencia, Alfonso, Vazquez, Miguel, Verbeke, Lieven PC, 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Subjects: Human Biology & Physiology, Ecology,Evolution & Ethology, Tumour Biology, Genetics & Genomics, Structural Biology & Biophysics, Computational & Systems Biology
Abstract: The discovery of driver mutations is one of the key motivations for cancer genome sequencing. Here, as part of the ICGC/TCGA Pan-Cancer Analysis of Whole Genomes (PCAWG) Consortium, which aggregated whole genome sequencing data from 2658 cancers across 38 tumour types, we describe DriverPower, a software package that uses mutational burden and functional impact evidence to identify driver mutations in coding and non-coding sites within cancer whole genomes. Using a total of 1373 genomic features derived from public sources, DriverPower’s background mutation model explains up to 93% of the regional variance in the mutation rate across multiple tumour types. By incorporating functional impact scores, we are able to further increase the accuracy of driver discovery. Testing across a collection of 2583 cancer genomes from the PCAWG project, DriverPower identifies 217 coding and 95 non-coding driver candidates. Comparing to six published methods used by the PCAWG Drivers and Functional Interpretation Working Group, DriverPower has the highest F1 score for both coding and non-coding driver discovery. This demonstrates that DriverPower is an effective framework for computational driver discovery.
Published: 2023
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39. Integrative pathway enrichment analysis of multivariate omics data

Author: Paczkowska, Marta, Barenboim, Jonathan, Sintupisut, Nardnisa, Fox, Natalie S, Zhu, Helen, Abd-Rabbo, Diala, Mee, Miles W, Boutros, Paul C, Abascal, Federico, Amin, Samirkumar B, Bader, Gary D, Beroukhim, Rameen, Bertl, Johanna, Boroevich, Keith A, Brunak, Søren, Campbell, Peter J, Carlevaro-Fita, Joana, Chakravarty, Dimple, Chan, Calvin Wing Yiu, Chen, Ken, Choi, Jung Kyoon, Deu-Pons, Jordi, Dhingra, Priyanka, Diamanti, Klev, Feuerbach, Lars, Fink, J Lynn, Fonseca, Nuno A, Frigola, Joan, Gambacorti-Passerini, Carlo, Garsed, Dale W, Gerstein, Mark, Getz, Gad, Gonzalez-Perez, Abel, Guo, Qianyun, Gut, Ivo G, Haan, David, Hamilton, Mark P, Haradhvala, Nicholas J, Harmanci, Arif O, Helmy, Mohamed, Herrmann, Carl, Hess, Julian M, Hobolth, Asger, Hodzic, Ermin, Hong, Chen, Hornshøj, Henrik, Isaev, Keren, Izarzugaza, Jose MG, Johnson, Rory, Johnson, Todd A, Juul, Malene, Juul, Randi Istrup, Kahles, Andre, Kahraman, Abdullah, Kellis, Manolis, Khurana, Ekta, Kim, Jaegil, Kim, Jong K, Kim, Youngwook, Komorowski, Jan, Korbel, Jan O, Kumar, Sushant, Lanzós, Andrés, Lawrence, Michael S, Lee, Donghoon, Lehmann, Kjong-Van, Li, Shantao, Li, Xiaotong, Lin, Ziao, Liu, Eric Minwei, Lochovsky, Lucas, Lou, Shaoke, Madsen, Tobias, Marchal, Kathleen, Martincorena, Iñigo, Martinez-Fundichely, Alexander, Maruvka, Yosef E, McGillivray, Patrick D, Meyerson, William, Muiños, Ferran, Mularoni, Loris, Nakagawa, Hidewaki, Nielsen, Morten Muhlig, Park, Keunchil, Park, Kiejung, Pedersen, Jakob Skou, Pich, Oriol, Pons, Tirso, Pulido-Tamayo, Sergio, Raphael, Benjamin J, Reyes-Salazar, Iker, Reyna, Matthew A, Rheinbay, Esther, Rubin, Mark A, Rubio-Perez, Carlota, Sabarinathan, Radhakrishnan, Sahinalp, S Cenk, Saksena, Gordon, Salichos, Leonidas, Sander, Chris, Schumacher, Steven E, Shackleton, Mark, Shapira, Ofer, Shen, Ciyue, Shrestha, Raunak, Shuai, Shimin, Sidiropoulos, Nikos, Sieverling, Lina, Sinnott-Armstrong, Nasa, Stein, Lincoln D, Stuart, Joshua M, Tamborero, David, Tiao, Grace, 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Qian, Xiao, Xiao, Xing, Rui, Xiong, Heng, Xu, Qinying, Xu, Yanxun, Xue, Hong, Yachida, Shinichi, Yakneen, Sergei, Yamaguchi, Rui, Yamaguchi, Takafumi N, Yamamoto, Masakazu, Yamamoto, Shogo, Yamaue, Hiroki, Yang, Fan, Yang, Huanming, Yang, Jean Y, Yang, Liming, Yang, Lixing, Yang, Shanlin, Yang, Tsun-Po, Yang, Yang, Yao, Xiaotong, Yaspo, Marie-Laure, Yates, Lucy, Yau, Christina, Ye, Chen, Ye, Kai, Yellapantula, Venkata D, Yoon, Christopher J, Yoon, Sung-Soo, Yousif, Fouad, Yu, Kaixian, Yu, Willie, Yu, Yingyan, Yuan, Ke, Yuan, Yuan, Yuen, Denis, Yung, Christina K, Zaikova, Olga, Zamora, Jorge, Zapatka, Marc, Zenklusen, Jean C, Zenz, Thorsten, Zeps, Nikolajs, Zhang, Cheng-Zhong, Zhang, Fan, Zhang, Hailei, Zhang, Hongwei, Zhang, Hongxin, Zhang, Jiashan, Zhang, Junjun, Zhang, Xiuqing, Zhang, Zemin, Zheng, Liangtao, Zheng, Xiuqing, Zhou, Wanding, Zhou, Yong, Zhu, Bin, Zhu, Hongtu, Zhu, Jingchun, Zhu, Shida, Zou, Xueqing, deFazio, Anna, van As, Nicholas, van Deurzen, Carolien HM, van de Vijver, Marc J, and Veer, L van’t
Subjects: Human Biology & Physiology, Ecology,Evolution & Ethology, Tumour Biology, Genetics & Genomics, Structural Biology & Biophysics, Computational & Systems Biology
Abstract: Multi-omics datasets represent distinct aspects of the central dogma of molecular biology. Such high-dimensional molecular profiles pose challenges to data interpretation and hypothesis generation. ActivePathways is an integrative method that discovers significantly enriched pathways across multiple datasets using statistical data fusion, rationalizes contributing evidence and highlights associated genes. As part of the ICGC/TCGA Pan-Cancer Analysis of Whole Genomes (PCAWG) Consortium, which aggregated whole genome sequencing data from 2658 cancers across 38 tumor types, we integrated genes with coding and non-coding mutations and revealed frequently mutated pathways and additional cancer genes with infrequent mutations. We also analyzed prognostic molecular pathways by integrating genomic and transcriptomic features of 1780 breast cancers and highlighted associations with immune response and anti-apoptotic signaling. Integration of ChIP-seq and RNA-seq data for master regulators of the Hippo pathway across normal human tissues identified processes of tissue regeneration and stem cell regulation. ActivePathways is a versatile method that improves systems-level understanding of cellular organization in health and disease through integration of multiple molecular datasets and pathway annotations.
Published: 2023
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40. Pathway and network analysis of more than 2500 whole cancer genomes

Author: Reyna, Matthew A, Haan, David, Paczkowska, Marta, Verbeke, Lieven PC, Vazquez, Miguel, Kahraman, Abdullah, Pulido-Tamayo, Sergio, Barenboim, Jonathan, Wadi, Lina, Dhingra, Priyanka, Shrestha, Raunak, Getz, Gad, Lawrence, Michael S, Pedersen, Jakob Skou, Rubin, Mark A, Wheeler, David A, Brunak, Søren, Izarzugaza, Jose MG, Khurana, Ekta, Marchal, Kathleen, von Mering, Christian, Sahinalp, S Cenk, Valencia, Alfonso, Abascal, Federico, Amin, Samirkumar B, Bader, Gary D, Bandopadhayay, Pratiti, Beroukhim, Rameen, Bertl, Johanna, Boroevich, Keith A, Busanovich, John, Campbell, Peter J, Carlevaro-Fita, Joana, Chakravarty, Dimple, Chan, Calvin Wing Yiu, Chen, Ken, Choi, Jung Kyoon, Deu-Pons, Jordi, Diamanti, Klev, Feuerbach, Lars, Fink, J Lynn, Fonseca, Nuno A, Frigola, Joan, Gambacorti-Passerini, Carlo, Garsed, Dale W, Gerstein, Mark, Guo, Qianyun, Gut, Ivo G, Hamilton, Mark P, Haradhvala, Nicholas J, Harmanci, Arif O, Helmy, Mohamed, Herrmann, Carl, Hess, Julian M, Hobolth, Asger, Hodzic, Ermin, Hong, Chen, Hornshøj, Henrik, Isaev, Keren, Johnson, Rory, Johnson, Todd A, Juul, Malene, Juul, Randi Istrup, Kahles, Andre, Kellis, Manolis, Kim, Jaegil, Kim, Jong K, Kim, Youngwook, Komorowski, Jan, Korbel, Jan O, Kumar, Sushant, Lanzós, Andrés, Larsson, Erik, Lee, Donghoon, Lehmann, Kjong-Van, Li, Shantao, Li, Xiaotong, Lin, Ziao, Liu, Eric Minwei, Lochovsky, Lucas, Lou, Shaoke, Madsen, Tobias, Martincorena, Iñigo, Martinez-Fundichely, Alexander, Maruvka, Yosef E, McGillivray, Patrick D, Meyerson, William, Muiños, Ferran, Mularoni, Loris, Nakagawa, Hidewaki, Nielsen, Morten Muhlig, Park, Keunchil, Park, Kiejung, Pons, Tirso, Reyes-Salazar, Iker, Rheinbay, Esther, Rubio-Perez, Carlota, Saksena, Gordon, Salichos, Leonidas, Sander, Chris, Schumacher, Steven E, Shackleton, Mark, Shapira, Ofer, Shen, Ciyue, Shuai, Shimin, Sidiropoulos, Nikos, Sieverling, Lina, Sinnott-Armstrong, Nasa, Stein, Lincoln D, Tamborero, David, Tiao, Grace, Tsunoda, Tatsuhiko, Umer, Husen M, 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Subjects: Human Biology & Physiology, Ecology,Evolution & Ethology, Tumour Biology, Genetics & Genomics, Structural Biology & Biophysics, Computational & Systems Biology
Abstract: The catalog of cancer driver mutations in protein-coding genes has greatly expanded in the past decade. However, non-coding cancer driver mutations are less well-characterized and only a handful of recurrent non-coding mutations, most notably TERT promoter mutations, have been reported. Here, as part of the ICGC/TCGA Pan-Cancer Analysis of Whole Genomes (PCAWG) Consortium, which aggregated whole genome sequencing data from 2658 cancer across 38 tumor types, we perform multi-faceted pathway and network analyses of non-coding mutations across 2583 whole cancer genomes from 27 tumor types compiled by the ICGC/TCGA PCAWG project that was motivated by the success of pathway and network analyses in prioritizing rare mutations in protein-coding genes. While few non-coding genomic elements are recurrently mutated in this cohort, we identify 93 genes harboring non-coding mutations that cluster into several modules of interacting proteins. Among these are promoter mutations associated with reduced mRNA expression in TP53, TLE4, and TCF4. We find that biological processes had variable proportions of coding and non-coding mutations, with chromatin remodeling and proliferation pathways altered primarily by coding mutations, while developmental pathways, including Wnt and Notch, altered by both coding and non-coding mutations. RNA splicing is primarily altered by non-coding mutations in this cohort, and samples containing non-coding mutations in well-known RNA splicing factors exhibit similar gene expression signatures as samples with coding mutations in these genes. These analyses contribute a new repertoire of possible cancer genes and mechanisms that are altered by non-coding mutations and offer insights into additional cancer vulnerabilities that can be investigated for potential therapeutic treatments.
Published: 2023
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41. Divergent mutational processes distinguish hypoxic and normoxic tumours

Author: Bhandari, Vinayak, Li, Constance H, Bristow, Robert G, Boutros, Paul C, Aaltonen, Lauri A, Abascal, Federico, Abeshouse, Adam, Aburatani, Hiroyuki, Adams, David J, Agrawal, Nishant, Ahn, Keun Soo, Ahn, Sung-Min, Aikata, Hiroshi, Akbani, Rehan, Akdemir, Kadir C, Al-Ahmadie, Hikmat, Al-Sedairy, Sultan T, Al-Shahrour, Fatima, Alawi, Malik, Albert, Monique, Aldape, Kenneth, Alexandrov, Ludmil B, Ally, Adrian, Alsop, Kathryn, Alvarez, Eva G, Amary, Fernanda, Amin, Samirkumar B, Aminou, Brice, Ammerpohl, Ole, Anderson, Matthew J, Ang, Yeng, Antonello, Davide, Anur, Pavana, Aparicio, Samuel, Appelbaum, Elizabeth L, Arai, Yasuhito, Aretz, Axel, Arihiro, Koji, Ariizumi, Shun-ichi, Armenia, Joshua, Arnould, Laurent, Asa, Sylvia, Assenov, Yassen, Atwal, Gurnit, Aukema, Sietse, Auman, J Todd, Aure, Miriam RR, Awadalla, Philip, Aymerich, Marta, Bader, Gary D, Baez-Ortega, Adrian, Bailey, Matthew H, Bailey, Peter J, Balasundaram, Miruna, Balu, Saianand, Bandopadhayay, Pratiti, Banks, Rosamonde E, Barbi, Stefano, Barbour, Andrew P, Barenboim, Jonathan, Barnholtz-Sloan, Jill, Barr, Hugh, Barrera, Elisabet, Bartlett, John, Bartolome, Javier, Bassi, Claudio, Bathe, Oliver F, Baumhoer, Daniel, Bavi, Prashant, Baylin, Stephen B, Bazant, Wojciech, Beardsmore, Duncan, Beck, Timothy A, Behjati, Sam, Behren, Andreas, Niu, Beifang, Bell, Cindy, Beltran, Sergi, Benz, Christopher, Berchuck, Andrew, Bergmann, Anke K, Bergstrom, Erik N, Berman, Benjamin P, Berney, Daniel M, Bernhart, Stephan H, Beroukhim, Rameen, Berrios, Mario, Bersani, Samantha, Bertl, Johanna, Betancourt, Miguel, Bhosle, Shriram G, Biankin, Andrew V, Bieg, Matthias, Bigner, Darell, Binder, Hans, Birney, Ewan, Birrer, Michael, Biswas, Nidhan K, Bjerkehagen, Bodil, Bodenheimer, Tom, Boice, Lori, Bonizzato, Giada, De Bono, Johann S, Boot, Arnoud, Bootwalla, Moiz S, Borg, Ake, Borkhardt, Arndt, Boroevich, Keith A, Borozan, Ivan, Borst, Christoph, Bosenberg, Marcus, Bosio, Mattia, Boultwood, Jacqueline, Bourque, Guillaume, Bova, G Steven, Bowen, David T, Bowlby, Reanne, Bowtell, David DL, Boyault, Sandrine, Boyce, Rich, Boyd, Jeffrey, Brazma, Alvis, Brennan, Paul, Brewer, Daniel S, Brinkman, Arie B, Broaddus, Russell R, Brock, Jane E, Brock, Malcolm, Broeks, Annegien, Brooks, Angela N, Brooks, Denise, Brors, Benedikt, Brunak, Søren, Bruxner, Timothy JC, Bruzos, Alicia L, Buchanan, Alex, Buchhalter, Ivo, Buchholz, Christiane, Bullman, Susan, Burke, Hazel, Burkhardt, Birgit, Burns, Kathleen H, Busanovich, John, Bustamante, Carlos D, Butler, Adam P, Butte, Atul J, Byrne, Niall J, Børresen-Dale, Anne-Lise, Caesar-Johnson, Samantha J, Cafferkey, Andy, Cahill, Declan, Calabrese, Claudia, Caldas, Carlos, Calvo, Fabien, Camacho, Niedzica, Campbell, Peter J, Campo, Elias, Cantù, Cinzia, Cao, Shaolong, Carey, Thomas E, Carlevaro-Fita, Joana, Carlsen, Rebecca, Cataldo, Ivana, Cazzola, Mario, Cebon, Jonathan, Cerfolio, Robert, Chadwick, Dianne E, Chakravarty, Dimple, Chalmers, Don, Chan, Calvin Wing Yiu, Chan, Kin, Chan-Seng-Yue, Michelle, Chandan, Vishal S, Chang, David K, Chanock, Stephen J, Chantrill, Lorraine A, Chateigner, Aurélien, Chatterjee, Nilanjan, Chayama, Kazuaki, Chen, Hsiao-Wei, Chen, Jieming, Chen, Ken, Chen, Yiwen, Chen, Zhaohong, Cherniack, Andrew D, Chien, Jeremy, Chiew, Yoke-Eng, Chin, Suet-Feung, Cho, Juok, Cho, Sunghoon, Choi, Jung Kyoon, Choi, Wan, Chomienne, Christine, Chong, Zechen, Choo, Su Pin, Chou, Angela, Christ, Angelika N, Christie, Elizabeth L, Chuah, Eric, Cibulskis, Carrie, Cibulskis, Kristian, Cingarlini, Sara, Clapham, Peter, Claviez, Alexander, Cleary, Sean, Cloonan, Nicole, Cmero, Marek, Collins, Colin C, Connor, Ashton A, Cooke, Susanna L, Cooper, Colin S, Cope, Leslie, Corbo, Vincenzo, Cordes, Matthew G, Cordner, Stephen M, Cortés-Ciriano, Isidro, Covington, Kyle, Cowin, Prue A, Craft, Brian, Craft, David, Creighton, Chad J, Cun, Yupeng, Curley, Erin, Cutcutache, Ioana, Czajka, Karolina, Czerniak, Bogdan, Dagg, Rebecca A, Danilova, Ludmila, Davi, Maria Vittoria, Davidson, Natalie R, Davies, Helen, Davis, Ian J, Davis-Dusenbery, Brandi N, Dawson, Kevin J, De La Vega, Francisco M, De Paoli-Iseppi, Ricardo, Defreitas, Timothy, Dei Tos, Angelo P, Delaneau, Olivier, Demchok, John A, Demeulemeester, Jonas, Demidov, German M, Demircioğlu, Deniz, Dennis, Nening M, Denroche, Robert E, Dentro, Stefan C, Desai, Nikita, Deshpande, Vikram, Deshwar, Amit G, Desmedt, Christine, Deu-Pons, Jordi, Dhalla, Noreen, Dhani, Neesha C, Dhingra, Priyanka, Dhir, Rajiv, DiBiase, Anthony, Diamanti, Klev, Ding, Li, Ding, Shuai, Dinh, Huy Q, Dirix, Luc, Doddapaneni, HarshaVardhan, Donmez, Nilgun, Dow, Michelle T, Drapkin, Ronny, Drechsel, Oliver, Drews, Ruben M, Serge, Serge, Dudderidge, Tim, Dueso-Barroso, Ana, Dunford, Andrew J, Dunn, Michael, Dursi, Lewis Jonathan, Duthie, Fraser R, Dutton-Regester, Ken, Eagles, Jenna, Easton, Douglas F, Edmonds, Stuart, Edwards, Paul A, Edwards, Sandra E, Eeles, Rosalind A, Ehinger, Anna, Eils, Juergen, Eils, Roland, El-Naggar, Adel, Eldridge, Matthew, Ellrott, Kyle, Erkek, Serap, Escaramis, Georgia, Espiritu, Shadrielle MG, Estivill, Xavier, Etemadmoghadam, Dariush, Eyfjord, Jorunn E, Faltas, Bishoy M, Fan, Daiming, Fan, Yu, Faquin, William C, Farcas, Claudiu, Fassan, Matteo, Fatima, Aquila, Favero, Francesco, Fayzullaev, Nodirjon, Felau, Ina, Fereday, Sian, Ferguson, Martin L, Ferretti, Vincent, Feuerbach, Lars, Field, Matthew A, Fink, J Lynn, Finocchiaro, Gaetano, Fisher, Cyril, Fittall, Matthew W, Fitzgerald, Anna, Fitzgerald, Rebecca C, Flanagan, Adrienne M, Fleshner, Neil E, Flicek, Paul, Foekens, John A, Fong, Kwun M, Fonseca, Nuno A, Foster, Christopher S, Fox, Natalie S, Fraser, Michael, Frazer, Scott, Frenkel-Morgenstern, Milana, Friedman, William, Frigola, Joan, Fronick, Catrina C, Fujimoto, Akihiro, Fujita, Masashi, Fukayama, Masashi, Fulton, Lucinda A, Fulton, Robert S, Furuta, Mayuko, Futreal, P Andrew, Füllgrabe, Anja, Gabriel, Stacey B, Gallinger, Steven, Gambacorti-Passerini, Carlo, Gao, Jianjiong, Gao, Shengjie, Garraway, Levi, Garred, Øystein, Garrison, Erik, Garsed, Dale W, Gehlenborg, Nils, Gelpi, Josep LL, George, Joshy, Gerhard, Daniela S, Gerhauser, Clarissa, Gershenwald, Jeffrey E, Gerstein, Mark, Gerstung, Moritz, Getz, Gad, Ghori, Mohammed, Ghossein, Ronald, Giama, Nasra H, Gibbs, Richard A, Gibson, Bob, Gill, Anthony J, Gill, Pelvender, Giri, Dilip D, Glodzik, Dominik, Gnanapragasam, Vincent J, Goebler, Maria Elisabeth, Goldman, Mary J, Gomez, Carmen, Gonzalez, Santiago, Gonzalez-Perez, Abel, Gordenin, Dmitry A, Gossage, James, Gotoh, Kunihito, Govindan, Ramaswamy, Grabau, Dorthe, Graham, Janet S, Grant, Robert C, Green, Anthony R, Green, Eric, Greger, Liliana, Grehan, Nicola, Grimaldi, Sonia, Grimmond, Sean M, Grossman, Robert L, Grundhoff, Adam, Gundem, Gunes, Guo, Qianyun, Gupta, Manaswi, Gupta, Shailja, Gut, Ivo G, Gut, Marta, Göke, Jonathan, Ha, Gavin, Haake, Andrea, Haan, David, Haas, Siegfried, Haase, Kerstin, Haber, 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Masakazu, Yamamoto, Shogo, Yamaue, Hiroki, Yang, Fan, Yang, Huanming, Yang, Jean Y, Yang, Liming, Yang, Lixing, Yang, Shanlin, Yang, Tsun-Po, Yang, Yang, Yao, Xiaotong, Yaspo, Marie-Laure, Yates, Lucy, Yau, Christina, Ye, Chen, Ye, Kai, Yellapantula, Venkata D, Yoon, Christopher J, Yoon, Sung-Soo, Yousif, Fouad, Yu, Jun, Yu, Kaixian, Yu, Willie, Yu, Yingyan, Yuan, Ke, Yuan, Yuan, Yuen, Denis, Yung, Christina K, Zaikova, Olga, Zamora, Jorge, Zapatka, Marc, Zenklusen, Jean C, Zenz, Thorsten, Zeps, Nikolajs, Zhang, Cheng-Zhong, Zhang, Fan, Zhang, Hailei, Zhang, Hongwei, Zhang, Hongxin, Zhang, Jiashan, Zhang, Jing, Zhang, Junjun, Zhang, Xiuqing, Zhang, Xuanping, Zhang, Yan, Zhang, Zemin, Zhao, Zhongming, Zheng, Liangtao, Zheng, Xiuqing, Zhou, Wanding, Zhou, Yong, Zhu, Bin, Zhu, Hongtu, Zhu, Jingchun, Zhu, Shida, Zou, Lihua, Zou, Xueqing, deFazio, Anna, van As, Nicholas, van Deurzen, Carolien HM, van de Vijver, Marc J, Veer, L van’t, and von Mering, Christian
Subjects: Human Biology & Physiology, Ecology,Evolution & Ethology, Tumour Biology, Genetics & Genomics, Structural Biology & Biophysics, Computational & Systems Biology
Abstract: Many primary tumours have low levels of molecular oxygen (hypoxia), and hypoxic tumours respond poorly to therapy. Pan-cancer molecular hallmarks of tumour hypoxia remain poorly understood, with limited comprehension of its associations with specific mutational processes, non-coding driver genes and evolutionary features. Here, as part of the ICGC/TCGA Pan-Cancer Analysis of Whole Genomes (PCAWG) Consortium, which aggregated whole genome sequencing data from 2658 cancers across 38 tumour types, we quantify hypoxia in 1188 tumours spanning 27 cancer types. Elevated hypoxia associates with increased mutational load across cancer types, irrespective of underlying mutational class. The proportion of mutations attributed to several mutational signatures of unknown aetiology directly associates with the level of hypoxia, suggesting underlying mutational processes for these signatures. At the gene level, driver mutations in TP53, MYC and PTEN are enriched in hypoxic tumours, and mutations in PTEN interact with hypoxia to direct tumour evolutionary trajectories. Overall, hypoxia plays a critical role in shaping the genomic and evolutionary landscapes of cancer.
Published: 2023
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42. Genomic footprints of activated telomere maintenance mechanisms in cancer

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Nakagawa, Hidewaki, Navarro, Fabio CP, Ossowski, Stephan, Pearson, John V, Puiggròs, Montserrat, Rippe, Karsten, Roberts, Nicola D, Roberts, Steven A, Rodriguez-Martin, Bernardo, Schumacher, Steven E, Scully, Ralph, Shackleton, Mark, Sidiropoulos, Nikos, Stewart, Chip, Torrents, David, MC Tubio, Jose, Villasante, Izar, Waddell, Nicola, Wala, Jeremiah A, Weischenfeldt, Joachim, Yang, Lixing, Yao, Xiaotong, Yoon, Sung-Soo, Zamora, Jorge, Zhang, Cheng-Zhong, Aaltonen, Lauri A, Abascal, Federico, Abeshouse, Adam, Aburatani, Hiroyuki, Adams, David J, Agrawal, Nishant, Ahn, Keun Soo, Ahn, Sung-Min, Aikata, Hiroshi, Akbani, Rehan, Al-Ahmadie, Hikmat, Al-Sedairy, Sultan T, Al-Shahrour, Fatima, Alawi, Malik, Albert, Monique, Aldape, Kenneth, Alexandrov, Ludmil B, Ally, Adrian, Alsop, Kathryn, Amary, Fernanda, Amin, Samirkumar B, Aminou, Brice, Ammerpohl, Ole, Anderson, Matthew J, Ang, Yeng, Antonello, Davide, Anur, Pavana, Aparicio, Samuel, Appelbaum, Elizabeth L, Arai, Yasuhito, Aretz, Axel, 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Okusaka, Takuji, Omberg, Larsson, Ong, Choon Kiat, Ott, German, Ouellette, BF Francis, P’ng, Christine, Paczkowska, Marta, Paiella, Salvatore, Pairojkul, Chawalit, Pajic, Marina, Pan-Hammarström, Qiang, Papaemmanuil, Elli, Papatheodorou, Irene, Paramasivam, Nagarajan, Park, Ji Wan, Park, Joong-Won, Park, Keunchil, Park, Kiejung, Parker, Joel S, Parsons, Simon L, Pass, Harvey, Pasternack, Danielle, Pastore, Alessandro, Patch, Ann-Marie, Pauporté, Iris, Pea, Antonio, Pedamallu, Chandra Sekhar, Pedersen, Jakob Skou, Pederzoli, Paolo, Peifer, Martin, Pennell, Nathan A, Perou, Charles M, Perry, Marc D, Petersen, Gloria M, Peto, Myron, Petrelli, Nicholas, Petryszak, Robert, Pfister, Stefan M, Phillips, Mark, Pich, Oriol, Pickett, Hilda A, Pihl, Todd D, Pillay, Nischalan, Pinder, Sarah, Pinese, Mark, Pinho, Andreia V, Pitkänen, Esa, Pivot, Xavier, Piñeiro-Yáñez, Elena, Planko, Laura, Plass, Christoph, Polak, Paz, Pons, Tirso, Popescu, Irinel, Potapova, Olga, Prasad, Aparna, Preston, Shaun R, Prinz, Manuel, Pritchard, Antonia L, Prokopec, Stephenie D, Provenzano, Elena, Puente, Xose S, Puig, Sonia, Pulido-Tamayo, Sergio, Pupo, Gulietta M, Purdie, Colin A, Quinn, Michael C, Rabionet, Raquel, Rader, Janet S, Radlwimmer, Bernhard, Radovic, Petar, Raeder, Benjamin, Raine, Keiran M, Ramakrishna, Manasa, Ramakrishnan, Kamna, Ramalingam, Suresh, Raphael, Benjamin J, Rathmell, W Kimryn, Rausch, Tobias, Reifenberger, Guido, Reimand, Jüri, Reis-Filho, Jorge, Reuter, Victor, Reyes-Salazar, Iker, Reyna, Matthew A, Reynolds, Sheila M, Rheinbay, Esther, Riazalhosseini, Yasser, Richardson, Andrea L, Richter, Julia, Ringel, Matthew, Ringnér, Markus, Rino, Yasushi, Roach, Jeffrey, Roberts, Lewis R, Robertson, A Gordon, Robertson, Alan J, Rodriguez, Javier Bartolomé, Rodríguez-González, F Germán, Roehrl, Michael HA, Rohde, Marius, Rokutan, Hirofumi, Romieu, Gilles, Rooman, Ilse, Roques, Tom, Rosebrock, Daniel, Rosenberg, Mara, Rosenstiel, Philip C, Rosenwald, Andreas, Rowe, Edward W, Royo, Romina, Rozen, Steven G, Rubanova, Yulia, Rubin, Mark A, Rubio-Perez, Carlota, Rudneva, Vasilisa A, Rusev, Borislav C, Ruzzenente, Andrea, Rätsch, Gunnar, Sabarinathan, Radhakrishnan, Sabelnykova, Veronica Y, Sadeghi, Sara, Sahinalp, S Cenk, Saini, Natalie, Saito-Adachi, Mihoko, Saksena, Gordon, Salcedo, Adriana, Salgado, Roberto, Salichos, Leonidas, Sallari, Richard, Saller, Charles, Salvia, Roberto, Sam, Michelle, Samra, Jaswinder S, Sanchez-Vega, Francisco, Sander, Chris, Sanders, Grant, Sarin, Rajiv, Sarrafi, Iman, Sasaki-Oku, Aya, Sauer, Torill, Sauter, Guido, Saw, Robyn PM, Scardoni, Maria, Scarlett, Christopher J, Scarpa, Aldo, Scelo, Ghislaine, Schadendorf, Dirk, Schein, Jacqueline E, Schilhabel, Markus B, Schlomm, Thorsten, Schmidt, Heather K, Schramm, Sarah-Jane, Schreiber, Stefan, Schultz, Nikolaus, Schwarz, Roland F, Scolyer, Richard A, Scott, David, Seethala, Raja, Segre, Ayellet V, Selander, Iris, Semple, Colin A, Senbabaoglu, Yasin, Sengupta, Subhajit, Sereni, Elisabetta, Serra, Stefano, Sgroi, Dennis C, Shah, Nimish C, Shahabi, Sagedeh, Shang, Catherine A, Shang, Ping, Shapira, Ofer, Shelton, Troy, Shen, Ciyue, Shen, Hui, Shepherd, Rebecca, Shi, Ruian, Shi, Yan, Shiah, Yu-Jia, Shibata, Tatsuhiro, Shih, Juliann, Shimizu, Eigo, Shimizu, Kiyo, Shin, Seung Jun, Shiraishi, Yuichi, Shmaya, Tal, Shmulevich, Ilya, Shorser, Solomon I, Short, Charles, Shrestha, Raunak, Shringarpure, Suyash S, Shriver, Craig, Shuai, Shimin, Siebert, Reiner, Sieuwerts, Anieta M, Signoretti, Sabina, Sikora, Katarzyna O, Simbolo, Michele, Simon, Ronald, Simons, Janae V, Simpson, Jared T, Simpson, Peter T, Singer, Samuel, Sinnott-Armstrong, Nasa, Sipahimalani, Payal, Skelly, Tara J, Smid, Marcel, Smith, Jaclyn, Smith-McCune, Karen, Socci, Nicholas D, Sofia, Heidi J, Soloway, Matthew G, Song, Lei, Sood, Anil K, Sothi, Sharmila, Sotiriou, Christos, Soulette, Cameron M, Span, Paul N, Spellman, Paul T, Sperandio, Nicola, Spillane, Andrew J, Spiro, Oliver, Spring, Jonathan, Staaf, Johan, Stadler, Peter F, Staib, Peter, Stark, Stefan G, Stebbings, Lucy, Stefánsson, Ólafur Andri, Stegle, Oliver, Stein, Lincoln D, Stenhouse, Alasdair, Stilgenbauer, Stephan, Stobbe, Miranda D, Stratton, Michael R, Stretch, Jonathan R, Struck, Adam J, Stuart, Joshua M, Stunnenberg, Henk G, Su, Hong, Su, Xiaoping, Sun, Ren X, Sungalee, Stephanie, Susak, Hana, Suzuki, Akihiro, Sweep, Fred, Szczepanowski, Monika, Sültmann, Holger, Yugawa, Takashi, Tam, Angela, Tamborero, David, Tan, Benita Kiat Tee, Tan, Donghui, Tan, Patrick, Tanaka, Hiroko, Taniguchi, Hirokazu, Tanskanen, Tomas J, Tarabichi, Maxime, Tarnuzzer, Roy, Tarpey, Patrick, Taschuk, Morgan L, Tatsuno, Kenji, Tavaré, Simon, Taylor, Darrin F, Taylor-Weiner, Amaro, Teague, Jon W, Teh, Bin Tean, Tembe, Varsha, Temes, Javier, Thai, Kevin, Thayer, Sarah P, Thiessen, Nina, Thomas, Gilles, Thomas, Sarah, Thompson, Alan, Thompson, Alastair M, Thompson, John FF, Thompson, R Houston, Thorne, Heather, Thorne, Leigh B, Thorogood, Adrian, Tiao, Grace, Tijanic, Nebojsa, Timms, Lee E, Tirabosco, Roberto, Tojo, Marta, Tommasi, Stefania, Toon, Christopher W, Toprak, Umut H, Tortora, Giampaolo, Tost, Jörg, Totoki, Yasushi, Townend, David, Traficante, Nadia, Treilleux, Isabelle, Trotta, Jean-Rémi, Trümper, Lorenz HP, Tsao, Ming, Tsunoda, Tatsuhiko, Tucker, Olga, Turkington, Richard, Turner, Daniel J, Tutt, Andrew, Ueno, Masaki, Ueno, Naoto T, Umbricht, Christopher, Umer, Husen M, Underwood, Timothy J, Urban, Lara, Urushidate, Tomoko, Ushiku, Tetsuo, Uusküla-Reimand, Liis, Valencia, Alfonso, Van Den Berg, David J, Van Laere, Steven, Van Loo, Peter, Van Meir, Erwin G, Van den Eynden, Gert G, Van der Kwast, Theodorus, Vasudev, Naveen, Vazquez, Miguel, Vedururu, Ravikiran, Veluvolu, Umadevi, Vembu, Shankar, Verbeke, Lieven PC, Vermeulen, Peter, Verrill, Clare, Viari, Alain, Vicente, David, Vicentini, Caterina, VijayRaghavan, K, Viksna, Juris, Vilain, Ricardo E, Vincent-Salomon, Anne, Visakorpi, Tapio, Voet, Douglas, Vyas, Paresh, Vázquez-García, Ignacio, Waddell, Nick M, Wadelius, Claes, Wadi, Lina, Wagener, Rabea, Wang, Jian, Wang, Jiayin, Wang, Linghua, Wang, Qi, Wang, Wenyi, Wang, Yumeng, Wang, Zhining, Waring, Paul M, Warnatz, Hans-Jörg, Warrell, Jonathan, Warren, Anne Y, Waszak, Sebastian M, Wedge, David C, Weichenhan, Dieter, Weinberger, Paul, Weinstein, John N, Weisenberger, Daniel J, Welch, Ian, Wendl, Michael C, Werner, Johannes, Whalley, Justin P, Wheeler, David A, Whitaker, Hayley C, Wigle, Dennis, Wilkerson, Matthew D, Williams, Ashley, Wilmott, James S, Wilson, Gavin W, Wilson, Julie M, Wilson, Richard K, Winterhoff, Boris, Wintersinger, Jeffrey A, Wiznerowicz, Maciej, Wolf, Stephan, Wong, Bernice H, Wong, Tina, Wong, Winghing, Woo, Youngchoon, Wood, Scott, Wouters, Bradly G, Wright, Adam J, Wright, Derek W, Wright, Mark H, Wu, Chin-Lee, Wu, Dai-Ying, Wu, Guanming, Wu, Jianmin, Wu, Kui, Wu, Yang, Wu, Zhenggang, Xi, Liu, Xia, Tian, Xiang, Qian, Xiao, Xiao, Xing, Rui, Xiong, Heng, Xu, Qinying, Xu, Yanxun, Xue, Hong, Yachida, Shinichi, Yakneen, Sergei, Yamaguchi, Rui, Yamaguchi, Takafumi N, Yamamoto, Masakazu, Yamamoto, Shogo, Yamaue, Hiroki, Yang, Fan, Yang, Huanming, Yang, Jean Y, Yang, Liming, Yang, Shanlin, Yang, Tsun-Po, Yang, Yang, Yaspo, Marie-Laure, Yates, Lucy, Yau, Christina, Ye, Chen, Ye, Kai, Yellapantula, Venkata D, Yoon, Christopher J, Yousif, Fouad, Yu, Jun, Yu, Kaixian, Yu, Willie, Yu, Yingyan, Yuan, Ke, Yuan, Yuan, Yuen, Denis, Yung, Christina K, Zaikova, Olga, Zapatka, Marc, Zenklusen, Jean C, Zenz, Thorsten, Zeps, Nikolajs, Zhang, Fan, Zhang, Hailei, Zhang, Hongwei, Zhang, Hongxin, Zhang, Jiashan, Zhang, Jing, Zhang, Junjun, Zhang, Xiuqing, Zhang, Xuanping, Zhang, Yan, Zhang, Zemin, Zhao, Zhongming, Zheng, Liangtao, Zheng, Xiuqing, Zhou, Wanding, Zhou, Yong, Zhu, Bin, Zhu, Hongtu, Zhu, Jingchun, Zhu, Shida, Zou, Lihua, Zou, Xueqing, deFazio, Anna, van As, Nicholas, van Deurzen, Carolien HM, van de Vijver, Marc J, Veer, L van’t, and von Mering, Christian
Subjects: Human Biology & Physiology, Ecology,Evolution & Ethology, Tumour Biology, Genetics & Genomics, Structural Biology & Biophysics, Computational & Systems Biology
Abstract: Cancers require telomere maintenance mechanisms for unlimited replicative potential. They achieve this through TERT activation or alternative telomere lengthening associated with ATRX or DAXX loss. Here, as part of the ICGC/TCGA Pan-Cancer Analysis of Whole Genomes (PCAWG) Consortium, we dissect whole-genome sequencing data of over 2500 matched tumor-control samples from 36 different tumor types aggregated within the ICGC/TCGA Pan-Cancer Analysis of Whole Genomes (PCAWG) Consortium to characterize the genomic footprints of these mechanisms. While the telomere content of tumors with ATRX or DAXX mutations (ATRX/DAXXtrunc) is increased, tumors with TERT modifications show a moderate decrease of telomere content. One quarter of all tumor samples contain somatic integrations of telomeric sequences into non-telomeric DNA. This fraction is increased to 80% prevalence in ATRX/DAXXtrunc tumors, which carry an aberrant telomere variant repeat (TVR) distribution as another genomic marker. The latter feature includes enrichment or depletion of the previously undescribed singleton TVRs TTCGGG and TTTGGG, respectively. Our systematic analysis provides new insight into the recurrent genomic alterations associated with telomere maintenance mechanisms in cancer.
Published: 2023
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43. Genomic hallmarks of localized, non-indolent prostate cancer

Author: Fraser, Michael, Sabelnykova, Veronica Y., Yamaguchi, Takafumi N., Heisler, Lawrence E., Livingstone, Julie, Huang, Vincent, Shiah, Yu-Jia, Yousif, Fouad, Lin, Xihui, Masella, Andre P., Fox, Natalie S., Xie, Michael, Prokopec, Stephenie D., Berlin, Alejandro, Lalonde, Emilie, Ahmed, Musaddeque, Trudel, Dominique, Luo, Xuemei, Beck, Timothy A., Meng, Alice, Zhang, Junyan, DʼCosta, Alister, Denroche, Robert E., Kong, Haiying, Espiritu, Shadrielle Melijah G., Chua, Melvin L. K., Wong, Ada, Chong, Taryne, Sam, Michelle, Johns, Jeremy, Timms, Lee, Buchner, Nicholas B., Orain, Michèle, Picard, Valérie, Hovington, Helène, Murison, Alexander, Kron, Ken, Harding, Nicholas J., Pʼng, Christine, Houlahan, Kathleen E., Chu, Kenneth C., Lo, Bryan, Nguyen, Francis, Li, Constance H., Sun, Ren X., de Borja, Richard, Cooper, Christopher I., Hopkins, Julia F., Govind, Shaylan K., Fung, Clement, Waggott, Daryl, Green, Jeffrey, Haider, Syed, Chan-Seng-Yue, Michelle A., Jung, Esther, Wang, Zhiyuan, Bergeron, Alain, Pra, Alan Dal, Lacombe, Louis, Collins, Colin C., Sahinalp, Cenk, Lupien, Mathieu, Fleshner, Neil E., He, Housheng H., Fradet, Yves, Tetu, Bernard, van der Kwast, Theodorus, McPherson, John D., Bristow, Robert G., and Boutros, Paul C.
Published: 2017
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44. Cut homeobox 1 causes chromosomal instability by promoting bipolar division after cytokinesis failure

Author: Sansregret, Laurent, Vadnais, Charles, Livingstone, Julie, Kwiatkowski, Nicholas, Awan, Arif, Cadieux, Chantal, Leduy, Lam, Hallett, Michael T., Nepveu, Alain, and Cavenee, Webster K.
Published: 2011

45. Tumor cell total mRNA expression shapes the molecular and clinical phenotype of cancer

Author: Cao, Shaolong, primary, Wang, Jennifer, additional, Ji, Shuangxi, additional, Yang, Peng, additional, Montierth, Matthew, additional, Guo, Shuai, additional, Shen, John Paul, additional, Zhao, Xiao, additional, Chen, Jingxiao, additional, Lee, Jaewon, additional, Guerrero, Paola, additional, Spetsieris, Nicholas, additional, Engedal, Nikolai, additional, Taavitsainen, Sinja, additional, Yu, Kaixian, additional, Livingstone, Julie, additional, Bhandari, Vinayak, additional, Hubert, Shawna, additional, Daw, Najat, additional, Futreal, Andrew, additional, Efstathiou, Eleni, additional, Lim, Bora, additional, Viale, Andrea, additional, Zhang, Jianjun, additional, Nykter, Matti, additional, Czerniak, Bogdan, additional, Msaouel, Pavlos, additional, Maitra, Anirban, additional, Kopetz, Scott, additional, Campbell, Peter, additional, Speed, Terence, additional, Boutros, Paul, additional, Zhu, Hongtu, additional, Urbanucci, Alfonso, additional, Demeulemeester, Jonas, additional, Loo, Peter Van, additional, and Wang, Wenyi, additional
Published: 2021
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46. The Telomere Length Landscape of Localized Prostate Cancer

Author: Livingstone, Julie, primary, Shiah, Yu-Jia, additional, Yamaguchi, Takafumi N., additional, Heisler, Lawrence E., additional, Huang, Vincent, additional, Lesurf, Robert, additional, Drysdale, Erik, additional, Green, Jeffrey, additional, van der Kwast, Theodorus, additional, Bristow, Robert G., additional, Fraser, Michael, additional, and Boutros, Paul C., additional
Published: 2021
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47. Methylation Subtypes of Primary Prostate Cancer Predict Poor Prognosis.

Author: Xiaoyu Wang, Jordahl, Kristina M., Chenghao Zhu, Livingstone, Julie, Rhie, Suhn K., Wright, Jonathan L., Grady, William M., Boutros, Paul C., Stanford, Janet L., and Dai, James Y.
Abstract: Background: Patients with prostate cancer experience heterogeneous outcomes after radical prostatectomy. Genomic studies including The Cancer Genome Atlas (TCGA) have reported molecular signatures of prostate cancer, but few studies have assessed the prognostic effects of DNA methylation profiles. Methods: We conducted the largest methylome subtyping analysis for primary prostate tumors to date, using methylome data from three patient populations: TCGA, a prostate cancer cohort study conducted at the Fred Hutchinson Cancer Research Center (FH; Seattle, WA), and the Canadian International Cancer Genome Consortium (ICGC) cohort. Four subtypes were detected in the TCGA dataset, then independently assigned to FH and ICGC cohort data. The identified methylation subtypes were assessed for association with cancer prognosis in the above three patient populations. Results: Using a set of hypermethylated CpG sites, four methylation subtypes were identified in TCGA. Compared with subtype 1, subtype 4 had an HR of 2.09 (P = 0.029) for biochemical recurrence (BCR) in TCGA patients. HRs of 2.76 (P = 0.002) for recurrence and 9.73 (P = 0.002) for metastatic-lethal (metastasis or prostate cancer-specific death) outcomes were observed in the FH cohort. A similar pattern of association was noted in the Canadian ICGC cohort, though HRs were not statistically significant. Conclusions: A hypermethylated subtype was associated with an increased hazard of recurrence and mortality in three studies with prostate tumor methylome data. Further molecular work is needed to understand the effect of methylation subtypes on cancer prognosis. Impact: This study identified a DNA methylation subtype that was associated with worse prostate cancer prognosis after radical prostatectomy. [ABSTRACT FROM AUTHOR]
Published: 2022
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48. Abstract IA-018: Molecular landmarks of tumor hypoxia across cancer types

Author: Bhandari, Vinayak, primary, Hoey, Christianne, additional, Liu, Lydia, additional, Lalonde, Emilie, additional, Ray, Jessica, additional, Livingstone, Julie, additional, Lesurf, Robert, additional, Shiah, Yu-Jia, additional, Vujcic, Tina, additional, Huang, Xiaoyong, additional, Espiritu, Shadrielle M.G., additional, Heisler, Lawrence E., additional, Yousif, Fouad, additional, Huang, Vincent, additional, Yamaguchi, Takafumi N., additional, Yao, Cindy Q., additional, Sabelnykova, Veronica Y., additional, Fraser, Michael, additional, Chua, Melvin L.K., additional, van der Kwast, Theodorus, additional, Liu, Stanley K., additional, Boutros, Paul C., additional, and Bristow, Robert G., additional
Published: 2021
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49. Abstract PO052: Uncovering the evolution of Glioblastoma proteome landscape from primary to the recurrent stage for development of novel diagnostic and predictive biomarkers

Author: Tatari, Nazanin, primary, Khan, Shahbaz, additional, Livingstone, Julie, additional, Venugopal, Chitra, additional, Chan, Jennifer, additional, Hawkins, Cynthia, additional, Provias, John, additional, Lu, Jian-Qiang, additional, Ask, Kjetil, additional, Kislinger, Thomas, additional, and Singh, Sheila, additional
Published: 2021
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50. Molecular Profiles of Prostate Cancer in Men of Middle Eastern Ancestry Identifies Key Differences with Western Populations: A Multiethnic SNP Array Study

Author: Albawardi, Alia, primary, Livingstone, Julie, additional, Al Marzooqi, Saeeda, additional, Houlahan, Kathleen, additional, Awwad, Aktham Adnan Ahmad, additional, Abdelsalam, Ramy, additional, Boutros, Paul, additional, and Bismar, Tarek A, additional
Published: 2021
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