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1. Multi-ancestry genome-wide association study of kidney cancer identifies 63 susceptibility regions

Author

Purdue, Mark P., Dutta, Diptavo, Machiela, Mitchell J., Gorman, Bryan R., Winter, Timothy, Okuhara, Dayne, Cleland, Sara, Ferreiro-Iglesias, Aida, Scheet, Paul, Liu, Aoxing, Wu, Chao, Antwi, Samuel O., Larkin, James, Zequi, Stênio C., Sun, Maxine, Hikino, Keiko, Hajiran, Ali, Lawson, Keith A., Cárcano, Flavio, Blanchet, Odile, Shuch, Brian, Nepple, Kenneth G., Margue, Gaëlle, Sundi, Debasish, Diver, W. Ryan, Folgueira, Maria A. A. K., van Bokhoven, Adrie, Neffa, Florencia, Brown, Kevin M., Hofmann, Jonathan N., Rhee, Jongeun, Yeager, Meredith, Cole, Nathan R., Hicks, Belynda D., Manning, Michelle R., Hutchinson, Amy A., Rothman, Nathaniel, Huang, Wen-Yi, Linehan, W. Marston, Lori, Adriana, Ferragu, Matthieu, Zidane-Marinnes, Merzouka, Serrano, Sérgio V., Magnabosco, Wesley J., Vilas, Ana, Decia, Ricardo, Carusso, Florencia, Graham, Laura S., Anderson, Kyra, Bilen, Mehmet A., Arciero, Cletus, Pellegrin, Isabelle, Ricard, Solène, Scelo, Ghislaine, Banks, Rosamonde E., Vasudev, Naveen S., Soomro, Naeem, Stewart, Grant D., Adeyoju, Adebanji, Bromage, Stephen, Hrouda, David, Gibbons, Norma, Patel, Poulam, Sullivan, Mark, Protheroe, Andrew, Nugent, Francesca I., Fournier, Michelle J., Zhang, Xiaoyu, Martin, Lisa J., Komisarenko, Maria, Eisen, Timothy, Cunningham, Sonia A., Connolly, Denise C., Uzzo, Robert G., Zaridze, David, Mukeria, Anush, Holcatova, Ivana, Hornakova, Anna, Foretova, Lenka, Janout, Vladimir, Mates, Dana, Jinga, Viorel, Rascu, Stefan, Mijuskovic, Mirjana, Savic, Slavisa, Milosavljevic, Sasa, Gaborieau, Valérie, Abedi-Ardekani, Behnoush, McKay, James, Johansson, Mattias, Phouthavongsy, Larry, Hayman, Lindsay, Li, Jason, Lungu, Ilinca, Bezerra, Stephania M., Souza, Aline G., Sares, Claudia T. G., Reis, Rodolfo B., Gallucci, Fabio P., Cordeiro, Mauricio D., Pomerantz, Mark, Lee, Gwo-Shu M., Freedman, Matthew L., Jeong, Anhyo, Greenberg, Samantha E., Sanchez, Alejandro, Thompson, R. Houston, Sharma, Vidit, Thiel, David D., Ball, Colleen T., Abreu, Diego, Lam, Elaine T., Nahas, William C., Master, Viraj A., Patel, Alpa V., Bernhard, Jean-Christophe, Freedman, Neal D., Bigot, Pierre, Reis, Rui M., Colli, Leandro M., Finelli, Antonio, Manley, Brandon J., Terao, Chikashi, Choueiri, Toni K., Carraro, Dirce M., Houlston, Richard, Eckel-Passow, Jeanette E., Abbosh, Philip H., Ganna, Andrea, Brennan, Paul, Gu, Jian, and Chanock, Stephen J.

Published
2024
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2. Transcriptome- and proteome-wide association studies identify genes associated with renal cell carcinoma

Author

Purdue, Mark P., Dutta, Diptavo, Machiela, Mitchell J., Gorman, Bryan R., Winter, Timothy, Okuhara, Dayne, Cleland, Sara, Ferreiro-Iglesias, Aida, Scheet, Paul, Liu, Aoxing, Wu, Chao, Antwi, Samuel O., Larkin, James, Zequi, Stênio C., Sun, Maxine, Hikino, Keiko, Hajiran, Ali, Lawson, Keith A., Cárcano, Flavio, Blanchet, Odile, Shuch, Brian, Nepple, Kenneth G., Margue, Gaëlle, Sundi, Debasish, Diver, W. Ryan, Folgueira, Maria A.A.K., van Bokhoven, Adrie, Neffa, Florencia, Brown, Kevin M., Hofmann, Jonathan N., Rhee, Jongeun, Yeager, Meredith, Cole, Nathan R., Hicks, Belynda D., Manning, Michelle R., Hutchinson, Amy A., Rothman, Nathaniel, Huang, Wen-Yi, Linehan, W. Marston, Lori, Adriana, Ferragu, Matthieu, Zidane-Marinnes, Merzouka, Serrano, Sérgio, Magnabosco, Wesley J., BioBank Japan Project Consortium, Vilas, Ana, Decia, Ricardo, Carusso, Florencia, Graham, Laura S., Anderson, Kyra, Bilen, Mehmet A., Arciero, Cletus, Pellegrin, Isabelle, Ricard, Solène, FinnGen, Scelo, Ghislaine, Banks, Rosamonde E., Vasudev, Naveen S., Soomro, Naeem, Stewart, Grant D., Adeyoju, Adebanji, Bromage, Stephen, Hrouda, David, Gibbons, Norma, Patel, Poulam, Sullivan, Mark, Protheroe, Andrew, Nugent, Francesca I., Fournier, Michelle J., Zhang, Xiaoyu, Martin, Lisa J., Komisarenko, Maria, Eisen, Timothy, Cunningham, Sonia A., Connolly, Denise C., Uzzo, Robert G., Zaridze, David, Mukeria, Anush, Holcatova, Ivana, Hornakova, Anna, Foretova, Lenka, Janout, Vladimir, Mates, Dana, Jinga, Viorel, Rascu, Stefan, Mijuskovic, Mirjana, Savic, Slavisa, Milosavljevic, Sasa, Gaborieau, Valérie, Abedi-Ardekani, Behnoush, McKay, James, Johansson, Mattias, Phouthavongsy, Larry, Hayman, Lindsay, Li, Jason, Lungu, Ilinca, Bezerra, Stephania M., de Souza, Aline G., Sares, Claudia T.G., Reis, Rodolfo B., Gallucci, Fabio P., Cordeiro, Mauricio D., Pomerantz, Mark, Lee, Gwo-Shu M., Freedman, Matthew L., Jeong, Anhyo, Greenberg, Samantha E., Sanchez, Alejandro, Thompson, R. Houston, Sharma, Vidit, Thiel, David D., Ball, Colleen T., Abreu, Diego, Lam, Elaine T., Nahas, William C., Master, Viraj A., Patel, Alpa V., Bernhard, Jean-Christophe, Freedman, Neal D., Bigot, Pierre, Reis, Rui M., Colli, Leandro M., Finelli, Antonio, Manley, Brandon J., Terao, Chikashi, Choueiri, Toni K., Carraro, Dirce M., Houlston, Richard, Eckel-Passow, Jeanette E., Abbosh, Philip H., Ganna, Andrea, Brennan, Paul, Gu, Jian, Chanock, Stephen J., Guo, Xinyu, Winter, Timothy D., Jahagirdar, Om, Ha, Eunji, and Susztak, Katalin

Published
2024
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4. Tumor FAK orchestrates immunosuppression in ovarian cancer via the CD155/TIGIT axis

Author

Ozmadenci, Duygu, Narayanan, Jayanth S Shankara, Andrew, Jacob, Ojalill, Marjaana, Barrie, Allison M, Jiang, Shulin, Iyer, Samhita, Chen, Xiao Lei, Rose, Michael, Estrada, Valeria, Molinolo, Alfredo, Bertotto, Thomas, Mikulski, Zbigniew, McHale, Michael C, White, Rebekah R, Connolly, Denise C, Pachter, Jonathan A, Kuchroo, Vijay K, Stupack, Dwayne G, and Schlaepfer, David D

Subjects
Biomedical and Clinical Sciences, Oncology and Carcinogenesis, Immunology, Rare Diseases, Cancer, Ovarian Cancer, Development of treatments and therapeutic interventions, 5.1 Pharmaceuticals, Good Health and Well Being, Animals, Carcinoma, Ovarian Epithelial, Female, Focal Adhesion Kinase 1, Focal Adhesion Protein-Tyrosine Kinases, Humans, Immunosuppression Therapy, Ligands, Mice, Ovarian Neoplasms, Receptors, Immunologic, high-grade serous ovarian cancer, immunotherapy, FAK, CD155, tertiary lymphoid structures
Abstract

High-grade serous ovarian cancer (HGSOC) is a lethal malignancy characterized by an immunosuppressive tumor microenvironment containing few tumor infiltrating lymphocytes (TILs) and an insensitivity to checkpoint inhibitor immunotherapies. Gains in the PTK2 gene encoding focal adhesion kinase (FAK) at Chr8 q24.3 occur in ∼70% of HGSOC tumors, and elevated FAK messenger RNA (mRNA) levels are associated with poor patient survival. Herein, we show that active FAK, phosphorylated at tyrosine-576 within catalytic domain, is significantly increased in late-stage HGSOC tumors. Active FAK costained with CD155, a checkpoint receptor ligand for TIGIT (T cell immunoreceptor with immunoglobulin and immunoreceptor tyrosine-based inhibitory motif domains), in HGSOC tumors and a selective association between FAK and TIGIT checkpoint ligands were supported by patient transcriptomic database analysis. HGSOC tumors with high FAK expression were associated with low CD3 mRNA levels. Accordingly, late-stage tumors showed elevated active FAK staining and significantly lower levels of CD3+ TILs. Using the KMF (Kras, Myc, FAK) syngeneic ovarian tumor model containing spontaneous PTK2 (FAK) gene gains, the effects of tumor intrinsic genetic or oral small molecule FAK inhibitior (FAKi; VS-4718) were evaluated in vivo. Blocking FAK activity decreased tumor burden, suppressed ascites KMF-associated CD155 levels, and increased peritoneal TILs. The combination of FAKi with blocking TIGIT antibody (1B4) maintained elevated TIL levels and reduced TIGIT+ T regulatory cell levels, prolonged host survival, increased CXCL13 levels, and led to the formation of omental tertiary lymphoid structures. Collectively, our studies support FAK and TIGIT targeting as a rationale immunotherapy combination for HGSOC.

Published
2022

5. FAK activity sustains intrinsic and acquired ovarian cancer resistance to platinum chemotherapy.

Author

Diaz Osterman, Carlos J, Ozmadenci, Duygu, Kleinschmidt, Elizabeth G, Taylor, Kristin N, Barrie, Allison M, Jiang, Shulin, Bean, Lisa M, Sulzmaier, Florian J, Jean, Christine, Tancioni, Isabelle, Anderson, Kristen, Uryu, Sean, Cordasco, Edward A, Li, Jian, Chen, Xiao Lei, Fu, Guo, Ojalill, Marjaana, Rappu, Pekka, Heino, Jyrki, Mark, Adam M, Xu, Guorong, Fisch, Kathleen M, Kolev, Vihren N, Weaver, David T, Pachter, Jonathan A, Győrffy, Balázs, McHale, Michael T, Connolly, Denise C, Molinolo, Alfredo, Stupack, Dwayne G, and Schlaepfer, David D

Subjects
Stem Cells, Animals, Humans, Mice, Ovarian Neoplasms, Disease Models, Animal, Cisplatin, Platinum, Proto-Oncogene Proteins c-myc, Antineoplastic Agents, Signal Transduction, Drug Resistance, Neoplasm, Female, Proto-Oncogene Proteins p21(ras), Focal Adhesion Kinase 1, beta-catenin, cancer biology, focal adhesion kinase FAK, mouse, ovarian cancer, platinum chemotherapy, pluripotency, tumorspheres, Rare Diseases, Genetics, Stem Cell Research, Ovarian Cancer, Cancer, 2.1 Biological and endogenous factors, Biochemistry and Cell Biology
Abstract

Gene copy number alterations, tumor cell stemness, and the development of platinum chemotherapy resistance contribute to high-grade serous ovarian cancer (HGSOC) recurrence. Stem phenotypes involving Wnt-β-catenin, aldehyde dehydrogenase activities, intrinsic platinum resistance, and tumorsphere formation are here associated with spontaneous gains in Kras, Myc and FAK (KMF) genes in a new aggressive murine model of ovarian cancer. Adhesion-independent FAK signaling sustained KMF and human tumorsphere proliferation as well as resistance to cisplatin cytotoxicity. Platinum-resistant tumorspheres can acquire a dependence on FAK for growth. Accordingly, increased FAK tyrosine phosphorylation was observed within HGSOC patient tumors surviving neo-adjuvant chemotherapy. Combining a FAK inhibitor with platinum overcame chemoresistance and triggered cell apoptosis. FAK transcriptomic analyses across knockout and reconstituted cells identified 135 targets, elevated in HGSOC, that were regulated by FAK activity and β-catenin including Myc, pluripotency and DNA repair genes. These studies reveal an oncogenic FAK signaling role supporting chemoresistance.

Published
2019

6. FAK activity sustains intrinsic and acquired ovarian cancer resistance to platinum chemotherapy

Author

Osterman, Carlos J Diaz, Ozmadenci, Duygu, Kleinschmidt, Elizabeth G, Taylor, Kristin N, Barrie, Allison M, Jiang, Shulin, Bean, Lisa M, Sulzmaier, Florian J, Jean, Christine, Tancioni, Isabelle, Anderson, Kristen, Uryu, Sean, Cordasco, Edward A, Li, Jian, Chen, Xiao Lei, Fu, Guo, Ojalill, Marjaana, Rappu, Pekka, Heino, Jyrki, Mark, Adam M, Xu, Guorong, Fisch, Kathleen M, Kolev, Vihren N, Weaver, David T, Pachter, Jonathan A, Győrffy, Balázs, McHale, Michael T, Connolly, Denise C, Molinolo, Alfredo, Stupack, Dwayne G, and Schlaepfer, David D

Subjects
Biochemistry and Cell Biology, Biomedical and Clinical Sciences, Oncology and Carcinogenesis, Biological Sciences, Ovarian Cancer, Genetics, Rare Diseases, Women's Health, Cancer, Clinical Research, 2.1 Biological and endogenous factors, 5.1 Pharmaceuticals, Animals, Antineoplastic Agents, Cisplatin, Disease Models, Animal, Drug Resistance, Neoplasm, Female, Focal Adhesion Kinase 1, Humans, Mice, Ovarian Neoplasms, Platinum, Proto-Oncogene Proteins c-myc, Proto-Oncogene Proteins p21(ras), Signal Transduction, Stem Cells, beta-catenin, cancer biology, focal adhesion kinase FAK, mouse, ovarian cancer, platinum chemotherapy, pluripotency, tumorspheres, Biological sciences, Biomedical and clinical sciences, Health sciences
Abstract

Gene copy number alterations, tumor cell stemness, and the development of platinum chemotherapy resistance contribute to high-grade serous ovarian cancer (HGSOC) recurrence. Stem phenotypes involving Wnt-β-catenin, aldehyde dehydrogenase activities, intrinsic platinum resistance, and tumorsphere formation are here associated with spontaneous gains in Kras, Myc and FAK (KMF) genes in a new aggressive murine model of ovarian cancer. Adhesion-independent FAK signaling sustained KMF and human tumorsphere proliferation as well as resistance to cisplatin cytotoxicity. Platinum-resistant tumorspheres can acquire a dependence on FAK for growth. Accordingly, increased FAK tyrosine phosphorylation was observed within HGSOC patient tumors surviving neo-adjuvant chemotherapy. Combining a FAK inhibitor with platinum overcame chemoresistance and triggered cell apoptosis. FAK transcriptomic analyses across knockout and reconstituted cells identified 135 targets, elevated in HGSOC, that were regulated by FAK activity and β-catenin including Myc, pluripotency and DNA repair genes. These studies reveal an oncogenic FAK signaling role supporting chemoresistance.

Published
2019

7. Association of circulating tumor DNA with patient prognosis in surgically resected renal cell carcinoma.

Author

Correa, Andres F, Kalashnikova, Ekaterina, Wu, Hsin-Ta, Winters, Ryan M, Balcioglu, Mustafa, Sudhaman, Sumedha, Connolly, Denise C, Gong, Yulan, Uzzo, Robert G, Sethi, Himanshu, ElNaggar, Adam C, Aleshin, Alexey, Liu, Minetta C, and Abbosh, Philip H

Subjects
CANCER relapse, RESEARCH funding, DNA, DESCRIPTIVE statistics, RENAL cell carcinoma, NUCLEIC acids, EXTRACELLULAR space
Abstract

Background Despite complete resection, 20%-50% of patients with localized renal cell carcinoma (RCC) experience recurrence within 5 years. Accurate assessment of prognosis in high-risk patients would aid in improving outcomes. Here we evaluate the use of circulating tumor DNA (ctDNA) in RCC using banked samples and clinical data from a single institution. Methods The cohort consisted of 45 RCC patients (≥pT1b) who underwent complete resection. The presence of ctDNA in plasma was determined using a personalized, tumor-informed ctDNA assay (Signatera RUO, Natera, Inc.). Relationships with outcomes and other relevant clinical variables were assessed. The median follow-up was 62 months. Results Plasma ctDNA was detected in 18 out of 36 patients (50%) pre-operatively and was associated with increased tumor size (mean 9.3 cm vs. 7.0 cm, P  < .05) and high Fuhrman grade (60% grades III-IV vs 27% grade II, P  = .07). The presence of ctDNA, either pre-operatively or at any time post-operatively, was associated with inferior relapse-free survival (HR = 2.70, P  = .046; HR = 3.23, P  = .003, respectively). Among patients who were ctDNA positive at any time point, the sensitivity of relapse prediction was 84% with a PPV of 90%. Of note, ctDNA positivity at a post-surgical time point revealed a PPV of 100% and NPV of 64%. The lack of ctDNA detection at both time points yielded an NPV of 80%. Conclusions Detection of plasma ctDNA using a personalized assay is prognostic of recurrence in patients with resected RCC. Herein, we describe a successful approach for its application and identify potential limitations to be addressed in future studies. [ABSTRACT FROM AUTHOR]

Published
2024
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8. The BRCA1-Δ11q Alternative Splice Isoform Bypasses Germline Mutations and Promotes Therapeutic Resistance to PARP Inhibition and Cisplatin

Author

Wang, Yifan, Bernhardy, Andrea J, Cruz, Cristina, Krais, John J, Nacson, Joseph, Nicolas, Emmanuelle, Peri, Suraj, van der Gulden, Hanneke, van der Heijden, Ingrid, O'Brien, Shane W, Zhang, Yong, Harrell, Maribel I, Johnson, Shawn F, Dos Reis, Francisco J Candido, Pharoah, Paul DP, Karlan, Beth, Gourley, Charlie, Lambrechts, Diether, Chenevix-Trench, Georgia, Olsson, Håkan, Benitez, Javier J, Greene, Mark H, Gore, Martin, Nussbaum, Robert, Sadetzki, Siegal, Gayther, Simon A, Kjaer, Susanne K, Investigators, kConFab, D'Andrea, Alan D, Shapiro, Geoffrey I, Wiest, David L, Connolly, Denise C, Daly, Mary B, Swisher, Elizabeth M, Bouwman, Peter, Jonkers, Jos, Balmaña, Judith, Serra, Violeta, and Johnson, Neil

Subjects
Clinical Research, Ovarian Cancer, Breast Cancer, Cancer, Rare Diseases, Genetics, Aetiology, 2.1 Biological and endogenous factors, Good Health and Well Being, Alternative Splicing, Animals, BRCA1 Protein, Blotting, Western, Breast Neoplasms, Cisplatin, Drug Resistance, Neoplasm, Female, Fluorescent Antibody Technique, Germ-Line Mutation, Humans, Immunohistochemistry, Mice, Ovarian Neoplasms, Poly(ADP-ribose) Polymerase Inhibitors, Polymerase Chain Reaction, Protein Isoforms, Xenograft Model Antitumor Assays, kConFab Investigators, Oncology and Carcinogenesis, Oncology & Carcinogenesis
Abstract

Breast and ovarian cancer patients harboring BRCA1/2 germline mutations have clinically benefitted from therapy with PARP inhibitor (PARPi) or platinum compounds, but acquired resistance limits clinical impact. In this study, we investigated the impact of mutations on BRCA1 isoform expression and therapeutic response. Cancer cell lines and tumors harboring mutations in exon 11 of BRCA1 express a BRCA1-Δ11q splice variant lacking the majority of exon 11. The introduction of frameshift mutations to exon 11 resulted in nonsense-mediated mRNA decay of full-length, but not the BRCA1-Δ11q isoform. CRISPR/Cas9 gene editing as well as overexpression experiments revealed that the BRCA1-Δ11q protein was capable of promoting partial PARPi and cisplatin resistance relative to full-length BRCA1, both in vitro and in vivo Furthermore, spliceosome inhibitors reduced BRCA1-Δ11q levels and sensitized cells carrying exon 11 mutations to PARPi treatment. Taken together, our results provided evidence that cancer cells employ a strategy to remove deleterious germline BRCA1 mutations through alternative mRNA splicing, giving rise to isoforms that retain residual activity and contribute to therapeutic resistance. Cancer Res; 76(9); 2778-90. ©2016 AACR.

Published
2016

9. Contributors

Author

Agyemang, Amma F., primary, Alsop, Kathryn, additional, Au-Yeung, George, additional, Bates, Susan, additional, Bowtell, David D., additional, Christie, Elizabeth L., additional, Cole, Christopher B., additional, Connolly, Denise C., additional, Craig, Amaranta D., additional, deFazio, Anna, additional, Fereday, Sian, additional, Fojo, Antonio, additional, Freimund, Alison E., additional, Friedlander, Michael, additional, Gao, Bo, additional, Harnett, Paul R., additional, Hoang, Therese, additional, House, Carrie D., additional, Mapagu, Cristina, additional, Moore, Kathleen N., additional, Moujaber, Tania, additional, Odunsi, Kunle O., additional, Peri, Suraj, additional, Pishas, Kathleen, additional, Richardson, Debra L., additional, Sodi, Valerie L., additional, Soragni, Alice, additional, Trivedi, Meghna S., additional, Washington, Christina R., additional, and Waters, Jennifer A., additional

Published
2021
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11. Analyses of merlin/NF2 connection to FAK inhibitor responsiveness in serous ovarian cancer

Author

Shah, Nina R, Tancioni, Isabelle, Ward, Kristy K, Lawson, Christine, Chen, Xiao Lei, Jean, Christine, Sulzmaier, Florian J, Uryu, Sean, Miller, Nichol LG, Connolly, Denise C, and Schlaepfer, David D

Subjects
Biomedical and Clinical Sciences, Oncology and Carcinogenesis, Neurosciences, Rare Diseases, Neurofibromatosis, Ovarian Cancer, Cancer, Animals, Biomarkers, Tumor, Cell Line, Tumor, Cystadenocarcinoma, Serous, Female, Focal Adhesion Kinase 1, Gene Knockdown Techniques, Humans, Mice, Neurofibromin 2, Ovarian Neoplasms, Protein Kinase Inhibitors, Ovarian cancer, Focal adhesion kinase, Merlin, Tumor, Biomarker, Paediatrics and Reproductive Medicine, Oncology & Carcinogenesis, Clinical sciences, Oncology and carcinogenesis, Reproductive medicine
Abstract

ObjectiveFocal adhesion kinase (FAK) is overexpressed in serous ovarian cancer. Loss of merlin, a product of the neurofibromatosis 2 tumor suppressor gene, is being evaluated as a biomarker for FAK inhibitor sensitivity in mesothelioma. Connections between merlin and FAK in ovarian cancer remain undefined.MethodsNine human and two murine ovarian cancer cell lines were analyzed for growth in the presence of a small molecule FAK inhibitor (PF-271, also termed VS-6062) from 0.1 to 1 μM for 72 h. Merlin was evaluated by immunoblotting and immunostaining of a human ovarian tumor tissue array. Growth of cells was analyzed in an orthotopic tumor model and evaluated in vitro after stable shRNA-mediated merlin knockdown.ResultsGreater than 50% inhibition of OVCAR8, HEY, and ID8-IP ovarian carcinoma cell growth occurred with 0.1 μM PF-271 in anchorage-independent (p

Published
2014

13. Distinct expression levels and patterns of stem cell marker, aldehyde dehydrogenase isoform 1 (ALDH1), in human epithelial cancers.

Author

Deng, Shan, Yang, Xiaojun, Lassus, Heini, Liang, Shun, Kaur, Sippy, Ye, Qunrui, Li, Chunsheng, Wang, Li-Ping, Roby, Katherine F, Orsulic, Sandra, Connolly, Denise C, Zhang, Youcheng, Montone, Kathleen, Bützow, Ralf, Coukos, George, and Zhang, Lin

Subjects
Cell Line, Tumor, Epithelial Cells, Animals, Mice, Transgenic, Humans, Mice, Carcinoma, Ovarian Neoplasms, Isoenzymes, Prognosis, Immunohistochemistry, Gene Expression, Female, Retinal Dehydrogenase, Neoplastic Stem Cells, Biomarkers, Aldehyde Dehydrogenase 1, Cell Line, Tumor, Transgenic, General Science & Technology
Abstract

Aldehyde dehydrogenase isoform 1 (ALDH1) has been proved useful for the identification of cancer stem cells. However, our knowledge of the expression and activity of ALDH1 in common epithelial cancers and their corresponding normal tissues is still largely absent. Therefore, we characterized ALDH1 expression in 24 types of normal tissues and a large collection of epithelial tumor specimens (six cancer types, n = 792) by immunohistochemical staining. Using the ALDEFUOR assay, ALDH1 activity was also examined in 16 primary tumor specimens and 43 established epithelial cancer cell lines. In addition, an ovarian cancer transgenic mouse model and 7 murine ovarian cancer cell lines were analyzed. We found that the expression levels and patterns of ALDH1 in epithelial cancers are remarkably distinct, and they correlate with their corresponding normal tissues. ALDH1 protein expression levels are positively correlated with ALDH1 enzymatic activity measured by ALDEFLUOR assay. Long-term in vitro culture doesn't significantly affect ALDH1 activity in epithelial tumor cells. Consistent with research on other cancers, we found that high ALDH1 expression is significantly associated with poor clinical outcomes in serous ovarian cancer patients (n = 439, p = 0.0036). Finally, ALDH(br) tumor cells exhibit cancer stem cell properties and are resistant to chemotherapy. As a novel cancer stem cell marker, ALDH1 can be used for tumors whose corresponding normal tissues express ALDH1 in relatively restricted or limited levels such as breast, lung, ovarian or colon cancer.

Published
2010

14. Identification of BRCA1/2 mutation female carriers using circulating microRNA profiles

Author

Elias, Kevin, primary, Smyczynska, Urszula, additional, Stawiski, Konrad, additional, Nowicka, Zuzanna, additional, Webber, James, additional, Kaplan, Jakub, additional, Landen, Charles, additional, Lubinski, Jan, additional, Mukhopadhyay, Asima, additional, Chakraborty, Dona, additional, Connolly, Denise C., additional, Symecko, Heather, additional, Domchek, Susan M., additional, Garber, Judy E., additional, Konstantinopoulos, Panagiotis, additional, Fendler, Wojciech, additional, and Chowdhury, Dipanjan, additional

Published
2023
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15. Functional genomic landscape of acute myeloid leukaemia

Author

Tyner, Jeffrey W., Tognon, Cristina E., Bottomly, Daniel, Wilmot, Beth, Kurtz, Stephen E., Savage, Samantha L., Long, Nicola, Schultz, Anna Reister, Traer, Elie, Abel, Melissa, Agarwal, Anupriya, Blucher, Aurora, Borate, Uma, Bryant, Jade, Burke, Russell, Carlos, Amy, Carpenter, Richie, Carroll, Joseph, Chang, Bill H., Coblentz, Cody, d’Almeida, Amanda, Cook, Rachel, Danilov, Alexey, Dao, Kim-Hien T., Degnin, Michie, Devine, Deirdre, Dibb, James, Edwards, V, David K., Eide, Christopher A., English, Isabel, Glover, Jason, Henson, Rachel, Ho, Hibery, Jemal, Abdusebur, Johnson, Kara, Johnson, Ryan, Junio, Brian, Kaempf, Andy, Leonard, Jessica, Lin, Chenwei, Liu, Selina Qiuying, Lo, Pierrette, Loriaux, Marc M., Luty, Samuel, Macey, Tara, MacManiman, Jason, Martinez, Jacqueline, Mori, Motomi, Nelson, Dylan, Nichols, Ceilidh, Peters, Jill, Ramsdill, Justin, Rofelty, Angela, Schuff, Robert, Searles, Robert, Segerdell, Erik, Smith, Rebecca L., Spurgeon, Stephen E., Sweeney, Tyler, Thapa, Aashis, Visser, Corinne, Wagner, Jake, Watanabe-Smith, Kevin, Werth, Kristen, Wolf, Joelle, White, Libbey, Yates, Amy, Zhang, Haijiao, Cogle, Christopher R., Collins, Robert H., Connolly, Denise C., Deininger, Michael W., Drusbosky, Leylah, Hourigan, Christopher S., Jordan, Craig T., Kropf, Patricia, Lin, Tara L., Martinez, Micaela E., Medeiros, Bruno C., Pallapati, Rachel R., Pollyea, Daniel A., Swords, Ronan T., Watts, Justin M., Weir, Scott J., Wiest, David L., Winters, Ryan M., McWeeney, Shannon K., and Druker, Brian J.

Published
2018
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18. Supplementary Figures S1-S3 from Targeted Blockade of JAK/STAT3 Signaling Inhibits Ovarian Carcinoma Growth

Author

Gritsina, Galina, primary, Xiao, Fang, primary, O'Brien, Shane W., primary, Gabbasov, Rashid, primary, Maglaty, Marisa A., primary, Xu, Ren-Huan, primary, Thapa, Roshan J., primary, Zhou, Yan, primary, Nicolas, Emmanuelle, primary, Litwin, Samuel, primary, Balachandran, Siddharth, primary, Sigal, Luis J., primary, Huszar, Dennis, primary, and Connolly, Denise C., primary

Published
2023
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19. Data from Targeted Blockade of JAK/STAT3 Signaling Inhibits Ovarian Carcinoma Growth

Author

Gritsina, Galina, primary, Xiao, Fang, primary, O'Brien, Shane W., primary, Gabbasov, Rashid, primary, Maglaty, Marisa A., primary, Xu, Ren-Huan, primary, Thapa, Roshan J., primary, Zhou, Yan, primary, Nicolas, Emmanuelle, primary, Litwin, Samuel, primary, Balachandran, Siddharth, primary, Sigal, Luis J., primary, Huszar, Dennis, primary, and Connolly, Denise C., primary

Published
2023
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20. Supplementary Figure from Ovarian Cancers with Low CIP2A Tumor Expression Constitute an APR-246–Sensitive Disease Subtype

Author

Cvrljevic, Anna N., primary, Butt, Umar, primary, Huhtinen, Kaisa, primary, Grönroos, Tove J., primary, Böckelman, Camilla, primary, Lassus, Heini, primary, Butzow, Ralf, primary, Haglund, Caj, primary, Kaipio, Katja, primary, Arsiola, Tiina, primary, Laajala, Teemu D., primary, Connolly, Denise C., primary, Ristimäki, Ari, primary, Carpen, Olli, primary, Pouwels, Jeroen, primary, and Westermarck, Jukka, primary

Published
2023
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21. Supplemental Table 1 from Targeted Blockade of JAK/STAT3 Signaling Inhibits Ovarian Carcinoma Growth

Author

Gritsina, Galina, primary, Xiao, Fang, primary, O'Brien, Shane W., primary, Gabbasov, Rashid, primary, Maglaty, Marisa A., primary, Xu, Ren-Huan, primary, Thapa, Roshan J., primary, Zhou, Yan, primary, Nicolas, Emmanuelle, primary, Litwin, Samuel, primary, Balachandran, Siddharth, primary, Sigal, Luis J., primary, Huszar, Dennis, primary, and Connolly, Denise C., primary

Published
2023
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22. Supplementary Data from Ovarian Cancers with Low CIP2A Tumor Expression Constitute an APR-246–Sensitive Disease Subtype

Author

Cvrljevic, Anna N., primary, Butt, Umar, primary, Huhtinen, Kaisa, primary, Grönroos, Tove J., primary, Böckelman, Camilla, primary, Lassus, Heini, primary, Butzow, Ralf, primary, Haglund, Caj, primary, Kaipio, Katja, primary, Arsiola, Tiina, primary, Laajala, Teemu D., primary, Connolly, Denise C., primary, Ristimäki, Ari, primary, Carpen, Olli, primary, Pouwels, Jeroen, primary, and Westermarck, Jukka, primary

Published
2023
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23. Supplemental Table 2 from Targeted Blockade of JAK/STAT3 Signaling Inhibits Ovarian Carcinoma Growth

Author

Gritsina, Galina, primary, Xiao, Fang, primary, O'Brien, Shane W., primary, Gabbasov, Rashid, primary, Maglaty, Marisa A., primary, Xu, Ren-Huan, primary, Thapa, Roshan J., primary, Zhou, Yan, primary, Nicolas, Emmanuelle, primary, Litwin, Samuel, primary, Balachandran, Siddharth, primary, Sigal, Luis J., primary, Huszar, Dennis, primary, and Connolly, Denise C., primary

Published
2023
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24. Supplementary Table from Ovarian Cancers with Low CIP2A Tumor Expression Constitute an APR-246–Sensitive Disease Subtype

Author

Cvrljevic, Anna N., primary, Butt, Umar, primary, Huhtinen, Kaisa, primary, Grönroos, Tove J., primary, Böckelman, Camilla, primary, Lassus, Heini, primary, Butzow, Ralf, primary, Haglund, Caj, primary, Kaipio, Katja, primary, Arsiola, Tiina, primary, Laajala, Teemu D., primary, Connolly, Denise C., primary, Ristimäki, Ari, primary, Carpen, Olli, primary, Pouwels, Jeroen, primary, and Westermarck, Jukka, primary

Published
2023
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27. Supplementary Data from CIP2A Interacts with TopBP1 and Drives Basal-Like Breast Cancer Tumorigenesis

Author

Laine, Anni, primary, Nagelli, Srikar G., primary, Farrington, Caroline, primary, Butt, Umar, primary, Cvrljevic, Anna N., primary, Vainonen, Julia P., primary, Feringa, Femke M., primary, Grönroos, Tove J., primary, Gautam, Prson, primary, Khan, Sofia, primary, Sihto, Harri, primary, Qiao, Xi, primary, Pavic, Karolina, primary, Connolly, Denise C., primary, Kronqvist, Pauliina, primary, Elo, Laura L., primary, Maurer, Jochen, primary, Wennerberg, Krister, primary, Medema, Rene H., primary, Joensuu, Heikki, primary, Peuhu, Emilia, primary, de Visser, Karin, primary, Narla, Goutham, primary, and Westermarck, Jukka, primary

Published
2023
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28. Supplementary Figure S6 from The BRCA1-Δ11q Alternative Splice Isoform Bypasses Germline Mutations and Promotes Therapeutic Resistance to PARP Inhibition and Cisplatin

Author

Wang, Yifan, primary, Bernhardy, Andrea J., primary, Cruz, Cristina, primary, Krais, John J., primary, Nacson, Joseph, primary, Nicolas, Emmanuelle, primary, Peri, Suraj, primary, van der Gulden, Hanneke, primary, van der Heijden, Ingrid, primary, O'Brien, Shane W., primary, Zhang, Yong, primary, Harrell, Maribel I., primary, Johnson, Shawn F., primary, Candido Dos Reis, Francisco J., primary, Pharoah, Paul D. P., primary, Karlan, Beth, primary, Gourley, Charlie, primary, Lambrechts, Diether, primary, Chenevix-Trench, Georgia, primary, Olsson, Håkan, primary, Benitez, Javier J., primary, Greene, Mark H., primary, Gore, Martin, primary, Nussbaum, Robert, primary, Sadetzki, Siegal, primary, Gayther, Simon A., primary, Kjaer, Susanne K., primary, D'Andrea, Alan D., primary, Shapiro, Geoffrey I., primary, Wiest, David L., primary, Connolly, Denise C., primary, Daly, Mary B., primary, Swisher, Elizabeth M., primary, Bouwman, Peter, primary, Jonkers, Jos, primary, Balmaña, Judith, primary, Serra, Violeta, primary, and Johnson, Neil, primary

Published
2023
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29. Supplemental Figures and Legends from Follicle-Stimulating Hormone Receptor Is Expressed by Most Ovarian Cancer Subtypes and Is a Safe and Effective Immunotherapeutic Target

Author

Perales-Puchalt, Alfredo, primary, Svoronos, Nikolaos, primary, Rutkowski, Melanie R., primary, Allegrezza, Michael J., primary, Tesone, Amelia J., primary, Payne, Kyle K., primary, Wickramasinghe, Jayamanna, primary, Nguyen, Jenny M., primary, O'Brien, Shane W., primary, Gumireddy, Kiranmai, primary, Huang, Qihong, primary, Cadungog, Mark G., primary, Connolly, Denise C., primary, Tchou, Julia, primary, Curiel, Tyler J., primary, and Conejo-Garcia, Jose R., primary

Published
2023
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31. Data from The BRCA1-Δ11q Alternative Splice Isoform Bypasses Germline Mutations and Promotes Therapeutic Resistance to PARP Inhibition and Cisplatin

Author

Wang, Yifan, primary, Bernhardy, Andrea J., primary, Cruz, Cristina, primary, Krais, John J., primary, Nacson, Joseph, primary, Nicolas, Emmanuelle, primary, Peri, Suraj, primary, van der Gulden, Hanneke, primary, van der Heijden, Ingrid, primary, O'Brien, Shane W., primary, Zhang, Yong, primary, Harrell, Maribel I., primary, Johnson, Shawn F., primary, Candido Dos Reis, Francisco J., primary, Pharoah, Paul D. P., primary, Karlan, Beth, primary, Gourley, Charlie, primary, Lambrechts, Diether, primary, Chenevix-Trench, Georgia, primary, Olsson, Håkan, primary, Benitez, Javier J., primary, Greene, Mark H., primary, Gore, Martin, primary, Nussbaum, Robert, primary, Sadetzki, Siegal, primary, Gayther, Simon A., primary, Kjaer, Susanne K., primary, D'Andrea, Alan D., primary, Shapiro, Geoffrey I., primary, Wiest, David L., primary, Connolly, Denise C., primary, Daly, Mary B., primary, Swisher, Elizabeth M., primary, Bouwman, Peter, primary, Jonkers, Jos, primary, Balmaña, Judith, primary, Serra, Violeta, primary, and Johnson, Neil, primary

Published
2023
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34. Supplementary Tables S1-S4 from The BRCA1-Δ11q Alternative Splice Isoform Bypasses Germline Mutations and Promotes Therapeutic Resistance to PARP Inhibition and Cisplatin

Author

Wang, Yifan, primary, Bernhardy, Andrea J., primary, Cruz, Cristina, primary, Krais, John J., primary, Nacson, Joseph, primary, Nicolas, Emmanuelle, primary, Peri, Suraj, primary, van der Gulden, Hanneke, primary, van der Heijden, Ingrid, primary, O'Brien, Shane W., primary, Zhang, Yong, primary, Harrell, Maribel I., primary, Johnson, Shawn F., primary, Candido Dos Reis, Francisco J., primary, Pharoah, Paul D. P., primary, Karlan, Beth, primary, Gourley, Charlie, primary, Lambrechts, Diether, primary, Chenevix-Trench, Georgia, primary, Olsson, Håkan, primary, Benitez, Javier J., primary, Greene, Mark H., primary, Gore, Martin, primary, Nussbaum, Robert, primary, Sadetzki, Siegal, primary, Gayther, Simon A., primary, Kjaer, Susanne K., primary, D'Andrea, Alan D., primary, Shapiro, Geoffrey I., primary, Wiest, David L., primary, Connolly, Denise C., primary, Daly, Mary B., primary, Swisher, Elizabeth M., primary, Bouwman, Peter, primary, Jonkers, Jos, primary, Balmaña, Judith, primary, Serra, Violeta, primary, and Johnson, Neil, primary

Published
2023
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35. Supplementary Methods and References from The BRCA1-Δ11q Alternative Splice Isoform Bypasses Germline Mutations and Promotes Therapeutic Resistance to PARP Inhibition and Cisplatin

Author

Wang, Yifan, primary, Bernhardy, Andrea J., primary, Cruz, Cristina, primary, Krais, John J., primary, Nacson, Joseph, primary, Nicolas, Emmanuelle, primary, Peri, Suraj, primary, van der Gulden, Hanneke, primary, van der Heijden, Ingrid, primary, O'Brien, Shane W., primary, Zhang, Yong, primary, Harrell, Maribel I., primary, Johnson, Shawn F., primary, Candido Dos Reis, Francisco J., primary, Pharoah, Paul D. P., primary, Karlan, Beth, primary, Gourley, Charlie, primary, Lambrechts, Diether, primary, Chenevix-Trench, Georgia, primary, Olsson, Håkan, primary, Benitez, Javier J., primary, Greene, Mark H., primary, Gore, Martin, primary, Nussbaum, Robert, primary, Sadetzki, Siegal, primary, Gayther, Simon A., primary, Kjaer, Susanne K., primary, D'Andrea, Alan D., primary, Shapiro, Geoffrey I., primary, Wiest, David L., primary, Connolly, Denise C., primary, Daly, Mary B., primary, Swisher, Elizabeth M., primary, Bouwman, Peter, primary, Jonkers, Jos, primary, Balmaña, Judith, primary, Serra, Violeta, primary, and Johnson, Neil, primary

Published
2023
Full Text
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37. Supplemental Methods from Follicle-Stimulating Hormone Receptor Is Expressed by Most Ovarian Cancer Subtypes and Is a Safe and Effective Immunotherapeutic Target

Author

Perales-Puchalt, Alfredo, primary, Svoronos, Nikolaos, primary, Rutkowski, Melanie R., primary, Allegrezza, Michael J., primary, Tesone, Amelia J., primary, Payne, Kyle K., primary, Wickramasinghe, Jayamanna, primary, Nguyen, Jenny M., primary, O'Brien, Shane W., primary, Gumireddy, Kiranmai, primary, Huang, Qihong, primary, Cadungog, Mark G., primary, Connolly, Denise C., primary, Tchou, Julia, primary, Curiel, Tyler J., primary, and Conejo-Garcia, Jose R., primary

Published
2023
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41. Supplementary Figure Legends from The BRCA1-Δ11q Alternative Splice Isoform Bypasses Germline Mutations and Promotes Therapeutic Resistance to PARP Inhibition and Cisplatin

Author

Wang, Yifan, primary, Bernhardy, Andrea J., primary, Cruz, Cristina, primary, Krais, John J., primary, Nacson, Joseph, primary, Nicolas, Emmanuelle, primary, Peri, Suraj, primary, van der Gulden, Hanneke, primary, van der Heijden, Ingrid, primary, O'Brien, Shane W., primary, Zhang, Yong, primary, Harrell, Maribel I., primary, Johnson, Shawn F., primary, Candido Dos Reis, Francisco J., primary, Pharoah, Paul D. P., primary, Karlan, Beth, primary, Gourley, Charlie, primary, Lambrechts, Diether, primary, Chenevix-Trench, Georgia, primary, Olsson, Håkan, primary, Benitez, Javier J., primary, Greene, Mark H., primary, Gore, Martin, primary, Nussbaum, Robert, primary, Sadetzki, Siegal, primary, Gayther, Simon A., primary, Kjaer, Susanne K., primary, D'Andrea, Alan D., primary, Shapiro, Geoffrey I., primary, Wiest, David L., primary, Connolly, Denise C., primary, Daly, Mary B., primary, Swisher, Elizabeth M., primary, Bouwman, Peter, primary, Jonkers, Jos, primary, Balmaña, Judith, primary, Serra, Violeta, primary, and Johnson, Neil, primary

Published
2023
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45. Supplementary Figure 1 from NEDD9 Promotes Oncogenic Signaling in Mammary Tumor Development

Author

Izumchenko, Eugene, primary, Singh, Mahendra K., primary, Plotnikova, Olga V., primary, Tikhmyanova, Nadezhda, primary, Little, Joy L., primary, Serebriiskii, Ilya G., primary, Seo, Sachiko, primary, Kurokawa, Mineo, primary, Egleston, Brian L., primary, Klein-Szanto, Andres, primary, Pugacheva, Elena N., primary, Hardy, Richard R., primary, Wolfson, Marina, primary, Connolly, Denise C., primary, and Golemis, Erica A., primary

Published
2023
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46. Data from NEDD9 Promotes Oncogenic Signaling in Mammary Tumor Development

Author

Izumchenko, Eugene, primary, Singh, Mahendra K., primary, Plotnikova, Olga V., primary, Tikhmyanova, Nadezhda, primary, Little, Joy L., primary, Serebriiskii, Ilya G., primary, Seo, Sachiko, primary, Kurokawa, Mineo, primary, Egleston, Brian L., primary, Klein-Szanto, Andres, primary, Pugacheva, Elena N., primary, Hardy, Richard R., primary, Wolfson, Marina, primary, Connolly, Denise C., primary, and Golemis, Erica A., primary

Published
2023
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47. Supplementary Figure 2 from NEDD9 Promotes Oncogenic Signaling in Mammary Tumor Development

Author

Izumchenko, Eugene, primary, Singh, Mahendra K., primary, Plotnikova, Olga V., primary, Tikhmyanova, Nadezhda, primary, Little, Joy L., primary, Serebriiskii, Ilya G., primary, Seo, Sachiko, primary, Kurokawa, Mineo, primary, Egleston, Brian L., primary, Klein-Szanto, Andres, primary, Pugacheva, Elena N., primary, Hardy, Richard R., primary, Wolfson, Marina, primary, Connolly, Denise C., primary, and Golemis, Erica A., primary

Published
2023
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48. Supplementary Figure 3 from NEDD9 Promotes Oncogenic Signaling in Mammary Tumor Development

Author

Izumchenko, Eugene, primary, Singh, Mahendra K., primary, Plotnikova, Olga V., primary, Tikhmyanova, Nadezhda, primary, Little, Joy L., primary, Serebriiskii, Ilya G., primary, Seo, Sachiko, primary, Kurokawa, Mineo, primary, Egleston, Brian L., primary, Klein-Szanto, Andres, primary, Pugacheva, Elena N., primary, Hardy, Richard R., primary, Wolfson, Marina, primary, Connolly, Denise C., primary, and Golemis, Erica A., primary

Published
2023
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50. Supplementary Table 1 from NEDD9 Promotes Oncogenic Signaling in Mammary Tumor Development

Author

Izumchenko, Eugene, primary, Singh, Mahendra K., primary, Plotnikova, Olga V., primary, Tikhmyanova, Nadezhda, primary, Little, Joy L., primary, Serebriiskii, Ilya G., primary, Seo, Sachiko, primary, Kurokawa, Mineo, primary, Egleston, Brian L., primary, Klein-Szanto, Andres, primary, Pugacheva, Elena N., primary, Hardy, Richard R., primary, Wolfson, Marina, primary, Connolly, Denise C., primary, and Golemis, Erica A., primary

Published
2023
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