Author: "Chin, L" / Topic: neoplasms - Searchworks@Jio Institute Digital Library Search Results

40 results on '"Chin, L"'

1. Treatment times for delivering adjuvant breast radiotherapy at a cancer centre in Ontario, Canada.

Author: Chan S, MacKenzie S, Bosnic S, Wong G, Zhang L, Finkelstein S, Lam E, Russell S, Gallant F, Wronski M, Leung E, Chow E, and Chin L
Subjects: Humans, Middle Aged, Ontario, Radiotherapy, Adjuvant, Breath Holding, Time Factors, Neoplasms
Abstract: Background: Time is a valuable commodity that impacts hospital flow, patient experience and economic resources. This study aims to identify factors that affect daily treatment time over a course of radiation therapy (RT) in patients who underwent adjuvant breast RT., Methods: In all adjuvant breast/chestwall RT patients treated from October 2017 to May 2018, daily set-up, beam delivery time, and overall treatment times were collected. A multivariable linear regression analysis was conducted to identify significant predictive factors related to treatment time. A general linear regression model was used to determine whether there was a learning curve effect throughout the course of treatment that decreased treatment time as patient and staff familiarity with the treatment procedure increased., Results: A total of 567 patients were included with a median age of 61 years. The average overall treatment time for 2-field and 4-field RT was 8.3 (SD 2.4) and 13.1 (SD 5.6) minutes, respectively. Factors that significantly increased overall treatment times in patients prescribed 2-field RT were: bilateral techniques, breath-hold (BH) techniques, prone techniques (PR), reverse decubitus techniques (RD), wide tangents techniques, the use of bolus and number of segments delivered. (p < 0.05). Factors that significantly increased overall treatment times in patients who received 3-field and 4-field RT were: wide tangents volumes, a higher number of monitor units (MUs), bilateral techniques and BH techniques (p < 0.05). Older patients (≥60) who underwent 3-field and 4-field RT demonstrated a statistically significant increase in set-up time (p < 0.0001). Overall treatment time decreased from 10.0 to 9.3 min over the course of treatment, suggesting a minor learning curve (p = 0.009)., Conclusion: The use of bilateral RT, BH, PR, RD, wide tangents, bolus, increasing treatment volumes, and increasing plan complexity were associated with increased treatment times. Future research should quantify the impact of other factors (BMI, mobility, patient care assessments, and imaging protocols) and utility of technological tools (time-predicting models, machine learning tools, and operations research models) on treatment time to optimize RT scheduling and improve resource management., (Copyright © 2023. Published by Elsevier Inc.)
Published: 2023
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2. Stiff matrix induces exosome secretion to promote tumour growth.

Author: Wu B, Liu DA, Guan L, Myint PK, Chin L, Dang H, Xu Y, Ren J, Li T, Yu Z, Jabban S, Mills GB, Nukpezah J, Chen YH, Furth EE, Gimotty PA, Wells RG, Weaver VM, Radhakrishnan R, Wang XW, and Guo W
Subjects: Humans, Proteomics, Extracellular Matrix metabolism, Signal Transduction, Tumor Microenvironment, Exosomes metabolism, Neoplasms metabolism
Abstract: Tissue fibrosis and extracellular matrix (ECM) stiffening promote tumour progression. The mechanisms by which ECM regulates its contacting cells have been extensively studied. However, how stiffness influences intercellular communications in the microenvironment for tumour progression remains unknown. Here we report that stiff ECM stimulates the release of exosomes from cancer cells. We delineate a molecular pathway that links stiff ECM to activation of Akt, which in turn promotes GTP loading to Rab8 that drives exosome secretion. We further show that exosomes generated from cells grown on stiff ECM effectively promote tumour growth. Proteomic analysis revealed that the Notch signalling pathway is activated in cells treated with exosomes derived from tumour cells grown on stiff ECM, consistent with our gene expression analysis of liver tissues from patients. Our study reveals a molecular mechanism that regulates exosome secretion and provides insight into how mechanical properties of the ECM control the tumour microenvironment for tumour growth., (© 2023. The Author(s), under exclusive licence to Springer Nature Limited.)
Published: 2023
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3. A functional genomic approach to actionable gene fusions for precision oncology.

Author: Li J, Lu H, Ng PK, Pantazi A, Ip CKM, Jeong KJ, Amador B, Tran R, Tsang YH, Yang L, Song X, Dogruluk T, Ren X, Hadjipanayis A, Bristow CA, Lee S, Kucherlapati M, Parfenov M, Tang J, Seth S, Mahadeshwar HS, Mojumdar K, Zeng D, Zhang J, Protopopov A, Seidman JG, Creighton CJ, Lu Y, Sahni N, Shaw KR, Meric-Bernstam F, Futreal A, Chin L, Scott KL, Kucherlapati R, Mills GB, and Liang H
Subjects: Gene Fusion, Genome, Genomics, Humans, Precision Medicine, Neoplasms genetics
Abstract: Fusion genes represent a class of attractive therapeutic targets. Thousands of fusion genes have been identified in patients with cancer, but the functional consequences and therapeutic implications of most of these remain largely unknown. Here, we develop a functional genomic approach that consists of efficient fusion reconstruction and sensitive cell viability and drug response assays. Applying this approach, we characterize ~100 fusion genes detected in patient samples of The Cancer Genome Atlas, revealing a notable fraction of low-frequency fusions with activating effects on tumor growth. Focusing on those in the RTK-RAS pathway, we identify a number of activating fusions that can markedly affect sensitivity to relevant drugs. Last, we propose an integrated, level-of-evidence classification system to prioritize gene fusions systematically. Our study reiterates the urgent clinical need to incorporate similar functional genomic approaches to characterize gene fusions, thereby maximizing the utility of gene fusions for precision oncology.
Published: 2022
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4. Preface.

Author: Curtis C and Chin L
Subjects: Humans, Artificial Intelligence, Machine Learning, Neoplasms
Published: 2021
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5. Reimagining Global Oncology Clinical Trials for the Postpandemic Era: A Call to Arms.

Author: Saini KS, de Las Heras B, Plummer R, Moreno V, Romano M, de Castro J, Aftimos P, Fredriksson J, Bhattacharyya GS, Olivo MS, Schiavon G, Punie K, Garcia-Foncillas J, Rogata E, Pfeiffer R, Orbegoso C, Morrison K, Curigliano G, Chin L, Saini ML, Rekdal Ø, Anderson S, Cortes J, Leone M, Dancey J, Twelves C, and Awada A
Subjects: Humans, Medical Oncology, Neoplasms therapy
Published: 2020
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6. Disruption of chromatin folding domains by somatic genomic rearrangements in human cancer.

Author: Akdemir KC, Le VT, Chandran S, Li Y, Verhaak RG, Beroukhim R, Campbell PJ, Chin L, Dixon JR, and Futreal PA
Subjects: Gene Expression Regulation, Neoplastic, Humans, Chromatin genetics, Gene Rearrangement genetics, Genome, Human genetics, Genomic Structural Variation, Neoplasms genetics
Abstract: Chromatin is folded into successive layers to organize linear DNA. Genes within the same topologically associating domains (TADs) demonstrate similar expression and histone-modification profiles, and boundaries separating different domains have important roles in reinforcing the stability of these features. Indeed, domain disruptions in human cancers can lead to misregulation of gene expression. However, the frequency of domain disruptions in human cancers remains unclear. Here, as part of the Pan-Cancer Analysis of Whole Genomes (PCAWG) Consortium of the International Cancer Genome Consortium (ICGC) and The Cancer Genome Atlas (TCGA), which aggregated whole-genome sequencing data from 2,658 cancers across 38 tumor types, we analyzed 288,457 somatic structural variations (SVs) to understand the distributions and effects of SVs across TADs. Notably, SVs can lead to the fusion of discrete TADs, and complex rearrangements markedly change chromatin folding maps in the cancer genomes. Notably, only 14% of the boundary deletions resulted in a change in expression in nearby genes of more than twofold.
Published: 2020
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7. Global impact of somatic structural variation on the DNA methylome of human cancers.

Author: Zhang Y, Yang L, Kucherlapati M, Hadjipanayis A, Pantazi A, Bristow CA, Lee EA, Mahadeshwar HS, Tang J, Zhang J, Seth S, Lee S, Ren X, Song X, Sun H, Seidman J, Luquette LJ, Xi R, Chin L, Protopopov A, Park PJ, Kucherlapati R, and Creighton CJ
Subjects: CpG Islands, Humans, Epigenome, Genomic Structural Variation, Neoplasms genetics
Abstract: Background: Genomic rearrangements exert a heavy influence on the molecular landscape of cancer. New analytical approaches integrating somatic structural variants (SSVs) with altered gene features represent a framework by which we can assign global significance to a core set of genes, analogous to established methods that identify genes non-randomly targeted by somatic mutation or copy number alteration. While recent studies have defined broad patterns of association involving gene transcription and nearby SSV breakpoints, global alterations in DNA methylation in the context of SSVs remain largely unexplored., Results: By data integration of whole genome sequencing, RNA sequencing, and DNA methylation arrays from more than 1400 human cancers, we identify hundreds of genes and associated CpG islands (CGIs) for which the nearby presence of a somatic structural variant (SSV) breakpoint is recurrently associated with altered expression or DNA methylation, respectively, independently of copy number alterations. CGIs with SSV-associated increased methylation are predominantly promoter-associated, while CGIs with SSV-associated decreased methylation are enriched for gene body CGIs. Rearrangement of genomic regions normally having higher or lower methylation is often involved in SSV-associated CGI methylation alterations. Across cancers, the overall structural variation burden is associated with a global decrease in methylation, increased expression in methyltransferase genes and DNA damage response genes, and decreased immune cell infiltration., Conclusion: Genomic rearrangement appears to have a major role in shaping the cancer DNA methylome, to be considered alongside commonly accepted mechanisms including histone modifications and disruption of DNA methyltransferases.
Published: 2019
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8. Applying Artificial Intelligence to Address the Knowledge Gaps in Cancer Care.

Author: Simon G, DiNardo CD, Takahashi K, Cascone T, Powers C, Stevens R, Allen J, Antonoff MB, Gomez D, Keane P, Suarez Saiz F, Nguyen Q, Roarty E, Pierce S, Zhang J, Hardeman Barnhill E, Lakhani K, Shaw K, Smith B, Swisher S, High R, Futreal PA, Heymach J, and Chin L
Subjects: Clinical Decision-Making methods, Clinical Trials as Topic, Electronic Health Records statistics & numerical data, Evidence-Based Medicine statistics & numerical data, Feasibility Studies, Humans, Medical Oncology statistics & numerical data, Neoplasms therapy, Patient Selection, Artificial Intelligence, Decision Support Systems, Clinical, Evidence-Based Medicine methods, Medical Oncology methods, Neoplasms diagnosis
Abstract: Background: Rapid advances in science challenge the timely adoption of evidence-based care in community settings. To bridge the gap between what is possible and what is practiced, we researched approaches to developing an artificial intelligence (AI) application that can provide real-time patient-specific decision support., Materials and Methods: The Oncology Expert Advisor (OEA) was designed to simulate peer-to-peer consultation with three core functions: patient history summarization, treatment options recommendation, and management advisory. Machine-learning algorithms were trained to construct a dynamic summary of patients cancer history and to suggest approved therapy or investigative trial options. All patient data used were retrospectively accrued. Ground truth was established for approximately 1,000 unique patients. The full Medline database of more than 23 million published abstracts was used as the literature corpus., Results: OEA's accuracies of searching disparate sources within electronic medical records to extract complex clinical concepts from unstructured text documents varied, with F1 scores of 90%-96% for non-time-dependent concepts (e.g., diagnosis) and F1 scores of 63%-65% for time-dependent concepts (e.g., therapy history timeline). Based on constructed patient profiles, OEA suggests approved therapy options linked to supporting evidence (99.9% recall; 88% precision), and screens for eligible clinical trials on ClinicalTrials.gov (97.9% recall; 96.9% precision)., Conclusion: Our results demonstrated technical feasibility of an AI-powered application to construct longitudinal patient profiles in context and to suggest evidence-based treatment and trial options. Our experience highlighted the necessity of collaboration across clinical and AI domains, and the requirement of clinical expertise throughout the process, from design to training to testing., Implications for Practice: Artificial intelligence (AI)-powered digital advisors such as the Oncology Expert Advisor have the potential to augment the capacity and update the knowledge base of practicing oncologists. By constructing dynamic patient profiles from disparate data sources and organizing and vetting vast literature for relevance to a specific patient, such AI applications could empower oncologists to consider all therapy options based on the latest scientific evidence for their patients, and help them spend less time on information "hunting and gathering" and more time with the patients. However, realization of this will require not only AI technology maturation but also active participation and leadership by clincial experts., Competing Interests: Disclosures of potential conflicts of interest may be found at the end of this article., (© AlphaMed Press 2018.)
Published: 2019
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9. A Pan-Cancer Compendium of Genes Deregulated by Somatic Genomic Rearrangement across More Than 1,400 Cases.

Author: Zhang Y, Yang L, Kucherlapati M, Chen F, Hadjipanayis A, Pantazi A, Bristow CA, Lee EA, Mahadeshwar HS, Tang J, Zhang J, Seth S, Lee S, Ren X, Song X, Sun H, Seidman J, Luquette LJ, Xi R, Chin L, Protopopov A, Li W, Park PJ, Kucherlapati R, and Creighton CJ
Subjects: Base Sequence, Carcinogenesis genetics, Carcinogenesis pathology, DNA Copy Number Variations genetics, Enhancer Elements, Genetic genetics, Humans, Gene Expression Regulation, Neoplastic, Gene Rearrangement genetics, Genes, Neoplasm, Genome, Human, Neoplasms genetics
Abstract: A systematic cataloging of genes affected by genomic rearrangement, using multiple patient cohorts and cancer types, can provide insight into cancer-relevant alterations outside of exomes. By integrative analysis of whole-genome sequencing (predominantly low pass) and gene expression data from 1,448 cancers involving 18 histopathological types in The Cancer Genome Atlas, we identified hundreds of genes for which the nearby presence (within 100 kb) of a somatic structural variant (SV) breakpoint is associated with altered expression. While genomic rearrangements are associated with widespread copy-number alteration (CNA) patterns, approximately 1,100 genes-including overexpressed cancer driver genes (e.g., TERT, ERBB2, CDK12, CDK4) and underexpressed tumor suppressors (e.g., TP53, RB1, PTEN, STK11)-show SV-associated deregulation independent of CNA. SVs associated with the disruption of topologically associated domains, enhancer hijacking, or fusion transcripts are implicated in gene upregulation. For cancer-relevant pathways, SVs considerably expand our understanding of how genes are affected beyond point mutation or CNA., (Copyright © 2018 The Author(s). Published by Elsevier Inc. All rights reserved.)
Published: 2018
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10. A Pan-Cancer Proteogenomic Atlas of PI3K/AKT/mTOR Pathway Alterations.

Author: Zhang Y, Kwok-Shing Ng P, Kucherlapati M, Chen F, Liu Y, Tsang YH, de Velasco G, Jeong KJ, Akbani R, Hadjipanayis A, Pantazi A, Bristow CA, Lee E, Mahadeshwar HS, Tang J, Zhang J, Yang L, Seth S, Lee S, Ren X, Song X, Sun H, Seidman J, Luquette LJ, Xi R, Chin L, Protopopov A, Westbrook TF, Shelley CS, Choueiri TK, Ittmann M, Van Waes C, Weinstein JN, Liang H, Henske EP, Godwin AK, Park PJ, Kucherlapati R, Scott KL, Mills GB, Kwiatkowski DJ, and Creighton CJ
Subjects: Databases, Genetic, Gene Expression Profiling, Humans, Mutation, Neoplasms metabolism, Signal Transduction, Survival Analysis, Neoplasms genetics, Phosphatidylinositol 3-Kinases metabolism, Proteogenomics, Proto-Oncogene Proteins c-akt metabolism, TOR Serine-Threonine Kinases metabolism
Abstract: Molecular alterations involving the PI3K/AKT/mTOR pathway (including mutation, copy number, protein, or RNA) were examined across 11,219 human cancers representing 32 major types. Within specific mutated genes, frequency, mutation hotspot residues, in silico predictions, and functional assays were all informative in distinguishing the subset of genetic variants more likely to have functional relevance. Multiple oncogenic pathways including PI3K/AKT/mTOR converged on similar sets of downstream transcriptional targets. In addition to mutation, structural variations and partial copy losses involving PTEN and STK11 showed evidence for having functional relevance. A substantial fraction of cancers showed high mTOR pathway activity without an associated canonical genetic or genomic alteration, including cancers harboring IDH1 or VHL mutations, suggesting multiple mechanisms for pathway activation., (Copyright © 2017 Elsevier Inc. All rights reserved.)
Published: 2017
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11. Integrated molecular analysis of tumor biopsies on sequential CTLA-4 and PD-1 blockade reveals markers of response and resistance.

Author: Roh W, Chen PL, Reuben A, Spencer CN, Prieto PA, Miller JP, Gopalakrishnan V, Wang F, Cooper ZA, Reddy SM, Gumbs C, Little L, Chang Q, Chen WS, Wani K, De Macedo MP, Chen E, Austin-Breneman JL, Jiang H, Roszik J, Tetzlaff MT, Davies MA, Gershenwald JE, Tawbi H, Lazar AJ, Hwu P, Hwu WJ, Diab A, Glitza IC, Patel SP, Woodman SE, Amaria RN, Prieto VG, Hu J, Sharma P, Allison JP, Chin L, Zhang J, Wargo JA, and Futreal PA
Subjects: Biomarkers, Tumor metabolism, Biopsy, CTLA-4 Antigen metabolism, Clone Cells, Cohort Studies, DNA Copy Number Variations genetics, Gene Dosage, Genome, Humans, Mutation genetics, Neoplasms genetics, Neoplasms immunology, Programmed Cell Death 1 Receptor metabolism, T-Lymphocytes immunology, CTLA-4 Antigen antagonists & inhibitors, Drug Resistance, Neoplasm, Neoplasms drug therapy, Neoplasms pathology, Programmed Cell Death 1 Receptor antagonists & inhibitors
Abstract: Immune checkpoint blockade produces clinical benefit in many patients. However, better biomarkers of response are still needed, and mechanisms of resistance remain incompletely understood. To address this, we recently studied a cohort of melanoma patients treated with sequential checkpoint blockade against cytotoxic T lymphocyte antigen-4 (CTLA-4) followed by programmed death receptor-1 (PD-1) and identified immune markers of response and resistance. Building on these studies, we performed deep molecular profiling including T cell receptor sequencing and whole-exome sequencing within the same cohort and demonstrated that a more clonal T cell repertoire was predictive of response to PD-1 but not CTLA-4 blockade. Analysis of CNAs identified a higher burden of copy number loss in nonresponders to CTLA-4 and PD-1 blockade and found that it was associated with decreased expression of genes in immune-related pathways. The effect of mutational load and burden of copy number loss on response was nonredundant, suggesting the potential utility of a combinatorial biomarker to optimize patient care with checkpoint blockade therapy., (Copyright © 2017, American Association for the Advancement of Science.)
Published: 2017
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12. Analysis of Immune Signatures in Longitudinal Tumor Samples Yields Insight into Biomarkers of Response and Mechanisms of Resistance to Immune Checkpoint Blockade.

Author: Chen PL, Roh W, Reuben A, Cooper ZA, Spencer CN, Prieto PA, Miller JP, Bassett RL, Gopalakrishnan V, Wani K, De Macedo MP, Austin-Breneman JL, Jiang H, Chang Q, Reddy SM, Chen WS, Tetzlaff MT, Broaddus RJ, Davies MA, Gershenwald JE, Haydu L, Lazar AJ, Patel SP, Hwu P, Hwu WJ, Diab A, Glitza IC, Woodman SE, Vence LM, Wistuba II, Amaria RN, Kwong LN, Prieto V, Davis RE, Ma W, Overwijk WW, Sharpe AH, Hu J, Futreal PA, Blando J, Sharma P, Allison JP, Chin L, and Wargo JA
Subjects: B7-H1 Antigen antagonists & inhibitors, Biopsy, CTLA-4 Antigen antagonists & inhibitors, Cluster Analysis, Gene Expression Profiling, Humans, Immunohistochemistry, Lymphocytes, Tumor-Infiltrating drug effects, Lymphocytes, Tumor-Infiltrating immunology, Lymphocytes, Tumor-Infiltrating metabolism, Melanoma drug therapy, Melanoma immunology, Melanoma metabolism, Neoplasms diagnosis, Neoplasms drug therapy, Prognosis, Programmed Cell Death 1 Receptor antagonists & inhibitors, T-Lymphocyte Subsets drug effects, T-Lymphocyte Subsets immunology, T-Lymphocyte Subsets metabolism, Antibodies, Monoclonal pharmacology, Antineoplastic Agents pharmacology, Biomarkers, Drug Resistance, Neoplasm, Immunomodulation drug effects, Neoplasms immunology, Neoplasms metabolism
Abstract: Unlabelled: Immune checkpoint blockade represents a major breakthrough in cancer therapy; however, responses are not universal. Genomic and immune features in pretreatment tumor biopsies have been reported to correlate with response in patients with melanoma and other cancers, but robust biomarkers have not been identified. We studied a cohort of patients with metastatic melanoma initially treated with cytotoxic T-lymphocyte-associated antigen-4 (CTLA4) blockade (n = 53) followed by programmed death-1 (PD-1) blockade at progression (n = 46), and analyzed immune signatures in longitudinal tissue samples collected at multiple time points during therapy. In this study, we demonstrate that adaptive immune signatures in tumor biopsy samples obtained early during the course of treatment are highly predictive of response to immune checkpoint blockade and also demonstrate differential effects on the tumor microenvironment induced by CTLA4 and PD-1 blockade. Importantly, potential mechanisms of therapeutic resistance to immune checkpoint blockade were also identified., Significance: These studies demonstrate that adaptive immune signatures in early on-treatment tumor biopsies are predictive of response to checkpoint blockade and yield insight into mechanisms of therapeutic resistance. These concepts have far-reaching implications in this age of precision medicine and should be explored in immune checkpoint blockade treatment across cancer types. Cancer Discov; 6(8); 827-37. ©2016 AACR.See related commentary by Teng et al., p. 818This article is highlighted in the In This Issue feature, p. 803., Competing Interests: No other potential conflicts of interest were disclosed., (©2016 American Association for Cancer Research.)
Published: 2016
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13. Polygenic in vivo validation of cancer mutations using transposons.

Author: Chew SK, Lu D, Campos LS, Scott KL, Saci A, Wang J, Collinson A, Raine K, Hinton J, Teague JW, Jones D, Menzies A, Butler AP, Gamble J, O'Meara S, McLaren S, Chin L, Liu P, and Futreal PA
Subjects: Animals, Carcinogenesis genetics, Cells, Cultured, Coculture Techniques, DNA Transposable Elements, Genetic Predisposition to Disease, Humans, Mice, Inbred NOD, Mice, SCID, Mice, Transgenic, Multifactorial Inheritance, Mutation, Neoplasm Transplantation, Genetic Association Studies methods, Neoplasms genetics
Abstract: The in vivo validation of cancer mutations and genes identified in cancer genomics is resource-intensive because of the low throughput of animal experiments. We describe a mouse model that allows multiple cancer mutations to be validated in each animal line. Animal lines are generated with multiple candidate cancer mutations using transposons. The candidate cancer genes are tagged and randomly expressed in somatic cells, allowing easy identification of the cancer genes involved in the generated tumours. This system presents a useful, generalised and efficient means for animal validation of cancer genes.
Published: 2014
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14. A systems biology approach to personalizing therapeutic combinations.

Author: Kwong LN, Heffernan TP, and Chin L
Subjects: Computer Simulation, Databases, Factual, Evidence-Based Medicine, Humans, Precision Medicine, Antineoplastic Combined Chemotherapy Protocols, Molecular Targeted Therapy methods, Neoplasms drug therapy, Neoplasms genetics, Systems Biology methods
Abstract: The identification of evidence-based, efficacious drug combinations for each cancer, among thousands of potential permutations, is a daunting task. In this perspective, we propose a systematic approach to defining such combinations by molecularly benchmarking a drug against a desired state of efficacy using model systems., (©2013 AACR.)
Published: 2013
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15. Emerging patterns of somatic mutations in cancer.

Author: Watson IR, Takahashi K, Futreal PA, and Chin L
Subjects: Exome genetics, High-Throughput Nucleotide Sequencing, Humans, Mutation, Mutation Rate, Sequence Analysis, DNA, Genome, Human genetics, Genomics methods, Neoplasms genetics
Abstract: Recent advances in technological tools for massively parallel, high-throughput sequencing of DNA have enabled the comprehensive characterization of somatic mutations in a large number of tumour samples. In this Review, we describe recent cancer genomic studies that have assembled emerging views of the landscapes of somatic mutations through deep-sequencing analyses of the coding exomes and whole genomes in various cancer types. We discuss the comparative genomics of different cancers, including mutation rates and spectra, as well as the roles of environmental insults that influence these processes. We highlight the developing statistical approaches that are used to identify significantly mutated genes, and discuss the emerging biological and clinical insights from such analyses, as well as the future challenges of translating these genomic data into clinical impacts.
Published: 2013
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16. Diverse mechanisms of somatic structural variations in human cancer genomes.

Author: Yang L, Luquette LJ, Gehlenborg N, Xi R, Haseley PS, Hsieh CH, Zhang C, Ren X, Protopopov A, Chin L, Kucherlapati R, Lee C, and Park PJ
Subjects: Chromosome Aberrations, Genome-Wide Association Study, Glioblastoma genetics, Humans, Neoplasms pathology, Algorithms, Genome, Human, Mutation, Neoplasms genetics
Abstract: Identification of somatic rearrangements in cancer genomes has accelerated through analysis of high-throughput sequencing data. However, characterization of complex structural alterations and their underlying mechanisms remains inadequate. Here, applying an algorithm to predict structural variations from short reads, we report a comprehensive catalog of somatic structural variations and the mechanisms generating them, using high-coverage whole-genome sequencing data from 140 patients across ten tumor types. We characterize the relative contributions of different types of rearrangements and their mutational mechanisms, find that ~20% of the somatic deletions are complex deletions formed by replication errors, and describe the differences between the mutational mechanisms in somatic and germline alterations. Importantly, we provide detailed reconstructions of the events responsible for loss of CDKN2A/B and gain of EGFR in glioblastoma, revealing that these alterations can result from multiple mechanisms even in a single genome and that both DNA double-strand breaks and replication errors drive somatic rearrangements., (Copyright © 2013 Elsevier Inc. All rights reserved.)
Published: 2013
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17. Recapitulating human cancer in a mouse.

Author: Chin L, de Sauvage F, Egeblad M, Olive KP, Tuveson D, and Weiss W
Subjects: Animals, Humans, Mice, Species Specificity, Disease Models, Animal, Medical Oncology trends, Neoplasms physiopathology, Neoplasms therapy, Translational Research, Biomedical trends
Published: 2013
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18. Phosphoglycerate dehydrogenase diverts glycolytic flux and contributes to oncogenesis.

Author: Locasale JW, Grassian AR, Melman T, Lyssiotis CA, Mattaini KR, Bass AJ, Heffron G, Metallo CM, Muranen T, Sharfi H, Sasaki AT, Anastasiou D, Mullarky E, Vokes NI, Sasaki M, Beroukhim R, Stephanopoulos G, Ligon AH, Meyerson M, Richardson AL, Chin L, Wagner G, Asara JM, Brugge JS, Cantley LC, and Vander Heiden MG
Subjects: Cell Proliferation, Cell Transformation, Neoplastic genetics, Cell Transformation, Neoplastic pathology, Humans, Neoplasms genetics, Neoplasms pathology, Cell Transformation, Neoplastic metabolism, Glucose metabolism, Glycolysis, Neoplasms metabolism, Phosphoglycerate Dehydrogenase metabolism
Abstract: Most tumors exhibit increased glucose metabolism to lactate, however, the extent to which glucose-derived metabolic fluxes are used for alternative processes is poorly understood. Using a metabolomics approach with isotope labeling, we found that in some cancer cells a relatively large amount of glycolytic carbon is diverted into serine and glycine metabolism through phosphoglycerate dehydrogenase (PHGDH). An analysis of human cancers showed that PHGDH is recurrently amplified in a genomic region of focal copy number gain most commonly found in melanoma. Decreasing PHGDH expression impaired proliferation in amplified cell lines. Increased expression was also associated with breast cancer subtypes, and ectopic expression of PHGDH in mammary epithelial cells disrupted acinar morphogenesis and induced other phenotypic alterations that may predispose cells to transformation. Our findings show that the diversion of glycolytic flux into a specific alternate pathway can be selected during tumor development and may contribute to the pathogenesis of human cancer.
Published: 2011
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19. Making sense of cancer genomic data.

Author: Chin L, Hahn WC, Getz G, and Meyerson M
Subjects: Animals, Databases, Genetic, Gene Expression Regulation, Neoplastic, Genes, Neoplasm genetics, Humans, MicroRNAs genetics, MicroRNAs metabolism, Genome genetics, Genome-Wide Association Study methods, Neoplasms genetics
Abstract: High-throughput tools for nucleic acid characterization now provide the means to conduct comprehensive analyses of all somatic alterations in the cancer genomes. Both large-scale and focused efforts have identified new targets of translational potential. The deluge of information that emerges from these genome-scale investigations has stimulated a parallel development of new analytical frameworks and tools. The complexity of somatic genomic alterations in cancer genomes also requires the development of robust methods for the interrogation of the function of genes identified by these genomics efforts. Here we provide an overview of the current state of cancer genomics, appraise the current portals and tools for accessing and analyzing cancer genomic data, and discuss emerging approaches to exploring the functions of somatically altered genes in cancer.
Published: 2011
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20. Cancer genomics: from discovery science to personalized medicine.

Author: Chin L, Andersen JN, and Futreal PA
Subjects: Humans, Neoplasms genetics, Genomics, Neoplasms therapy, Precision Medicine
Abstract: Recent advances in genome technologies and the ensuing outpouring of genomic information related to cancer have accelerated the convergence of discovery science and clinical medicine. Successful examples of translating cancer genomics into therapeutics and diagnostics reinforce its potential to make possible personalized cancer medicine. However, the bottlenecks along the path of converting a genome discovery into a tangible clinical endpoint are numerous and formidable. In this Perspective, we emphasize the importance of establishing the biological relevance of a cancer genomic discovery in realizing its clinical potential and discuss some of the major obstacles to moving from the bench to the bedside.
Published: 2011
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21. Towards patient-based cancer therapeutics.

Author: Schreiber SL, Shamji AF, Clemons PA, Hon C, Koehler AN, Munoz B, Palmer M, Stern AM, Wagner BK, Powers S, Lowe SW, Guo X, Krasnitz A, Sawey ET, Sordella R, Stein L, Trotman LC, Califano A, Dalla-Favera R, Ferrando A, Iavarone A, Pasqualucci L, Silva J, Stockwell BR, Hahn WC, Chin L, DePinho RA, Boehm JS, Gopal S, Huang A, Root DE, Weir BA, Gerhard DS, Zenklusen JC, Roth MG, White MA, Minna JD, MacMillan JB, and Posner BA
Subjects: Animals, Disease Models, Animal, Drug Discovery, Gene Regulatory Networks genetics, Humans, Mice, National Cancer Institute (U.S.), Neoplasm Proteins metabolism, Neoplasms genetics, RNA, Small Interfering metabolism, United States, Antineoplastic Agents therapeutic use, Neoplasms drug therapy, Precision Medicine
Published: 2010
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22. Non-germline genetically engineered mouse models for translational cancer research.

Author: Heyer J, Kwong LN, Lowe SW, and Chin L
Subjects: Animals, Humans, Translational Research, Biomedical, Animals, Genetically Modified, Disease Models, Animal, Germ-Line Mutation genetics, Mice genetics, Neoplasms genetics
Abstract: Genetically engineered mouse models (GEMMs) of cancer have affected virtually all areas of cancer research. However, the accelerated discovery of new cancer genes emerging from large-scale cancer genomics and new chemical entities pouring from the drug discovery pipeline have strained the capacity of traditional germline mouse models to provide crucial insights. This Review introduces new approaches to modelling cancer, with emphasis on a growing collection of non-germline GEMMs (nGEMMs). These offer flexibility, speed and uniformity at reduced costs, thus paving the way for much needed throughput and practical preclinical therapeutic testing models.
Published: 2010
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23. International network of cancer genome projects.

Author: Hudson TJ, Anderson W, Artez A, Barker AD, Bell C, Bernabé RR, Bhan MK, Calvo F, Eerola I, Gerhard DS, Guttmacher A, Guyer M, Hemsley FM, Jennings JL, Kerr D, Klatt P, Kolar P, Kusada J, Lane DP, Laplace F, Youyong L, Nettekoven G, Ozenberger B, Peterson J, Rao TS, Remacle J, Schafer AJ, Shibata T, Stratton MR, Vockley JG, Watanabe K, Yang H, Yuen MM, Knoppers BM, Bobrow M, Cambon-Thomsen A, Dressler LG, Dyke SO, Joly Y, Kato K, Kennedy KL, Nicolás P, Parker MJ, Rial-Sebbag E, Romeo-Casabona CM, Shaw KM, Wallace S, Wiesner GL, Zeps N, Lichter P, Biankin AV, Chabannon C, Chin L, Clément B, de Alava E, Degos F, Ferguson ML, Geary P, Hayes DN, Hudson TJ, Johns AL, Kasprzyk A, Nakagawa H, Penny R, Piris MA, Sarin R, Scarpa A, Shibata T, van de Vijver M, Futreal PA, Aburatani H, Bayés M, Botwell DD, Campbell PJ, Estivill X, Gerhard DS, Grimmond SM, Gut I, Hirst M, López-Otín C, Majumder P, Marra M, McPherson JD, Nakagawa H, Ning Z, Puente XS, Ruan Y, Shibata T, Stratton MR, Stunnenberg HG, Swerdlow H, Velculescu VE, Wilson RK, Xue HH, Yang L, Spellman PT, Bader GD, Boutros PC, Campbell PJ, Flicek P, Getz G, Guigó R, Guo G, Haussler D, Heath S, Hubbard TJ, Jiang T, Jones SM, Li Q, López-Bigas N, Luo R, Muthuswamy L, Ouellette BF, Pearson JV, Puente XS, Quesada V, Raphael BJ, Sander C, Shibata T, Speed TP, Stein LD, Stuart JM, Teague JW, Totoki Y, Tsunoda T, Valencia A, Wheeler DA, Wu H, Zhao S, Zhou G, Stein LD, Guigó R, Hubbard TJ, Joly Y, Jones SM, Kasprzyk A, Lathrop M, López-Bigas N, Ouellette BF, Spellman PT, Teague JW, Thomas G, Valencia A, Yoshida T, Kennedy KL, Axton M, Dyke SO, Futreal PA, Gerhard DS, Gunter C, Guyer M, Hudson TJ, McPherson JD, Miller LJ, Ozenberger B, Shaw KM, Kasprzyk A, Stein LD, Zhang J, Haider SA, Wang J, Yung CK, Cros A, Liang Y, Gnaneshan S, Guberman J, Hsu J, Bobrow M, Chalmers DR, Hasel KW, Joly Y, Kaan TS, Kennedy KL, Knoppers BM, Lowrance WW, Masui T, Nicolás P, Rial-Sebbag E, Rodriguez LL, Vergely C, Yoshida T, Grimmond SM, Biankin AV, Bowtell DD, Cloonan N, deFazio A, Eshleman JR, Etemadmoghadam D, Gardiner BB, Kench JG, Scarpa A, Sutherland RL, Tempero MA, Waddell NJ, Wilson PJ, McPherson JD, Gallinger S, Tsao MS, Shaw PA, Petersen GM, Mukhopadhyay D, Chin L, DePinho RA, Thayer S, Muthuswamy L, Shazand K, Beck T, Sam M, Timms L, Ballin V, Lu Y, Ji J, Zhang X, Chen F, Hu X, Zhou G, Yang Q, Tian G, Zhang L, Xing X, Li X, Zhu Z, Yu Y, Yu J, Yang H, Lathrop M, Tost J, Brennan P, Holcatova I, Zaridze D, Brazma A, Egevard L, Prokhortchouk E, Banks RE, Uhlén M, Cambon-Thomsen A, Viksna J, Ponten F, Skryabin K, Stratton MR, Futreal PA, Birney E, Borg A, Børresen-Dale AL, Caldas C, Foekens JA, Martin S, Reis-Filho JS, Richardson AL, Sotiriou C, Stunnenberg HG, Thoms G, van de Vijver M, van't Veer L, Calvo F, Birnbaum D, Blanche H, Boucher P, Boyault S, Chabannon C, Gut I, Masson-Jacquemier JD, Lathrop M, Pauporté I, Pivot X, Vincent-Salomon A, Tabone E, Theillet C, Thomas G, Tost J, Treilleux I, Calvo F, Bioulac-Sage P, Clément B, Decaens T, Degos F, Franco D, Gut I, Gut M, Heath S, Lathrop M, Samuel D, Thomas G, Zucman-Rossi J, Lichter P, Eils R, Brors B, Korbel JO, Korshunov A, Landgraf P, Lehrach H, Pfister S, Radlwimmer B, Reifenberger G, Taylor MD, von Kalle C, Majumder PP, Sarin R, Rao TS, Bhan MK, Scarpa A, Pederzoli P, Lawlor RA, Delledonne M, Bardelli A, Biankin AV, Grimmond SM, Gress T, Klimstra D, Zamboni G, Shibata T, Nakamura Y, Nakagawa H, Kusada J, Tsunoda T, Miyano S, Aburatani H, Kato K, Fujimoto A, Yoshida T, Campo E, López-Otín C, Estivill X, Guigó R, de Sanjosé S, Piris MA, Montserrat E, González-Díaz M, Puente XS, Jares P, Valencia A, Himmelbauer H, Quesada V, Bea S, Stratton MR, Futreal PA, Campbell PJ, Vincent-Salomon A, Richardson AL, Reis-Filho JS, van de Vijver M, Thomas G, Masson-Jacquemier JD, Aparicio S, Borg A, Børresen-Dale AL, Caldas C, Foekens JA, Stunnenberg HG, van't Veer L, Easton DF, Spellman PT, Martin S, Barker AD, Chin L, Collins FS, Compton CC, Ferguson ML, Gerhard DS, Getz G, Gunter C, Guttmacher A, Guyer M, Hayes DN, Lander ES, Ozenberger B, Penny R, Peterson J, Sander C, Shaw KM, Speed TP, Spellman PT, Vockley JG, Wheeler DA, Wilson RK, Hudson TJ, Chin L, Knoppers BM, Lander ES, Lichter P, Stein LD, Stratton MR, Anderson W, Barker AD, Bell C, Bobrow M, Burke W, Collins FS, Compton CC, DePinho RA, Easton DF, Futreal PA, Gerhard DS, Green AR, Guyer M, Hamilton SR, Hubbard TJ, Kallioniemi OP, Kennedy KL, Ley TJ, Liu ET, Lu Y, Majumder P, Marra M, Ozenberger B, Peterson J, Schafer AJ, Spellman PT, Stunnenberg HG, Wainwright BJ, Wilson RK, and Yang H
Subjects: DNA Methylation, DNA Mutational Analysis trends, Databases, Genetic, Genes, Neoplasm genetics, Genetics, Medical trends, Genomics trends, Humans, Intellectual Property, Mutation, Neoplasms classification, Neoplasms pathology, Neoplasms therapy, Genetics, Medical organization & administration, Genome, Human genetics, Genomics organization & administration, International Cooperation, Neoplasms genetics
Abstract: The International Cancer Genome Consortium (ICGC) was launched to coordinate large-scale cancer genome studies in tumours from 50 different cancer types and/or subtypes that are of clinical and societal importance across the globe. Systematic studies of more than 25,000 cancer genomes at the genomic, epigenomic and transcriptomic levels will reveal the repertoire of oncogenic mutations, uncover traces of the mutagenic influences, define clinically relevant subtypes for prognosis and therapeutic management, and enable the development of new cancer therapies.
Published: 2010
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24. Signaling from the Golgi: mechanisms and models for Golgi phosphoprotein 3-mediated oncogenesis.

Author: Scott KL and Chin L
Subjects: Carcinogens metabolism, Humans, Cell Transformation, Neoplastic, Golgi Apparatus metabolism, Membrane Proteins physiology, Neoplasms pathology, Oncogene Proteins physiology, Signal Transduction
Abstract: Golgi phosphoprotein 3 (GOLPH3; also known as GPP34/GMx33/MIDAS) represents an exciting new class of oncoproteins involved in vesicular trafficking. Encoded by a gene residing on human chromosome 5p13, which is frequently amplified in multiple solid tumor types, GOLPH3 was initially discovered as a phosphorylated protein localized to the Golgi apparatus. Recent functional, cell biological, and biochemical analyses show that GOLPH3 can function as an oncoprotein to promote cell transformation and tumor growth by enhancing activity of the mammalian target of rapamycin, a serine/threonine protein kinase known to regulate cell growth, proliferation, and survival. Although its precise mode of action in cancer remains to be elucidated, the fact that GOLPH3 has been implicated in protein trafficking, receptor recycling, and glycosylation points to potential links of these cellular processes to tumorigenesis. Understanding how these processes may be deregulated and contribute to cancer pathogenesis and drug response will uncover new avenues for therapeutic intervention.
Published: 2010
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25. A comprehensive catalogue of somatic mutations from a human cancer genome.

Author: Pleasance ED, Cheetham RK, Stephens PJ, McBride DJ, Humphray SJ, Greenman CD, Varela I, Lin ML, Ordóñez GR, Bignell GR, Ye K, Alipaz J, Bauer MJ, Beare D, Butler A, Carter RJ, Chen L, Cox AJ, Edkins S, Kokko-Gonzales PI, Gormley NA, Grocock RJ, Haudenschild CD, Hims MM, James T, Jia M, Kingsbury Z, Leroy C, Marshall J, Menzies A, Mudie LJ, Ning Z, Royce T, Schulz-Trieglaff OB, Spiridou A, Stebbings LA, Szajkowski L, Teague J, Williamson D, Chin L, Ross MT, Campbell PJ, Bentley DR, Futreal PA, and Stratton MR
Subjects: Adult, Cell Line, Tumor, DNA Damage genetics, DNA Mutational Analysis, DNA Repair genetics, Gene Dosage genetics, Humans, Loss of Heterozygosity genetics, Male, Melanoma etiology, Melanoma genetics, MicroRNAs genetics, Mutagenesis, Insertional genetics, Neoplasms etiology, Polymorphism, Single Nucleotide genetics, Precision Medicine, Sequence Deletion genetics, Ultraviolet Rays, Genes, Neoplasm genetics, Genome, Human genetics, Mutation genetics, Neoplasms genetics
Abstract: All cancers carry somatic mutations. A subset of these somatic alterations, termed driver mutations, confer selective growth advantage and are implicated in cancer development, whereas the remainder are passengers. Here we have sequenced the genomes of a malignant melanoma and a lymphoblastoid cell line from the same person, providing the first comprehensive catalogue of somatic mutations from an individual cancer. The catalogue provides remarkable insights into the forces that have shaped this cancer genome. The dominant mutational signature reflects DNA damage due to ultraviolet light exposure, a known risk factor for malignant melanoma, whereas the uneven distribution of mutations across the genome, with a lower prevalence in gene footprints, indicates that DNA repair has been preferentially deployed towards transcribed regions. The results illustrate the power of a cancer genome sequence to reveal traces of the DNA damage, repair, mutation and selection processes that were operative years before the cancer became symptomatic.
Published: 2010
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26. GOLPH3 modulates mTOR signalling and rapamycin sensitivity in cancer.

Author: Scott KL, Kabbarah O, Liang MC, Ivanova E, Anagnostou V, Wu J, Dhakal S, Wu M, Chen S, Feinberg T, Huang J, Saci A, Widlund HR, Fisher DE, Xiao Y, Rimm DL, Protopopov A, Wong KK, and Chin L
Subjects: Animals, Cell Line, Tumor drug effects, DNA-Binding Proteins genetics, Female, Gene Knockdown Techniques, Humans, Membrane Proteins genetics, Mice, Mice, Nude, Protein Kinases genetics, Saccharomyces cerevisiae genetics, TOR Serine-Threonine Kinases, Transcription Factors genetics, Antibiotics, Antineoplastic pharmacology, Membrane Proteins metabolism, Neoplasms physiopathology, Protein Kinases metabolism, Signal Transduction, Sirolimus pharmacology
Abstract: Genome-wide copy number analyses of human cancers identified a frequent 5p13 amplification in several solid tumour types, including lung (56%), ovarian (38%), breast (32%), prostate (37%) and melanoma (32%). Here, using integrative analysis of a genomic profile of the region, we identify a Golgi protein, GOLPH3, as a candidate targeted for amplification. Gain- and loss-of-function studies in vitro and in vivo validated GOLPH3 as a potent oncogene. Physically, GOLPH3 localizes to the trans-Golgi network and interacts with components of the retromer complex, which in yeast has been linked to target of rapamycin (TOR) signalling. Mechanistically, GOLPH3 regulates cell size, enhances growth-factor-induced mTOR (also known as FRAP1) signalling in human cancer cells, and alters the response to an mTOR inhibitor in vivo. Thus, genomic and genetic, biological, functional and biochemical data in yeast and humans establishes GOLPH3 as a new oncogene that is commonly targeted for amplification in human cancer, and is capable of modulating the response to rapamycin, a cancer drug in clinical use.
Published: 2009
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27. Translating insights from the cancer genome into clinical practice.

Author: Chin L and Gray JW
Subjects: Animals, Gene Amplification genetics, Humans, Mutation genetics, Neoplasms pathology, Neoplasms physiopathology, Translocation, Genetic genetics, Genome, Human genetics, Genomics trends, Neoplasms genetics, Neoplasms therapy
Abstract: Cancer cells have diverse biological capabilities that are conferred by numerous genetic aberrations and epigenetic modifications. Today's powerful technologies are enabling these changes to the genome to be catalogued in detail. Tomorrow is likely to bring a complete atlas of the reversible and irreversible alterations that occur in individual cancers. The challenge now is to work out which molecular abnormalities contribute to cancer and which are simply 'noise' at the genomic and epigenomic levels. Distinguishing between these will aid in understanding how the aberrations in a cancer cell collaborate to drive pathophysiology. Past successes in converting information from genomic discoveries into clinical tools provide valuable lessons to guide the translation of emerging insights from the genome into clinical end points that can affect the practice of cancer medicine.
Published: 2008
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28. High-resolution global profiling of genomic alterations with long oligonucleotide microarray.

Author: Brennan C, Zhang Y, Leo C, Feng B, Cauwels C, Aguirre AJ, Kim M, Protopopov A, and Chin L
Subjects: Animals, Cell Line, Tumor, DNA, Neoplasm genetics, Female, Gene Dosage, Humans, Male, Mice, Neoplasms, Experimental genetics, Nucleic Acid Hybridization, Polymerase Chain Reaction methods, Chromosome Aberrations, Computational Biology methods, Gene Expression Profiling methods, Neoplasms genetics, Oligonucleotide Array Sequence Analysis methods
Abstract: Cancer represents the phenotypic end point of multiple genetic lesions that endow cells with a full range of biological properties required for tumorigenesis. Among the hallmark features of the cancer genome are recurrent regional gains and losses that, upon detailed characterization, have provided highly productive discovery paths for new oncogenes and tumor suppressor genes. In this study, we describe the use of an oligonucleotide-based microarray platform and development of requisite assay conditions and bioinformatic mining tools that permits high-resolution genome-wide array-comparative genome hybridization profiling of human and mouse tumors. Using a commercially available 60-mer oligonucleotide microarray, we demonstrate that this platform provides sufficient sensitivity to detect single-copy difference in gene dosage of full complexity genomic DNA while offering high resolution. The commercial availability of the microarrays and associated reagents, along with the technical protocols and analytical tools described in this report, should provide investigators with the immediate capacity to perform DNA analysis of normal and diseased genomes in a global and detailed manner.
Published: 2004
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29. Telomere dysfunction provokes regional amplification and deletion in cancer genomes.

Author: O'Hagan RC, Chang S, Maser RS, Mohan R, Artandi SE, Chin L, and DePinho RA
Subjects: Animals, Chromosome Aberrations, DNA, Neoplasm genetics, Genes, p53, Genome, Humans, Mice, RNA genetics, Synteny, Telomerase genetics, Telomere genetics, Chromosomes, Mammalian genetics, Gene Amplification, Gene Deletion, Neoplasms genetics, Telomere metabolism
Abstract: Telomere dysfunction and associated fusion-breakage in the mouse encourages epithelial carcinogenesis and a more humanized genomic profile that includes nonreciprocal translocations (NRTs). Here, array comparative genomic hybridization was used to determine the pathogenic significance of NRTs and to determine whether telomere dysfunction also drives amplifications and deletions of cancer-relevant loci. Compared to tumors arising in mice with intact telomeres, tumors with telomere dysfunction possessed higher levels of genomic instability and showed numerous amplifications and deletions in regions syntenic to human cancer hotspots. These observations suggest that telomere-based crisis provides a mechanism of chromosomal instability, including regional amplifications and deletions, that drives carcinogenesis. This model provides a platform for discovery of genes responsible for the major cancers affecting aged humans.
Published: 2002
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30. Genetic analysis of Pten and Ink4a/Arf interactions in the suppression of tumorigenesis in mice.

Author: You MJ, Castrillon DH, Bastian BC, O'Hagan RC, Bosenberg MW, Parsons R, Chin L, and DePinho RA
Subjects: Adrenal Gland Neoplasms genetics, Adrenal Gland Neoplasms pathology, Animals, Cell Transformation, Neoplastic genetics, Chromosome Mapping, Chromosomes, Human, Pair 1, Crosses, Genetic, Cyclin-Dependent Kinase Inhibitor p16 deficiency, Cyclin-Dependent Kinase Inhibitor p16 genetics, Genes, Tumor Suppressor, Heterozygote, Humans, Mice, Mice, Inbred C57BL, Mice, Knockout, Neoplasms prevention & control, Nucleic Acid Hybridization, PTEN Phosphohydrolase, Phenotype, Pheochromocytoma genetics, Pheochromocytoma pathology, Phosphoric Monoester Hydrolases deficiency, Phosphoric Monoester Hydrolases genetics, Tumor Suppressor Proteins deficiency, Tumor Suppressor Proteins genetics, Chromosome Aberrations, Cyclin-Dependent Kinase Inhibitor p16 metabolism, Neoplasms genetics, Phosphoric Monoester Hydrolases metabolism, Tumor Suppressor Proteins metabolism
Abstract: Dual inactivation of PTEN and INK4a/ARF tumor suppressor genes is a common feature observed in a broad spectrum of human cancer types. To validate functional collaboration between these genes in tumor suppression, we examined the biological consequences of Pten and/or Ink4a/Arf deficiency in cells and mice. Relative to single mutant controls, Ink4a/Arf-/-Pten+/- mouse embryonic fibroblast cultures exhibited faster rates of growth in reduced serum, grew to higher saturation densities, produced more colonies upon low density seeding, and showed increased susceptibility to transformation by oncogenic H-Ras. Ink4a/Arf deficiency reduced tumor-free survival and shortened the latency of neoplasias associated with Pten heterozygosity, specifically pheochromocytoma, prostatic intraepithelial neoplasia, and endometrial hyperplasia. Compound mutant mice also exhibited an expanded spectrum of tumor types including melanoma and squamous cell carcinoma. Functional synergy between Ink4a/Arf and Pten manifested most prominently in the development of pheochromocytoma, prompting an analysis of genes and loci implicated in this rare human neoplasm. The classical pheochromocytoma genes Ret, Vhl, and Nf-1 remained intact, a finding consistent with the intersection of these genes with pathways engaged by Pten and Ink4a/Arf. Notably, conventional and array-comparative genomic hybridization revealed frequent loss of distal mouse chromosome 4 in a region syntenic to human chromosome 1p that is implicated in human pheochromocytoma. This study provides genetic evidence of collaboration between Pten and Ink4a/Arf in constraining the growth and oncogenic transformation of cultured cells and in suppressing a wide spectrum of tumors in vivo.
Published: 2002
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31. Telomere dysfunction alters the chemotherapeutic profile of transformed cells.

Author: Lee KH, Rudolph KL, Ju YJ, Greenberg RA, Cannizzaro L, Chin L, Weiler SR, and DePinho RA
Subjects: Animals, Cell Line, Transformed, Cisplatin pharmacology, Cyclin-Dependent Kinase Inhibitor p16 genetics, Cyclin-Dependent Kinase Inhibitor p16 physiology, Doxorubicin pharmacology, Etoposide pharmacology, Fluorouracil pharmacology, Mice, Proto-Oncogene Proteins c-myc genetics, RNA genetics, Telomerase genetics, Tumor Suppressor Protein p53 genetics, Tumor Suppressor Protein p53 physiology, ras Proteins genetics, Antineoplastic Agents pharmacology, Neoplasms drug therapy, RNA physiology, Telomerase physiology, Telomere physiology
Abstract: Telomerase inhibition has been touted as a novel cancer-selective therapeutic goal based on the observation of high telomerase levels in most cancers and the importance of telomere maintenance in long-term cellular growth and survival. Here, the impact of telomere dysfunction on chemotherapeutic responses was assessed in normal and neoplastic cells derived from telomerase RNA null (mTERC(-/-)) mice. Telomere dysfunction, rather than telomerase per se, was found to be the principal determinant governing chemosensitivity specifically to agents that induced double-stranded DNA breaks (DSB). Enhanced chemosensitivity in telomere dysfunctional cells was linked to therapy-induced fragmentation and multichromosomal fusions, whereas telomerase reconstitution restored genomic integrity and chemoresistance. Loss of p53 function muted the cytotoxic effects of DSB-inducing agents in cells with telomere dysfunction. Together, these results point to the combined use of DSB-inducing agents and telomere maintenance inhibition as an effective anticancer therapeutic approach particularly in cells with intact p53-dependent checkpoint responses.
Published: 2001
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32. Disruption of the Cockayne syndrome B gene impairs spontaneous tumorigenesis in cancer-predisposed Ink4a/ARF knockout mice.

Author: Lu Y, Lian H, Sharma P, Schreiber-Agus N, Russell RG, Chin L, van der Horst GT, and Bregman DB
Subjects: Age Factors, Animals, Apoptosis, Cell Division, Crosses, Genetic, DNA Repair, DNA Repair Enzymes, Fibroblasts metabolism, Fibrosarcoma metabolism, Flow Cytometry, Genes, p53 genetics, Genetic Predisposition to Disease, Genotype, Immunoblotting, In Situ Nick-End Labeling, Lymphoma metabolism, Mice, Mice, Knockout, Poly-ADP-Ribose Binding Proteins, RNA, Messenger metabolism, Time Factors, Transformation, Genetic, Tumor Suppressor Protein p14ARF, Tumor Suppressor Protein p53 metabolism, Ultraviolet Rays, ras Proteins metabolism, Cockayne Syndrome genetics, Cyclin-Dependent Kinase Inhibitor p16 genetics, DNA Helicases genetics, DNA Helicases physiology, Neoplasms genetics, Proteins genetics
Abstract: Cells isolated from individuals with Cockayne syndrome (CS) have a defect in transcription-coupled DNA repair, which rapidly corrects certain DNA lesions located on the transcribed strand of active genes. Despite this DNA repair defect, individuals with CS group A (CSA) or group B (CSB) do not exhibit an increased spontaneous or UV-induced cancer rate. In order to investigate the effect of CSB deficiency on spontaneous carcinogenesis, we crossed CSB(-/-) mice with cancer-prone mice lacking the p16(Ink4a)/p19(ARF) tumor suppressor locus. CSB(-/-) mice are sensitive to UV-induced skin cancer but show no increased rate of spontaneous cancer. CSB(-/-) Ink4a/ARF(-/-) mice developed 60% fewer tumors than Ink4a/ARF(-/-) animals and demonstrated a longer tumor-free latency time (260 versus 150 days). Moreover, CSB(-/-) Ink4a/ARF(-/-) mouse embryo fibroblasts (MEFs) exhibited a lower colony formation rate after low-density seeding, a lower rate of H-Ras-induced transformation, slower proliferation, and a lower mRNA synthesis rate than Ink4a/ARF(-/-) MEFs. CSB(-/-) Ink4a/ARF(-/-) MEFs were also more sensitive to UV-induced p53 induction and UV-induced apoptosis than were Ink4a/ARF(-/-) MEFs. In order to investigate whether the apparent antineoplastic effect of CSB gene disruption was caused by sensitization to genotoxin-induced (p53-mediated) apoptosis or by p53-independent sequelae, we also generated p53(-/-) and CSB(-/-) p53(-/-) MEFs. The CSB(-/-) p53(-/-) MEFs demonstrated lower colony formation efficiency, a lower proliferation rate, a lower mRNA synthesis rate, and a higher rate of UV-induced cell death than p53(-/-) MEFs. Collectively, these results indicate that the antineoplastic effect of CSB gene disruption is at least partially p53 independent; it may result from impaired transcription or from apoptosis secondary to environmental or endogenous DNA damage.
Published: 2001
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33. Short dysfunctional telomeres impair tumorigenesis in the INK4a(delta2/3) cancer-prone mouse.

Author: Greenberg RA, Chin L, Femino A, Lee KH, Gottlieb GJ, Singer RH, Greider CW, and DePinho RA
Subjects: Animals, Antigens, Polyomavirus Transforming, Cell Division, Cell Line, Transformed, Cyclin-Dependent Kinase Inhibitor p16 genetics, Mice, Mice, SCID, Phenotype, Telomere metabolism, Cyclin-Dependent Kinase Inhibitor p16 physiology, Neoplasms etiology, Telomerase metabolism, Telomere physiology
Abstract: Maintenance of telomere length is predicted to be essential for bypass of senescence and crisis checkpoints in cancer cells. The impact of telomere dysfunction on tumorigenesis was assessed in successive generations of mice doubly null for the telomerase RNA (mTR) and the INK4a tumor suppressor genes. Significant reductions in tumor formation in vivo and oncogenic potential in vitro were observed in late generations of telomerase deficiency, coincident with severe telomere shortening and associated dysfunction. Reintroduction of mTR into cells significantly restored the oncogenic potential, indicating telomerase activation is a cooperating event in the malignant transformation of cells containing critically short telomeres. The results described here demonstrate that loss of telomere function in a cancer-prone mouse model possessing intact DNA damage responses impairs, but does not prevent, tumor formation.
Published: 1999
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34. p53 deficiency rescues the adverse effects of telomere loss and cooperates with telomere dysfunction to accelerate carcinogenesis.

Author: Chin L, Artandi SE, Shen Q, Tam A, Lee SL, Gottlieb GJ, Greider CW, and DePinho RA
Subjects: Animals, Apoptosis, Male, Mice, Mice, Inbred C57BL, Phenotype, Spermatozoa cytology, Telomerase genetics, Testis cytology, Tumor Suppressor Protein p53 genetics, Neoplasms etiology, Telomerase physiology, Telomere physiology, Tumor Suppressor Protein p53 physiology
Abstract: Maintenance of telomere length and function is critical for the efficient proliferation of eukaryotic cells. Here, we examine the interactions between telomere dysfunction and p53 in cells and organs of telomerase-deficient mice. Coincident with severe telomere shortening and associated genomic instability, p53 is activated, leading to growth arrest and/or apoptosis. Deletion of p53 significantly attenuated the adverse cellular and organismal effects of telomere dysfunction, but only during the earliest stages of genetic crisis. Correspondingly, the loss of telomere function and p53 deficiency cooperated to initiate the transformation process. Together, these studies establish a key role for p53 in the cellular response to telomere dysfunction in both normal and neoplastic cells, question the significance of crisis as a tumor suppressor mechanism, and identify a biologically relevant stage of advanced crisis, termed genetic catastrophe.
Published: 1999
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35. The INK4a/ARF tumor suppressor: one gene--two products--two pathways.

Author: Chin L, Pomerantz J, and DePinho RA
Subjects: Animals, Cyclin-Dependent Kinase Inhibitor p16 genetics, Genes, p53, Humans, Melanoma genetics, Neoplasms metabolism, Proteins genetics, Proto-Oncogene Proteins genetics, Proto-Oncogene Proteins metabolism, Proto-Oncogene Proteins c-mdm2, Retinoblastoma Protein genetics, Retinoblastoma Protein metabolism, Tumor Suppressor Protein p14ARF, Cyclin-Dependent Kinase Inhibitor p16 metabolism, Genes, Tumor Suppressor, Neoplasms genetics, Nuclear Proteins, Proteins metabolism
Abstract: Functional inactivation of the retinoblastoma (RB) and p53 pathways appears to be a rite of passage for all cancerous cells and results in disruption of cell-cycle regulation and deactivation of the apoptotic response that normally ensues. The INK4a/ARF locus sits at the nexus of these two growth-control pathways, by virtue of its ability to generate two distinct products: the p16INK4a protein, a cyclin-dependent kinase inhibitor that functions upstream of RB; and the p19ARF protein, which blocks MDM2 inhibition of p53 activity. This 'one gene--two products--two pathways' arrangement provides a basis for the prominence of INK4a/ARF in tumorigenesis.
Published: 1998
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36. Growth and radiation response of cells grown in macroporous gelatin microcarriers (CultiSpher-G).

Author: Rasey JS, Cornwell MM, Maurer BJ, Boyles DJ, Hofstrand P, Chin L, and Cerveny C
Subjects: Animals, CHO Cells, Cell Communication, Cell Division, Cricetinae, Gelatin, Humans, Spheroids, Cellular, Tumor Cells, Cultured, Cell Survival radiation effects, Neoplasms pathology
Abstract: Four cell lines have been cultured in macroporous gelatin microcarrier beads (CultiSpher-G) to test this as a new model of three-dimensional cell growth for use in experimental cancer therapy. A549, KB 3-1, KB 8-5 and V79 cells were successfully grown in CultiSphers, albeit with longer doubling times than observed for the respective cell type in monolayer cultures. MTT staining and histology demonstrated three-dimensional contact of cells in the microcarriers. A549 cells populated the microcarriers more densely than KB 3-1 cells, and with both cell types there is bead-to-bead variation in occupancy by cells. [3H]TdR autoradiography reveals labelled cells throughout A549 and KB 3-1 CultiSphers, with no proliferation gradient from edge to centre. Central necrosis has not been observed. A549 cells but not KB 3-1 cells demonstrated a radiation contact effect (i.e. resistance) when irradiated in CultiSphers, compared with monolayers. We conclude that CultiSphers may be a useful model for three-dimensional growth and cell contact when investigators want to investigate these phenomena without the microenvironmental gradients of spheroids.
Published: 1996

37. Optimization of radiation therapy: integral-response of a model biological system.

Author: Wolbarst AB, Chin LM, and Svensson GK
Subjects: Humans, Mathematics, Models, Biological, Patient Care Planning, Radiotherapy Dosage, Neoplasms radiotherapy
Abstract: Several radiotherapy treatment planning criteria have been proposed for dose distribution optimization. Here we present a simple mathematical model of an idealized biological system. From it we have derived an objective function designed to achieve an extremum for that particular plan which minimizes the probabilities of occurrence of unacceptable complications in healthy tissue and of recurrence or spread of disease. The model assumes that an organism is separable into physiologically discrete compartments or organs, each consisting of a set of microscopic functional units with their own dose-response characteristics. In analogy to the integral-dose, we define an integral-response parameter v as a measure of radiation-induced damage; the value of this v may be calculated for any given spatial distribution of dose in a compartment or organ. A Probability of Serious Complications function, PSC(v), then provides an estimate of the likelihood of occurrence of unacceptable complications. Special problems arising with paired organs (kidneys), "series" organs (spinal cord), and the recurrence and spread of disease are addressed. The PSC for the various organs and neoplasia can be combined to form a compound Complication Factor (CF) objective function; the lower the value of the CF, the better the overall plan. Prospects for making the model explicitly time/fractionation dependent, and for incorporating utility theoretic ideas, are discussed.
Published: 1982
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38. Towards patient-based cancer therapeutics

Author: Discovery, C. T., Network, D., Schreiber, S. L., Shamji, A. F., Clemons, P. A., Hon, C., Koehler, A. N., Munoz, B., Palmer, M., Stern, A. M., Wagner, B. K., Powers, S., Lowe, S. W., Guo, X., Krasnitz, A., Sawey, E. T., Sordella, R., Stein, L., Trotman, L. C., Califano, A., Dalla Favera, R., Ferrando, A., Iavarone, A., Pasqualucci, Laura, Silva, J., Stockwell, B. R., Hahn, W. C., Chin, L., Depinho, R. A., Boehm, J. S., Gopal, S., Huang, A., Root, D. E., Weir, B. A., Gerhard, D. S., Zenklusen, J. C., Roth, M. G., White, M. A., Minna, J. D., Macmillan, J. B., and Posner, B. A.
Subjects: Biomedical Engineering, MEDLINE, Bioengineering, Antineoplastic Agents, Bioinformatics, Small Interfering, Applied Microbiology and Biotechnology, Article, Mice, Neoplasms, Drug Discovery, medicine, Animals, Humans, Gene Regulatory Networks, Precision Medicine, RNA, Small Interfering, Drug discovery, business.industry, Animal, Cancer, Individualized Medicine, Precision medicine, medicine.disease, National Cancer Institute (U.S.), United States, Neoplasm Proteins, Cancer drug discovery, Disease Models, Animal, Disease Models, Molecular Medicine, RNA, business, Biotechnology
Abstract: A new approach to the discovery of cancer therapeutics is emerging that begins with the cancer patient. Genomic analysis of primary tumors is providing an unprecedented molecular characterization of the disease. The next step requires relating the genetic features of cancers to acquired gene and pathway dependencies and identifying small-molecule therapeutics that target them.
Published: 2010

39. Effects of hospital facilities on patient outcomes after cancer surgery

Author: Knight, Sr, Chu, K, Lapitan, Mc, Dare, Aj, Pius, R, Shaw, Ca, Drake, Tm, Norman, L, Ademuyiwa, Ao, Adisa, Ao, Aguilera, Ml, Al-Saqqa, Sw, Al-Slaibi, I, Bhangu, A, Biccard, Bm, Brocklehurst, P, Costas-Chavarri, A, Elhadi, M, Fairfield, Cj, Fitzgerald, Je, Ghosh, D, Glasbey, J, Henegouwen, Miv, Ingabire, Jca, Kingham, Tp, Lawani, I, Lieske, B, Lilford, R, Martin, J, Mclean, Ka, Moore, R, Morton, D, Nepogodiev, D, Ntirenganya, F, Pata, F, Pinkney, T, Stephen, R Knight, Catherine, A Shaw, Riinu, Pius, Thomas, M Drake, Lisa, Norman, Adesoji, O Ademuyiwa, Adewale, O Adisa, Maria Lorena Aguilera, Sara, W Al-Saqqa, Ibrahim, Al-Slaibi, Aneel, Bhangu, Bruce, M Biccard, Peter, Brocklehurst, Ainhoa, Costas-Chavarri, Kathryn, Chu, Anna, Dare, Muhammed, Elhadi, Cameron, J Fairfield, J Edward Fitzgerald, Dhruv, Ghosh, James, Glasbey, Mark, I van Berge Henegouwen, C Allen Ingabire, J, T Peter Kingham, Marie Carmela Lapitan, Ismaïl, Lawani, Bettina, Lieske, Richard, Lilford, Janet, Martin, Kenneth, A McLean, Rachel, Moore, Dion, Morton, Dmitri, Nepogodiev, Faustin, Ntirenganya, Francesco, Pata, Thomas, Pinkney, Ahmad Uzair Qureshi, Antonio Ramos-De la Medina, Aya, Riad, Hosni Khairy Salem, Joana, Simões, Richard, Spence, Neil, Smart, Stephen, Tabiri, Hannah, Thomas, Thomas, G Weiser, Malcolm, West, John, Whitaker, Ewen, M Harrison, Arben, Gjata, Maria Marta Modolo, Sebastian, King, Erick, Chan, Sayeda Nazmun Nahar, Ade, Waterman, Dominique, Vervoort, Alemayehu Ginbo Bedada, Bernardo De Azevedo, Ana Gabriela Figueiredo, Manol, Sokolov, Venerand, Barendegere, Gerald, Ekwen, Arnav, Agarwal, Qinyang, Liu, Juan Camilo Correa, Kalisya Luc Malemo, Jacques, Bake, Jakov, Mihanovic, Kamila, Kunčarová, Julius, Orhalmi, Hosni, Salem, Jyri, Teras, Aristotelis, Kechagias, Alexis, P Arnaud, Judith, Lindert, Vasileios, Kalles, Maria-Lorena, Aguilera-Arevalo, Gustavo, Recinos, Zsolt, Baranyai, Basant, Kumar, Harish Neelamraju Lakshmi, Sanoop Koshy Zachariah, Philip, Alexander, Sunil Kumar Venkatappa, Pramesh, C, Radhian, Amandito, Christina, Fleming, Luca, Ansaloni, Gianluca, Pellino, Ahmed, M Altibi, Ibrahim, Nour, Intisar, Hamdun, Ali, M Ghellai, Donatas, Venskutonis, Tomas, Poskus, Justas, Zilinskas, Precious, Malemia, Yong Yong Tew, Elaine, Borg, Sarah, Ellul, Fatima Zahraa Wafqui, David, W Borowski, Anne Sophie van Dalen, Cameron, Wells, Harissou, Adamou, Adesoji, Ademuyiwa, Adewale, Adisa, Kjetil, Søreide, Sara Al Saqqa, Osaid, Alser, Haya, Tahboub, Helmut Alfredo Segovia Lohse, Sebastian Shu Yip, Piotr, Major, António Sampaio Soares, Matei Razvan Bratu, Andrey, Litvin, Armen, Vardanyan, Ahmad, Gudal, Naif, Albati, Jovan, Juloski, Miran, Rems, Sarah, Rayne, Stephanie Van Straten, Yoshan, Moodley, Irene Ortega Vázquez, Jaime, Ruiz-Tovar, Kithsiri Janakantha Senanayake, Sujeewa Priyantha Bandara Thalgaspitiya, Omer Abdelbagi Omer, Anmar, Homeida, Yucel, Cengiz, Daniel, Clerc, Muhammad, Alshaar, Hanen, Bouaziz, Yuksel, Altinel, Matthew, Doe, Maryna, Freigofer, Ella, Teasdale, Rakan, Kabariti, Joshua Michael Clements, Stephen Richard Knight, Ahsan, Ashfaq, Ijeoma, Azodo, Gabriela, Wagner, Ivan, Trostchansky, Mayaba, Maimbo, David, Linyama, Helidon, Nina, Amanda, Zeko, Claudio Gabriel Fermani, Santiago, Villalobos, Federico, Carballo, Pablo, Farina, Sebastian, Guckenheimer, Marilla, Dickfos, Ankit, Ajmera, Chester, Chong, Ralph, Gourlay, Sikandar, Hussaini, Yi Jia Lee, Adeeb, Majid, Peter, Martin, Rebecca, Miles, Owen James Morris, Jamie, Phua, William, Ridley, Tarunpreet, Saluja, Ryan Renxin Tan, Jen, Teh, Anna, Wells, Bharti, Arora, Qaasim, Dollie, Debbie, Ho, Yanru, Ma, Omattage Mahasha Perera, Anthony, Truong, Amanda Caroline Dawson, Bryan, Lim, Upuli, Pahalawatta, Jacqueline, Phan, Xiao-Ming Sarah Woon-Shoo-Tong, Andrea, Yeoh, Lillian, Charman, Andrew, Drane, Sharon, Laura, Charmaine Chu Wen Lo, Amy, Mozes, Rita, Poon, Hao Han Tan, Ellen, Wall, Prakshi, Chopra, Jasmine De Giovanni, Bal, Dhital, Brian, Draganic, Alexander, Duller, Jonathan, Gani, Yao Kuan Goh, Jun Young Jeong, Brendan, Mcmanus, Prakash, Nagappan, Peter, Pockney, Anya, Rugendyke, Mahsa, Sarrami, Stephen, Smith, Vanessa, Wills, Hsu Ven Wong, Geoffrey, Ye, Geoffrey, Zhang, Ethan, Brooker, Daniel, Feng, Bonnie, Lau, Carlin, Ngai, Sarah, Birks, David, Gyorki, Jaime Otero de Pablos, Ali, Abbosh, Chris, Gillespie, Ahmed, Mahmoud, Bianca, Kwan, Joshua, Lawson, Andrea, Warwick, Janne, Bingham, Andrew, J Cockbain, Nagendra Naidu Dudi-Venkata, Jordan, Ellaby-Hall, Ben, Finlay, Emily, Humphries, Jade, Pisaniello, Monique, Pisaniello, Salma, Salih, Tarik, Sammour, Haidar Hadri Abd Wahab, April De Silva, Nicola, Hayward, Kartik, Iyer, Guy, Maddern, Gian Andrea Prevost, Naga, Annapureddy, Krishna Pranathi Settipalli, Jeremy, Yeo, Lucy, Hempenstall, Lily, Pham, Shaun, Purcell, Cherry, Talavera, Ashish, I Vaska, Gurpreet, Chaggar, Phillip, Chrapko, Annelise, Cocco, Sarah Michelle Crystal Jade Coulter-Nile, Grahame, Ctercteko, James, French, Houchen, Gong, Martijn, Gosselink, Thuvarahan, Jegathees, Ivan, Jin, Michelle, Kalachov, Kathryn, Kiefhaber, Katherine, Lee, Jason, Luong, Steven, Phan, Henry, Pleass, Kelly, Veale, Zhi, Zeng, Angela, Au, Ashe, Debiasio, Idy, Deng, Jananee, Myooran, Amrita, Nair, Peter, Stewart, Anton, Stift, Lukas Walter Unger, Kerstin, Wimmer, Nabila, Ahmed, Syed, Hasan, Saber, Rahman, Margaret, O'Shea, Greg, Padmore, Adrian, Peters, Pietro, Perduca, Guenda, Pulcina, Nicolas, Tinton, Frederic, Buxant, Elsa, Dabin, Giulia, Garofalo, Francis, Dossou, Freddy Houehanou Rodrigue Gnangnon, Yacoubou Imorou Souaibou, Pako, Motlaleselelo, Omphile, Tlhomelang, Igor Lima Buarque, Gustavo Mendonça Ataíde Gomes, Aldo Vieira Barros, Ilia, Batashki, Nikolai, Damianov, Vladislav, Stoyanov, Dragomir, Dardanov, Svilen, Maslyankov, Plamen, Petkov, George, Todorov, Evgeni, Zhivkov, Aygulya, Akisheva, Miguel Angel Castilla Moreno, Geno, Genov, Ivelina, Ilieva, Tsvetomir, Ivanov, Martin, Karamanliev, Azhar, Khan, Emil, Mitkov, Tsanko, Yotsov, Boyko, Atanasov, Nikolay, Belev, Mihail, Slavchev, Carlos, Nsengiyumva, Elgan, Jones, Simon, Stock, Steve, Kyota, James, Brown, Tresor Mabanza, K, Lemery Nigo Samuel, Chidi, Otuneme, Ngwang, Prosper, Franklin, Umenze, Marylise, Boutros, Natasha, Caminsky, Sinziana, Dumitra, Richard, Garfinkle, Dominique, Morency, Ebram, Salama, Alexander, Banks, Lorenzo, Ferri, Haitian, He, Amit, Katz, Alexander Sender Liberman, Sarkis, Meterissian, Allison, Pang, Elena, Parvez, Usmaan, Hameed, Fahima, Osman, Sangita, Sequeira, Natalie, Coburn, Alisha, Jaffer, Paul, Karanicolas, Matthew, Mosseler, Reilly, Musselman, Xinyuan, Liu, Ching Wan Yip, Juan Sebastian Garces-Otero, Carolina, Guzman, Sebastian, Sierra, Andres Uribe Valencia, Paulo Andrés Cabrera Rivera, Saul, Camelo, Andrea, Gonzalez, Alejandro, González-Orozco, Manuel Santiago Mosquera Paz, Carlos J- Perez Rivera, Felipe, Gonzalez, Andres, Isaza-Restrepo, Laura, Nino-Torres, Natalia Arias Madrid, Maria Clara Mendoza Arango, Justin, Tsandiraki, Damir, Jemendžić, Branislav, Kocman, Oliver, Šuman, Renata, Canic, Darko, Jurišić, Ivana, Karakas, Ana Krizanovic Rupcic, Vlatka, Pitlovic, Josip, Samardžić, Mario, Kopljar, Ivan, Bacic, Edgar, Domini, Robert, Karlo, Danijela, Miljanić, Andrea, Simic, Mariam, Ahmed, Majdi Al Nassrallah, Rabiya, Altaf, Talal, Amjad, Ruba, Eltoum, Heba, Haidar, Alhassan, Hassan, Omar, Khalil, Marwan, Qasem, Rommel, Ramesh, Gautham, Sajith, Maham, Wisal, Jan, Žatecký, Michele, Bujda, Katerina, Jirankova, Ales, Paclik, Aya, Abdallah, Mariam Abdulgawad Almogy, Esraa Ayman El-Sawy, Ahmed Moustafa ElFayoumy, Nourhan, Elghareeb, Nourhan Ahmed Esmat, Ahmed, Fadel, Abdullah, Habater, Heba, Hamdy, Amr, Hefni, Marwa, Kamal, Norhan Mohamed Abobakr, Ahmed, Sayed, Nancy, Shaker, Ehab, Taha, Hoda, Tharwat, Omar, Zakaria, Ibrahem, Abdelmotaleb, Ali, Al-Dhufri, Hamza, S Al-Himyari, Enas El Sheikh, Asmaa, Eldmaty, Aya, Elkhalawy, Ahmed, M Elkhashen, Kithara, Magdy, Safa, Mostafa, Habib Doutoum Sadia, Mohamed Mahmoud Saleh, Dina, Samir, Mohamed Yahia Mohamed Ali, Mahmoud, A Nassar, Samar, Abdelhady, Aly, Abdelrazek, Israa, Abdelsalam, Aya, El-Sawy, Eman, Essam, Mohamed, Gadelkarim, Khaled, Ghaly, Mohamed, Hassabalnaby, Rana, Masarani, Nourhan Mohamed Shaaban, Ahmed, Sabry, Menatalla, Salem, Nourhan Akram Soliman, Diaaaldin, Zahran, Moustafa Ramadan Abou El Soud, Esraa Tarek Badr, Hala, Borham, Nehal, Elmeslemany, Mohammad, Elsayed, Fawzia, Elsherif, Sara, Eslam, Gehad, Gaber, Sondos, Ibrahim, Yara, Kamh, Abdelrahman, Mahmoud, Shimaa Gamal Mohamed, Eman, Morshedy, Cinderella, Omar, Fatima Salem Soliman, Shaza, Abdelkawy, Naglaa, Abdelmohsen, Mahmoud, Abdelshakour, Ahmed, Dahy, Norhan, Gamal, Mohammed, Gamal, Ahmad, Hasan, Helal, Hetta, Nehad, Mousa, Mohamed, Omar, Somia, Rabie, Mahmoud, Saad, Bakeer, Saleh, Marwa Sayed Mohamed, Muhammad, Shawqi, Heba Abdelhady Mousa, Mostafa, Alnoury, Mohamed, Elbealawy, Ahmed, Elshafey, Muhammad Essam Ibrahim El Desouki Muhammad Ahmed, Mennatullah, Ghonaim, Fawzy, Hgag, Mohamed, Ibrahim, Mahmoud, Morsy, Mohamed Reda Loaloa, Ahmed, Refaat, Hadeer, Samir, Fatma, Shahien, Mohamed, Sobhy, Fathy, Sroor, Esraa, Abdellatif, Marina, Adel, Amr Abdelghani Afifi, Eman, Afifi, Marco, Antaky, Amr, Dawoud, Naira El Zoghby, Amira, El-Remaily, Ali Abdelazez Elzanfaly, Ahmed, Gadallah, Fatma Alzahraa Gamal, Omar, Hashem, Shrouk Medhat Youssef, Aliaa Muhammad Attyah, Malak, Munir, Omar, Shazly, Esraa, Taha, Karim, Wilson, Sawsan, Adel, Asmaa, Ali, Esraa, Eid, Esraa, Elhelow, Marwa, Elmahdy, Bassant, Elshatby, Amany Hossam El-Din Zakaria, Ahmad, Hossny, Eman, Ibrahim, Ahmed, M Yonis, Maram, Metwalli, Basant, Yousry, Esraa, Zid, Mina, A Yacoub, Ahmed, Abdelhakim, Nervana, Abouelsoad, Mo'Min, Alkhatib, Ahmed, Ashraf, Alaa, Ashraf, Yasmin, Elazab, Mahmoud, Elfanty, Osama, Elkabir, Mai, Elsayed, Ahmed, Elshimy, Hager, Elsobky, John, Eskander, Ahmed, Gad, Ward, Hamsho, Noura Khaled Abdelwahed, Menna, Magdy, Dalia, Moharam, Abeer, Osama, Shereen, Ramadan, Radwa, Roum, Taqwa, Sayed, Tarneem, Shehada, Ahmed Mohy Zidan, Khalid, Abbas, Amr, Ali, Mohamed, Attia, Mohamed, Balata, Ayman El Nakeeb, Mohamed Ibrahim Elsayed Elewaily, Ahmed, Elfallal, Hossam, Elfeki, Ahmed, Elkhadragy, Sameh, Emile, Helmy, Ezzat, Hasnaa, Hosni, Islam, Mansour, Waleed, Omar, Gehad, Othman, Kareem, Sadek, Mostafa, Shalaby, Noura, Shehab-Eldeen, Rawda Anas Khalifa, Helmy, Badr, Mostafa, Eldeep, Ahmed, Eldeep, Amany Eldoseuky Mohammed, Salwa, Khallaf, Eman Magdy Hegazy, Rokia, Mahmoud, Pola, Mikhail, Mahmoud, Morsi, Sara, Mowafy, Dina, Raafat, Amina, Safy, Marwa, Sera, Ahmed Shible Sera, Mostafa Salim Mohamed AbdAllah, Muhammad, Abdelkader, Abdulrahman Osama Abdou, Ahmedgaber, Ahmed, Shireen, Gaafar, Fatma Ibrahim Negm, Mina, Lapic, Ahmed, Maher, Hagar, Mahmoud, Ahmed, Mostafa, Mohamed, Samir, Fatma, Samy, Nourhan, Semeda, Hind, I Shalaby, Alaa, El-Taweel, Ahmed Galal Elnagar, Ahmed Gamal Hemidan, Mohamed, Hussein, Ahmed, A Kandil, Moawad, Mf, Ayat Allah Nasser Hamamah, Mostafa, Soliman, Mohamed, Abdelkhalek, Noura Abdelmaksoud Tawakel, Ahmed Mohamed Abdelwahed, Alrawy, Abdou, Khalid, Atallah, Mohammed Yasser Elsherbeny, Eman, Emara, Mohamed, Hamdy, Omar, Hamdy, Amira, Haron, Salma, Ismail, Islam Hany Metwally, Nihal Mohamed Hamed Elgaml, Ahmed, Nassar, Basel, Refky, Mirna, Sadek, Mahmoud, Saleh, Asmaa, Yunes, Mai, Zakaria, Mohammed, Zuhdy, Notila, Fayed, Mohammed Mustafa Hassan Mohammed, Sander, Kütner, Priit, Melnik, Indrek, Seire, Toomas, Ümarik, Eppu, Ainoa, Verner, Eerola, Hanna, Koppatz, Laura, Koskenvuo, Ville, Sallinen, Sini, Takala, Jevgeni, Katunin, Arto, Turunen, Niki, Christou, Muriel, Mathonnet, Vincent, Lavoue, Krystel Nyangoh Timoh, Lucie, Soulabaille, Romain, Lesourd, Aude, Merdrignac, Laurent, Sulpice, Benoît, André, Elodie, Chantalat, Charlotte, Vaysse, Bertrand, Dousset, Sebastien, Gaujoux, Gregory, Martin, Octavian, Clonda, Domantas, Juodis, Klaus, Kienle, Andras, Mravik, Samuel, Palmer, Gabor, Szabadhegyi, Anita Eseenam Agbeko, Solomon, Gyabaah, Frank Enoch Gyamfi, Nuhu, Naabo, Atta Owusu Senior, Joseph, Yorke, Frank, Owusu, Francis, Abantanga, Theophilus Teddy Kojo Anyomih, Abdul-Jalilu Mohammed Muntaka, Emmanuel Owusu Abem, Mohammed, Sheriff, Paul, M Wondoh, Dimitrios, Balalis, Dimitrios, Korkolis, Georgios, Gkiokas, Eirini, Pantiora, Theodosios, Theodosopoulos, Argyrios, Ioannidis, Konstantinos, Konstantinidis, Sofia, Konstantinidou, Nikolaos, Machairas, Anna, Paspala, Anastasia, Prodromidou, Christos, Chouliaras, Konstantinos, Papadopoulos, Ioannis, Baloyiannis, Ioannis, Mamaloudis, George, Tzovaras, Ioanna, Akrida, Maria-Ioanna, Argentou, Stylianos, Germanos, Evangelos, Iliopoulos, Ioannis, Maroulis, George, Skroubis, George, Theofanis, Christos, Chatzakis, Orestis, Ioannidis, Lydia, Loutzidou, Panagiotis, Karathanasis, Nikolaos, Michalopoulos, Charalampos, Theodoropoulos, Dimitrios, Theodorou, Tania, Triantafyllou, Zoe, Garoufalia, Natasha, Hasemaki, Michalis, Kontos, Gregory, Kouraklis, Stylianos, Kykalos, Theodore, Liakakos, Eustratia, Mpaili, Alexandros, Papalampros, Dimitrios, Schizas, Athanasios, Syllaios, Ekaterini Christina Tampaki, Antonios, Tsimpoukelis, Maria Ioanna Antonopoulou, Eirini, Deskou, Dimitrios, K Manatakis, Dimitrios, Papageorgiou, Menelaos, Zoulamoglou, Christos, Anthoulakis, Michalis, Margaritis, Nikolaos, Nikoloudis, Veronica, Campo, André, Ceballos, Mario-Andrés, Flores, Waleska, Giron, Donghyun, Ko, Gabriel, Martinez, Verónica Rivera Lara, Nataly, Rueda, Andres, Sanchez, Jorge Carlos Guillermo Tejeda Garrido, Alvaro Eduardo Alvarez Rivera, Elvis Benjamin Bamaca Ixcajoc, Lilian Elizabeth Barreda Zelaya, Patricia, Chacòn-Herrera, Ligia Margarita Corea Ruiz, Guillermo, Echeverria-Davila, Mario, Garcia, Danilo, García, Edgar Fernando Gutiérrez Mayen, Noriega, José, Nery, Mazariegos, Diego, Méndez, Michael Paniagua Espinoza, David, Bardos, Marton, Benke, Kristof, Illes, Balint András Kokas, Réka, Szabó, Akhila, Appukuttan, Anjitha, Asok, D K, Vijaykumar, Kapil, Malik, Praveen, Ravishankaran, Ritesh, Tapkire, Guru, Moorthy, Joyner, Abraham, Ramesh, Muthuvel, John, Alapatt, Abhay, Kattepur, Nizamudheen, Pareekutty, Mebanshanbor, Garod, Caleb, Harris, Cliff, Wanniang, Ashish, Gupta, Deepak, Nehra, Sanjeev, Parshad, Rajgopal, Acharya, Rajendra, Badwe, Manish, Bhandare, Urvashi, Jain, Karishma, Kirti, Nita, Nair, Shailesh, Shrikhande, Purvi, Thakkar, Premkumar, Anandan, C S, Archana, Arun Holenarasipur Narasannaiah, Tejaswi, Jagarlamudi, M R, Rashmi, Mallikarjuna, Manangi, Abhishek, Raghavendra, K Seshagiri Rao, Vinay, S, Vinay, Sajjan, Aneesh, Shenoy, Santhosh Shivashankar Chikkanayakanahalli, Kavya, Tharanath, Sushmita, V, Peter, Adidharma, Raksheeth, Agarwal, Phebe Anggita Gultom, Ghafur Rasyid Arifin, Matthew, Billy, Zatira, Elfizri, Alessa, Fahira, Devi, Felicia, Triana Hardianti Gunardi, Nadya, Johanna, Nadia Rahmadiani Nugrahadi, Sonar Soni Panigoro, Siti, Rahmayanti, Retta Catherina Sihotang, Santi Yuanita Brata, Hadi, Winoto, Nastaran, Barati, Manoochehr, Karami, Hamidreza, Khorshidi, Homa, Naderifar, Mazin, A Abdulla, Maggie, Coleman, Ronan, J Doherty, Rob, Hannon, Brenda, Murphy, Aine, Stakelum, Des, Winter, Lylas, Aljohmani, Richard, Farnan, Yeshey, Seldon, Tanna, Tan, Shriya, Varghese, Mohammad, Alherz, Muaaz, Ather, Mohammad, Bajilan, Vivien, Graziadei, Isobel, Pilkington, Omar, Quidwai, Paul, Ridgway, Haaris, Shiwani, Abd Al-Rahman Tahir, Eimear, Blunnie, Daniel, Burke, Niall, Kennedy, Kate, Macdonagh, Maeve, O'Neill, Siobhan, Rooney, Giuseppe, Falco, Guglielmo, Ferrari, Simone, Mele, Gabriela Elisa Nita, Lara, Ugoletti, Maurizio, Zizzo, Gianmaria, Confalonieri, Giovanni, Pesenti, Fulvio, Tagliabue, Gianluca, Baronio, Deborah, Ongaro, Giacomo, Pata, Bruno, Compagnoni, Renato, Salvadori, Lucio, Taglietti, Nicola, D'Alessandro, Pierpaolo Di Lascio, Giovanni, Pascale, Luca, Bortolasi, Tommaso, Campagnaro, Massimo, Carlini, Giorgio, Lisi, Davide, Lombardi, Corrado, Pedrazzani, Domenico, Spoletini, Giulia, Turri, Paola, Violi, Donato Francesco Altomare, Fabrizio, Aquilino, Nicola, Musa, Vincenzo, Papagni, Arcangelo, Picciariello, Leonardo, Vincenti, Dario, Andreotti, Savino, Occhionorelli, Matteo, Tondo, Stefano Maria Massimiliano Basso, Paolo, Ubiali, Riccardo, Cirelli, Marco Enrico Mario Maino, Guglielmo Niccolò Piozzi, Emanuele, Picone, Rosa, Scaramuzzo, Giovanni, Sinibaldi, Alfonso, Amendola, Lorenzo, Anastasio, Luigi, Bucci, Emanuele, Caruso, Antonio, Castaldi, Sara Di Maso, Vincenza Paola Dinuzzi, Giovanni, Esposito, Maria, Gaudiello, Mariano Cesare Giglio, Paola Antonella Greco, Gaetano, Luglio, Andrea, Manfreda, Ester, Marra, Federica, Mastella, Gianluca, Pagano, Roberto, Peltrini, Vincenzo, Pepe, Michele, Sacco, Viviana, Sollazzo, Giovanni, Spiezio, Ettore, Cianchetti, Nunzia, Menduni, Michele Maria Carvello, Francesca Di Candido, Antonino, Spinelli, Fabio, Corsi, Luca, Sorrentino, Fabio, Marino, Emanuele Luigi Giuseppe Asti, Luigi, Bonavina, Emanuele, Rausa, Martina, Asta, Andrea, Belli, Francesco, Bianco, Carmela, Cervone, Paolo, Delrio, Armando, Falato, Andrea Fares Bucci, Rita, Guarino, Ugo, Pace, Daniela, Rega, Emilia De Luca, Gaetano, Gallo, Giuseppe, Sammarco, Giuseppe, Sena, Giuseppina, Vescio, Letizia, Santandrea, Giampaolo, Ugolini, Davide, Zattoni, Nicola, Chetta, Gaetano, Logrieco, Serafino, Vanella, Gianluca, Garulli, Nicola, Zanini, Andrea, Bondurri, Francesco, Cammarata, Francesco, Colombo, Diego, Foschi, Giulia Maria Beatrice Lamperti, Anna, Maffioli, Gianluca Matteo Sampietro, Al'Ona, Yakushkina, Gloria, Zaffaroni, Enrico, Cicuttin, Maria Grazia Sibilla, Harmony, Impellizzeri, Marco, Inama, Gianluigi, Moretto, Sylvie, Mochet, Elisa, Ponte, Antonella, Usai, Stefano, Mancini, Andrea, Sagnotta, Luigi, Solinas, Elisa, Bolzonaro, Nicolò, Tamini, Gianluca, Curletti, Raffaele, Galleano, Michele, Malerba, Sofia, Campanella, Gianfranco, Cocorullo, Francesco, Colli, Paolino De Marco, Nicolò, Falco, Tommaso, Fontana, Leonel Jospin Kamdem Mambou, Antonella La Brocca, Leo, Licari, Brenda, Randisi, Giovanna, Rizzo, Giulia, Rotolo, Giuseppe, Salamone, Roberta, Tutino, Paolina, Venturelli, Stefano, Malabarba, Alessandro, Sgrò, Ivan, Vella, Bruno, Cirillo, Daniele, Crocetti, Giorgio De Toma, Pierfrancesco, Lapolla, Andrea, Mingoli, Paolo, Sapienza, Angela, Belvedere, Stefania, Bianchini, Margherita, Binetti, Arianna, Birindelli, Valeria, Tonini, Mauro, Podda, Fabio, Pulighe, Michele De Rosa, Lorenzo, Bono, Felice, Borghi, Paolo, Geretto, Maria Carmela Giuffrida, Corrado, Lauro, Alessandra, Marano, Luca, Pellegrino, Paola, Salusso, Diego, Sasia, Michela, Campanelli, Alberto Realis Luc, Mario, Trompetto, Roberto, Cardia, Nicola, Cillara, Antonio Nicola Giordano, Antonio, Costanzo, Mario Alessandro Giovilli, Luca, Turati, Silvestro, Canonico, Sciaudone, Guido, Francesco, Selvaggi, Lucio, Selvaggi, Nader, Albsoul, Ahmad, Albsoul, Ala'a Aldeen Alkhatib, Osama, Alsallaq, Justin, Z Amarin, Rami, Ayoub, Isam, Bsisu, S El Muhtaseb, M, Mohammad, Jabaiti, Jamal, Melhem, Yasmeen, Z Qwaider, Mohammad Hasan Salameh, Ahmad, Suleihat, Haya, H Suradi, Mohammad, Alammarin, Almoutuz, Aljaafreh, Mohammad Bani Hani, Zeina Bani Hani, Farah Bani Hani, Toqa, Fahmawee, Shadi, Hamouri, Cyrine, Katanani, Ra'Fat, Tawalbeh, Tamara, Tawalbeh, Hassan, Zawahrah, Mohamad, K Abou Chaar, Lana, Abusalem, Mahmoud, Al-Masri, Hani, Al-Najjar, Lutfi, Barghuthi, Zahra, Ahmed, Adnan, Maulana, Omar, Ngotho, Charbel, Kamau, Aruyaru Stanley Mwenda, Fridah, Bosire, Elizabeth, Mwachiro, Robert, Parker, Ian, Simel, Kimutai, Sylvester, Abdulmunem Ahmed Mustafa Althini, Sofian, Elbarouni, Aya Elseed Elbeshina, Ahmed, Gwea, Ans, Malek, Wedad Albashir Masoud Farag, Abdulwahab, Abdalei, Abu Baker Abdel Malik, Areej, Abo-Khammash, Ma'Aly, Abuhlaiga, Nour, Adnan, Marwa, Albaggar, Asma, Alfitory, Asma, Aljanfi, Fakhruddin, Almuzghi, Zohoor, Altumei, Fatima, Alzabti, Hana, Ashoushan, Mohamed, Assalhi, Joma, Azzubia, Sondos, Bnhameida, Malik, Delhen, Houssein, 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Alcides Ylatoma Díaz, Mark Anthony Fontanilla, Joseph Roy Fuentes, Anna Leah Salazar, Genieve, Dominguez, Marc Paul Lopez, Shiela, Macalindong, Mark Augustine Onglao, Arjel, Ramirez, Marie Dione Sacdalan, Mayou Martin Tampo, Gemma Leonora Uy, Jeremiah, Mangahas, Kenneth, Yabut, Joannes Paul Cañete, Bernalynn Eris Cansana, Ernes John Castro, Maria Kaiserin Lipana, Manuel Francisco Roxas, Vlu Jean Zara, Maciej, Chroł, Paula, Franczak, Michał, Orłowski, Piotr, Budzyński, Andrzej, Budzyński, Pawel, Bury, Agata, Czerwińska, Jadwiga, Dworak, Jacek, Dziedzic, Michał, Kisielewski, Jan, Kulawik, Anna, Lasek, Piotr, Małczak, Marcin, Migaczewski, Michał, Pędziwiatr, Magdalena, Pisarska, Dorota, Radkowiak, Mateusz, Rubinkiewicz, Anna, Rzepa, Tomasz, Skoczylas, Maciej, Stanek, Katarzyna, Truszkiewicz, Mateusz, Wierdak, Marek, Winiarski, Piotr, Zarzycki, Anna, Zub-Pokrowiecka, Piotr, Kowalewski, Rafał, Roszkowski, Maciej, Walędziak, Miguel, Tomé, Sara, Patrocinio, Ines, Guerreiro, Filipe, Almeida, 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García, Pastora Rodriguez Fraga, Gonzalo De Castro Parga, Maria Pilar Fernández Veiga, Lucía Garrido López, Hugo Infante Pino, Irene Lages Cal, Marta López Otero, Manuel Nogueira Sixto, Marta Paniagua García Señorans, Laura Rodríguez Fernández, Alejandro Ruano Poblador, Erika Rufo Crespo, Raquel, Sanchez-Santos, Vincenzo, Vigorita, Ester Alonso Batanero, Dorisme, Asnel, Isabel Cifrian Canales, Elisa Contreras Saiz, Irene De Santiago Alvarez, Tamara Díaz Vico, Sebastian Fernandez Arias, Daniel Fernández Martínez, Carmen García Bernardo, Luis Joaquín García Flórez, Carmen Garcia Gutierrez, Manuel García Munar, Carlos Alberto Márquez Zorrilla Molina, Marta, Merayo, José Luis Michi Campos, Maria Moreno Gijon, Jorge, L Otero-Diez, Jose Luis Rodicio Miravalles, Lorena, Solar-Garcia, Aida Suárez Sánchez, Nuria, Truan, Cristina Alejandre Villalobos, Yurena Caballero Díaz, Marta, Jimenez, Dacil, Montesdeoca, Antonio, Navarro-Sánchez, Victor, Vega, Juan Beltrán de Heredia, Zahira, Gómez, Carlos, 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M., Srinivas, A., Sung, C. -Y., Tai, A., Valle Aranda, Y. C., Venturini, S., Wilguens Lartigue, J., Public and occupational health, AMS - Sports, APH - Health Behaviors & Chronic Diseases, CCA - Cancer Treatment and quality of life, Amsterdam Gastroenterology Endocrinology Metabolism, Cancer Center Amsterdam, and Albarella, Sara
Subjects: global surgery, hospitals, humans, income, neoplasms, postoperative period, poverty, prospective studies, no keywords listed, General Medicine, Prospective Studie, Hospital, Settore MED/18 - Chirurgia Generale, outcome, Hospitals, Humans, Income, Neoplasms, surgery, Postoperative Period, Poverty, Prospective Studies, cancer surgery, Human, hospital facilities
Abstract: © 2022 The Author(s). Published by Elsevier Ltd. This is an Open Access article under the CC BY 4.0 licenseBackground: Early death after cancer surgery is higher in low-income and middle-income countries (LMICs) compared with in high-income countries, yet the impact of facility characteristics on early postoperative outcomes is unknown. The aim of this study was to examine the association between hospital infrastructure, resource availability, and processes on early outcomes after cancer surgery worldwide. Methods: A multimethods analysis was performed as part of the GlobalSurg 3 study—a multicentre, international, prospective cohort study of patients who had surgery for breast, colorectal, or gastric cancer. The primary outcomes were 30-day mortality and 30-day major complication rates. Potentially beneficial hospital facilities were identified by variable selection to select those associated with 30-day mortality. Adjusted outcomes were determined using generalised estimating equations to account for patient characteristics and country-income group, with population stratification by hospital. Findings: Between April 1, 2018, and April 23, 2019, facility-level data were collected for 9685 patients across 238 hospitals in 66 countries (91 hospitals in 20 high-income countries; 57 hospitals in 19 upper-middle-income countries; and 90 hospitals in 27 low-income to lower-middle-income countries). The availability of five hospital facilities was inversely associated with mortality: ultrasound, CT scanner, critical care unit, opioid analgesia, and oncologist. After adjustment for case-mix and country income group, hospitals with three or fewer of these facilities (62 hospitals, 1294 patients) had higher mortality compared with those with four or five (adjusted odds ratio [OR] 3·85 [95% CI 2·58–5·75]; p
Published: 2022

40. Comprehensive, Integrative Genomic Analysis of Diffuse Lower-Grade Gliomas

Author: Noreen Dhalla, Saianand Balu, Alexander Potapov, Yiling Lu, Antonio Iavarone, Roel G.W. Verhaak, Alessandro Perin, Bradley A. Murray, Lee Lichtenstein, Nils Gehlenborg, Zhenlin Ju, Simon G. Coetzee, Stephanie Weaver, Gaetano Finocchiaro, Susan M. Staugaitis, Scott Morris, Da Yang, Rosy Singh, Erik Zmuda, Wei Zhang, Aaron D. Black, Roger E. McLendon, J. Bradley Elder, J. Todd Auman, Arvind Rao, Harshad S. Mahadeshwar, Yunhu Wan, Liming Yang, Stacey Gabriel, Andreas Unterberg, Adam E. Flanders, Piotr A. Mieczkowski, Jianjiong Gao, Robert Penny, Andrew Wei Xu, Peter W. Laird, Gad Getz, Cynthia Taylor, Adrian Ally, Ilya Shmulevich, Tina Wong, Christopher M. McPherson, Heidi J. Sofia, Matthew G. Soloway, Jonna Grimsby, Caterina Giannini, Mark L. Cohen, Johanna Gardner, Semin Lee, Alan P. Hoyle, Jianhua Zhang, Thais S. Sabedot, Felicia Williams, Mia Grifford, Daniela Pretti da Cunha Tirapelli, David Van Den Berg, Margi Sheth, Ye Wu, Jenny Eschbacher, Marco A. Marra, Katherine A. Hoadley, Angeliki Pantazi, Chris Benz, Michael S. Noble, Christopher R. Pierson, Kristen M. Leraas, Roy Tarnuzzer, Suzanne Sifri, Huandong Sun, Greg Eley, Eyas M. Hattab, David I. Heiman, Rehan Akbani, Todd Pihl, Michael Parfenov, Erwin G. Van Meir, Jill S. Barnholtz-Sloan, Peggy Yena, Josh Stuart, Richard A. Moore, Toshinori Hinoue, Kelly Senecal, Andrew D. Cherniack, Donald W. Parsons, Rileen Sinha, Dennis T. Maglinte, Timothy A. Chan, Reanne Bowlby, Phuong L. Nguyen, Juok Cho, Andrew E. Sloan, Alexei Protopopov, Matthew Schniederjan, Yun Wang, Yuexin Liu, Rameen Beroukhim, Kristian Cibulskis, Ty Abel, Ronald E. Warnick, Sahil Seth, Richard A. Gibbs, Rebecca Duell, W. Kimryn Rathmell, Jay Bowen, Michael S. Lawrence, Darell D. Bigner, Mary McGraw, Wen-Bin Liu, Xiaojia Ren, Umadevi Veluvolu, Erin Curley, Lynda Chin, Andy Chu, Laila M. Poisson, Harindra Arachchi, Jean C. Zenklusen, Ardene Noss, Sue E. Bell, Karen Devine, Moiz S. Bootwalla, Rebecca Carlsen, David Mallery, Eric S. Lipp, Hailei Zhang, Bradley A. Ozenberger, Andrew J. Mungall, Amie Radenbaugh, Luciano Neder, Sol Katzman, Lisa Iype, Shaowu Meng, Wendi Barrett, S. Onur Sumer, Katie Dicostanzo, Mark Vitucci, Phillip H. Lai, Vsevolod Shurkhay, D. Neil Hayes, Jiabin Tang, Hui Shen, Christopher A. Bristow, Stefania Cuzzubbo, Quinn T. Ostrom, Yasin Senbabaoglu, Ruth Steele, Peter J. Park, Jacqueline E. Schein, Lior Pachter, Jia Liu, Payal Sipahimalani, Angela Hadjipanayis, Scott L. Carter, Donghui Tan, Travis I. Zack, Kristen Shimmel, Steven E. Schumacher, Leigh B. Thorne, Kenna R. Mills Shaw, Troy Shelton, Julien Baboud, Jianan Zhang, Olga Potapova, Stuart R. Jefferys, Andreas von Deimling, B. Arman Aksoy, Carrie Sougnez, Howard Colman, Tom Mikkelsen, Amanda Clarke, Houtan Noushmehr, Daniel Crain, Mark A. Jensen, D L Rotin, Stephen B. Baylin, Barry S. Taylor, Gordon Saksena, Benito Campos, Sudha Chudamani, Ouida Liu, Lisle E. Mose, Jonathan G. Seidman, Corbin D. Jones, Norman L. Lehman, Eric S. Lander, David Haussler, Franklin W. Huang, Nina Thiessen, Charles M. Perou, Gregory N. Fuller, Kosuke Yoshihara, C. Ryan Miller, Brenda Ayala, Dina Aziz, Sara Sadeghi, Cameron Brennan, Randy Mandt, Aditya Raghunathan, Jeffrey Roach, Robert A. Holt, Timothy J. Triche, Barbara Tabak, Kenneth Aldape, John N. Weinstein, Kevin Lau, Ady Kendler, Lee Cooper, Carlos Gilberto Carlotti, Siyuan Zheng, Isaac Joseph, Jason T. Huse, Steven J.M. Jones, Brady Bernard, Chip Stewart, Lixing Yang, Lisa Wise, A. Gordon Robertson, Ronglai Shen, Lisa Scarpace, Richard Kreisberg, Shiyun Ling, Michael Mayo, Jordonna Fulop, Cathy Brewer, Denise Brooks, Daniel E. Carlin, Nils Weinhold, Angela Tam, Beth Hermes, Kalle Leinonen, Giovanni Ciriello, Mahitha Vallurupalli, John A. Demchok, Bianca Pollo, Christel Herold-Mende, Rajan Jain, Liu Xi, Francesco DiMeco, Nilsa C. Ramirez, Tara M. Lichtenberg, Ashley Fehrenbach, Yingchun Liu, Miruna Balasundaram, Sofie R. Salama, Rivka R. Colen, Olena Morozova, Yussanne Ma, Zhining Wang, W. K. Alfred Yung, Scott R. VandenBerg, Esther Rheinbay, Junyuan Wu, Katayoon Kasaian, Tanja M. Davidsen, William A. Friedman, Kathy Smolenski, Yichao Sun, Anders Jacobsen, Chiara Calatozzolo, Matthew D. Wilkerson, Lucia Cuppini, Gordon B. Mills, Xingzhi Song, Joseph Paulauskis, Jaegil Kim, Pei Lin, Scott Frazer, William M. Lee, Evan O. Paull, Sheila A. Fisher, Carolyn M. Hutter, Janae V. Simons, Gene Barnett, Mara Rosenberg, Scot Waring, Timothy R. Fennell, Raju Kucherlapati, Christine Jungk, Martin L. Ferguson, Julie M. Gastier-Foster, Cathy Schilero, Yingli Wolinsky, Rohini Raman, Zack Sanborn, Ranabir Guin, Matthew Meyerson, Daniel J. Brat, Cheryl A. Palmer, Nikolaus Schultz, Erik P. Sulman, Eric Chuah, Mark E. Sherman, Theo A. Knijnenburg, Mitchel S. Berger, Lihua Zou, Hoon Kim, Daniel DiCara, Sam Ng, Joel S. Parker, Sheila Reynolds, Raffaele Nunziata, Daniel J. Weisenberger, Natalie Tasman, Chris Sander, Doug Voet, Yaron S.N. Butterfield, Brian P. O'Neill, Lori Boice, Brat D.J., Verhaak R.G.W., Aldape K.D., Yung W.K.A., Salama S.R., Cooper L.A.D., Rheinbay E., Miller C.R., Vitucci M., Morozova O., Robertson A.G., Noushmehr H., Laird P.W., Cherniack A.D., Akbani R., Huse J.T., Ciriello G., Poisson L.M., Barnholtz-Sloan J.S., Berger M.S., Brennan C., Colen R.R., Colman H., Flanders A.E., Giannini C., Grifford M., Iavarone A., Jain R., Joseph I., Kim J., Kasaian K., Mikkelsen T., Murray B.A., O'Neill B.P., Pachter L., Parsons D.W., Sougnez C., Sulman E.P., Vandenberg S.R., Van Meir E.G., Von Deimling A., Zhang H., Crain D., Lau K., Mallery D., Morris S., Paulauskis J., Penny R., Shelton T., Sherman M., Yena P., Black A., Bowen J., Dicostanzo K., Gastier-Foster J., Leraas K.M., Lichtenberg T.M., Pierson C.R., Ramirez N.C., Taylor C., Weaver S., Wise L., Zmuda E., Davidsen T., Demchok J.A., Eley G., Ferguson M.L., Hutter C.M., Shaw K.R.M., Ozenberger B.A., Sheth M., Sofia H.J., Tarnuzzer R., Wang Z., Yang L., Zenklusen J.C., Ayala B., Baboud J., Chudamani S., Jensen M.A., Liu J., Pihl T., Raman R., Wan Y., Wu Y., Ally A., Auman J.T., Balasundaram M., Balu S., Baylin S.B., Beroukhim R., Bootwalla M.S., Bowlby R., Bristow C.A., Brooks D., Butterfield Y., Carlsen R., Carter S., Chin L., Chu A., Chuah E., Cibulskis K., Clarke A., Coetzee S.G., Dhalla N., Fennell T., Fisher S., Gabriel S., Getz G., Gibbs R., Guin R., Hadjipanayis A., Hayes D.N., Hinoue T., Hoadley K., Holt R.A., Hoyle A.P., Jefferys S.R., Jones S., Jones C.D., Kucherlapati R., Lai P.H., Lander E., Lee S., Lichtenstein L., Ma Y., Maglinte D.T., Mahadeshwar H.S., Marra M.A., Mayo M., Meng S., Meyerson M.L., Mieczkowski P.A., Moore R.A., Mose L.E., Mungall A.J., Pantazi A., Parfenov M., Park P.J., Parker J.S., Perou C.M., Protopopov A., Ren X., Roach J., Sabedot T.S., Schein J., Schumacher S.E., Seidman J.G., Seth S., Shen H., Simons J.V., Sipahimalani P., Soloway M.G., Song X., Sun H., Tabak B., Tam A., Tan D., Tang J., Thiessen N., Triche T., Van Den Berg D.J., Veluvolu U., Waring S., Weisenberger D.J., Wilkerson M.D., Wong T., Wu J., Xi L., Xu A.W., Zack T.I., Zhang J., Aksoy B.A., Arachchi H., Benz C., Bernard B., Carlin D., Cho J., DiCara D., Frazer S., Fuller G.N., Gao J., Gehlenborg N., Haussler D., Heiman D.I., Iype L., Jacobsen A., Ju Z., Katzman S., Kim H., Knijnenburg T., Kreisberg R.B., Lawrence M.S., Lee W., Leinonen K., Lin P., Ling S., Liu W., Liu Y., Lu Y., Mills G., Ng S., Noble M.S., Paull E., Rao A., Reynolds S., Saksena G., Sanborn Z., Sander C., Schultz N., Senbabaoglu Y., Shen R., Shmulevich I., Sinha R., Stuart J., Sumer S.O., Sun Y., Tasman N., Taylor B.S., Voet D., Weinhold N., Weinstein J.N., Yang D., Yoshihara K., Zheng S., Zhang W., Zou L., Abel T., Sadeghi S., Cohen M.L., Eschbacher J., Hattab E.M., Raghunathan A., Schniederjan M.J., Aziz D., Barnett G., Barrett W., Bigner D.D., Boice L., Brewer C., Calatozzolo C., Campos B., Carlotti C.G., Chan T.A., Cuppini L., Curley E., Cuzzubbo S., Devine K., DiMeco F., Duell R., Elder J.B., Fehrenbach A., Finocchiaro G., Friedman W., Fulop J., Gardner J., Hermes B., Herold-Mende C., Jungk C., Kendler A., Lehman N.L., Lipp E., Liu O., Mandt R., McGraw M., Mclendon R., McPherson C., Neder L., Nguyen P., Noss A., Nunziata R., Ostrom Q.T., Palmer C., Perin A., Pollo B., Potapov A., Potapova O., Rathmell W.K., Rotin D., Scarpace L., Schilero C., Senecal K., Shimmel K., Shurkhay V., Sifri S., Singh R., Sloan A.E., Smolenski K., Staugaitis S.M., Steele R., Thorne L., Tirapelli D.P.C., Unterberg A., Vallurupalli M., Wang Y., Warnick R., Williams F., Wolinsky Y., Bell S., Rosenberg M., Stewart C., Huang F., Grimsby J.L., and Radenbaugh A.J.
Subjects: Adult, Male, Pathology, medicine.medical_specialty, IDH1, Adolescent, Kaplan-Meier Estimate, 1p/19q Codeletion, Biology, Article, Glioma, Molecular genetics, Grade II Glioma, medicine, Cluster Analysis, Humans, neoplasms, Exome, ATRX, Proportional Hazards Models, Aged, Cluster Analysi, DNA, Neoplasm, Sequence Analysis, DNA, General Medicine, Middle Aged, Genes, p53, medicine.disease, Chromosomes, Human, Pair 1, Mutation, Proportional Hazards Model, Cancer research, GLIOMA, Female, Oligodendroglioma, Neoplasm Grading, Glioblastoma, Chromosomes, Human, Pair 19, Human, Signal Transduction
Abstract: BACKGROUND: Diffuse low-grade and intermediate-grade gliomas (which together make up the lower-grade gliomas, World Health Organization grades II and III) have highly variable clinical behavior that is not adequately predicted on the basis of histologic class. Some are indolent; others quickly progress to glioblastoma. The uncertainty is compounded by interobserver variability in histologic diagnosis. Mutations in IDH, TP53, and ATRX and codeletion of chromosome arms 1p and 19q (1p/19q codeletion) have been implicated as clinically relevant markers of lower-grade gliomas. METHODS: We performed genomewide analyses of 293 lower-grade gliomas from adults, incorporating exome sequence, DNA copy number, DNA methylation, messenger RNA expression, microRNA expression, and targeted protein expression. These data were integrated and tested for correlation with clinical outcomes. RESULTS: Unsupervised clustering of mutations and data from RNA, DNA-copy-number, and DNA-methylation platforms uncovered concordant classification of three robust, nonoverlapping, prognostically significant subtypes of lower-grade glioma that were captured more accurately by IDH, 1p/19q, and TP53 status than by histologic class. Patients who had lower-grade gliomas with an IDH mutation and 1p/19q codeletion had the most favorable clinical outcomes. Their gliomas harbored mutations in CIC, FUBP1, NOTCH1, and the TERT promoter. Nearly all lower-grade gliomas with IDH mutations and no 1p/19q codeletion had mutations in TP53 (94%) and ATRX inactivation (86%). The large majority of lower-grade gliomas without an IDH mutation had genomic aberrations and clinical behavior strikingly similar to those found in primary glioblastoma. CONCLUSIONS: The integration of genomewide data from multiple platforms delineated three molecular classes of lower-grade gliomas that were more concordant with IDH, 1p/19q, and TP53 status than with histologic class. Lower-grade gliomas with an IDH mutation either had 1p/19q codeletion or carried a TP53 mutation. Most lower-grade gliomas without an IDH mutation were molecularly and clinically similar to glioblastoma. (Funded by the National Institutes of Health.)
Published: 2015

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