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2. Mechanism-centric regulatory network identifies NME2 and MYC programs as markers of Enzalutamide resistance in CRPC

Author

Panja, Sukanya, Truica, Mihai Ioan, Yu, Christina Y., Saggurthi, Vamshi, Craige, Michael W., Whitehead, Katie, Tuiche, Mayra V., Al-Saadi, Aymen, Vyas, Riddhi, Ganesan, Shridar, Gohel, Suril, Coffman, Frederick, Parrott, James S., Quan, Songhua, Jha, Shantenu, Kim, Isaac, Schaeffer, Edward, Kothari, Vishal, Abdulkadir, Sarki A., and Mitrofanova, Antonina

Published
2024
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4. Computational pathology improves risk stratification of a multi-gene assay for early stage ER+ breast cancer

Author

Chen, Yuli, Li, Haojia, Janowczyk, Andrew, Toro, Paula, Corredor, Germán, Whitney, Jon, Lu, Cheng, Koyuncu, Can F., Mokhtari, Mojgan, Buzzy, Christina, Ganesan, Shridar, Feldman, Michael D., Fu, Pingfu, Corbin, Haley, Harbhajanka, Aparna, Gilmore, Hannah, Goldstein, Lori J., Davidson, Nancy E., Desai, Sangeeta, Parmar, Vani, and Madabhushi, Anant

Published
2023
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6. The Pan‐Cancer Landscape of Coamplification of the Tyrosine Kinases KIT, KDR, and PDGFRA

Author

Disel, Umut, Madison, Russell, Abhishek, Kumar, Chung, Jon H, Trabucco, Sally E, Matos, Asli O, Frampton, Garrett M, Albacker, Lee A, Reddy, Venkataprasanth, Karadurmus, Nuri, Benson, Adam, Webster, Jennifer, Paydas, Semra, Cabanillas, Ruben, Nangia, Chaitali, Ozturk, MA, Millis, Sherri Z, Pal, Sumanta K, Wilky, Breelyn, Sokol, Ethan S, Gay, Laurie M, Soman, Salil, Ganesan, Shridar, Janeway, Katherine, Stephens, Phil J, Zhu, Viola W, Ou, Sai‐Hong Ignatius, Lovly, Christine M, Gounder, Mrinal, Schrock, Alexa B, Ross, Jeffrey S, Miller, Vincent A, Klempner, Samuel J, and Ali, Siraj M

Subjects
Cancer, Rare Diseases, Adolescent, Adult, Aged, Aged, 80 and over, Child, Child, Preschool, Gene Amplification, Humans, Middle Aged, Neoplasms, Receptor Protein-Tyrosine Kinases, Receptor, Platelet-Derived Growth Factor alpha, Vascular Endothelial Growth Factor Receptor-2, Young Adult, amplification, tyrosine kinase inhibitor, KIT, PDGFRA, genomic profiling, sarcoma, Oncology and Carcinogenesis, Oncology & Carcinogenesis
Abstract

PurposeAmplifications of receptor tyrosine kinases (RTKS) are therapeutic targets in multiple tumor types (e.g. HER2 in breast cancer), and amplification of the chromosome 4 segment harboring the three RTKs KIT, PDGFRA, and KDR (4q12amp) may be similarly targetable. The presence of 4q12amp has been sporadically reported in small tumor specific series but a large-scale analysis is lacking. We assess the pan-cancer landscape of 4q12amp and provide early clinical support for the feasibility of targeting this amplicon.Experimental designTumor specimens from 132,872 patients with advanced cancer were assayed with hybrid capture based comprehensive genomic profiling which assays 186-315 genes for all classes of genomic alterations, including amplifications. Baseline demographic data were abstracted, and presence of 4q12amp was defined as 6 or more copies of KIT/KDR/PDGFRA. Concurrent alterations and treatment outcomes with matched therapies were explored in a subset of cases.ResultsOverall 0.65% of cases harbored 4q12amp at a median copy number of 10 (range 6-344). Among cancers with >100 cases in this series, glioblastomas, angiosarcomas, and osteosarcomas were enriched for 4q12amp at 4.7%, 4.8%, and 6.4%, respectively (all p < 0.001), giving an overall sarcoma (n = 6,885) incidence of 1.9%. Among 99 pulmonary adenocarcinoma cases harboring 4q12amp, 50 (50%) lacked any other known driver of NSLCC. Four index cases plus a previously reported case on treatment with empirical TKIs monotherapy had stable disease on average exceeding 20 months.ConclusionWe define 4q12amp as a significant event across the pan-cancer landscape, comparable to known pan-cancer targets such as NTRK and microsatellite instability, with notable enrichment in several cancers such as osteosarcoma where standard treatment is limited. The responses to available TKIs observed in index cases strongly suggest 4q12amp is a druggable oncogenic target across cancers that warrants a focused drug development strategy.Implications for practiceCoamplification of the receptor tyrosine kinases (rtks) KIT/KDR/PDGFRA (4q12amp) is present broadly across cancers (0.65%), with enrichment in osteosarcoma and gliomas. Evidence for this amplicon having an oncogenic role is the mutual exclusivity of 4q12amp to other known drivers in 50% of pulmonary adenocarcinoma cases. Furthermore, preliminary clinical evidence for driver status comes from four index cases of patients empirically treated with commercially available tyrosine kinase inhibitors with activity against KIT/KDR/PDGFRA who had stable disease for 20 months on average. The sum of these lines of evidence suggests further clinical and preclinical investigation of 4q12amp is warranted as the possible basis for a pan-cancer drug development strategy.

Published
2020

7. Truncated FGFR2 is a clinically actionable oncogene in multiple cancers

Author

Zingg, Daniel, Bhin, Jinhyuk, Yemelyanenko, Julia, Kas, Sjors M., Rolfs, Frank, Lutz, Catrin, Lee, Jessica K., Klarenbeek, Sjoerd, Silverman, Ian M., Annunziato, Stefano, Chan, Chang S., Piersma, Sander R., Eijkman, Timo, Badoux, Madelon, Gogola, Ewa, Siteur, Bjørn, Sprengers, Justin, de Klein, Bim, de Goeij-de Haas, Richard R., Riedlinger, Gregory M., Ke, Hua, Madison, Russell, Drenth, Anne Paulien, van der Burg, Eline, Schut, Eva, Henneman, Linda, van Miltenburg, Martine H., Proost, Natalie, Zhen, Huiling, Wientjens, Ellen, de Bruijn, Roebi, de Ruiter, Julian R., Boon, Ute, de Korte-Grimmerink, Renske, van Gerwen, Bastiaan, Féliz, Luis, Abou-Alfa, Ghassan K., Ross, Jeffrey S., van de Ven, Marieke, Rottenberg, Sven, Cuppen, Edwin, Chessex, Anne Vaslin, Ali, Siraj M., Burn, Timothy C., Jimenez, Connie R., Ganesan, Shridar, Wessels, Lodewyk F. A., and Jonkers, Jos

Published
2022
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9. BRAF in Lung Cancers: Analysis of Patient Cases Reveals Recurrent BRAF Mutations, Fusions, Kinase Duplications, and Concurrent Alterations.

Author

Sheikine, Yuri, Pavlick, Dean, Klempner, Samuel J, Trabucco, Sally E, Chung, Jon H, Rosenzweig, Mark, Wang, Kai, Velcheti, Vamsidhar, Frampton, Garrett M, Peled, Nir, Murray, Molly, Chae, Young Kwang, Albacker, Lee A, Gay, Laurie, Husain, Hatim, Suh, James H, Millis, Sherri Z, Reddy, Venkataprasanth P, Elvin, Julia A, Hartmaier, Ryan J, Dowlati, Afshin, Stephens, Phil, Ross, Jeffrey S, Bivona, Trever G, Miller, Vincent A, Ganesan, Shridar, Schrock, Alexa B, Ou, Sai-Hong Ignatius, and Ali, Siraj M

Subjects
Cancer, Lung Cancer, Genetics, Human Genome, Lung, Development of treatments and therapeutic interventions, 5.1 Pharmaceuticals, Good Health and Well Being
Abstract

Dabrafenib and trametinib are approved for the management of advanced non-small-cell lung cancers (NSCLCs) that harbor BRAF V600E mutations. Small series and pan-cancer analyses have identified non-V600 alterations as therapeutic targets. We sought to examine a large genomic data set to comprehensively characterize non-V600 BRAF alterations in lung cancer. A total of 23,396 patients with lung cancer provided data to assay with comprehensive genomic profiling. Data were reviewed for predicted pathogenic BRAF base substitutions, short insertions and deletions, copy number changes, and rearrangements. Adenocarcinomas represented 65% of the occurrences; NSCLC not otherwise specified (NOS), 15%; squamous cell carcinoma, 12%; and small-cell lung carcinoma, 5%. BRAF was altered in 4.5% (1,048 of 23,396) of all tumors; 37.4% (n = 397) were BRAF V600E, 38% were BRAF non-V600E activating mutations, and 18% were BRAF inactivating. Rearrangements were observed at a frequency of 4.3% and consisted of N-terminal deletions (NTDs; 0.75%), kinase domain duplications (KDDs; 0.75%), and BRAF fusions (2.8%). The fusions involved three recurrent fusion partners: ARMC10, DOCK4, and TRIM24. BRAF V600E was associated with co-occurrence of SETD2 alterations, but other BRAF alterations were not and were instead associated with CDKN2A, TP53, and STK11 alterations (P < .05). Potential mechanisms of acquired resistance to BRAF V600E inhibition are demonstrated. This series characterized the frequent occurrence (4.4%) of BRAF alterations in lung cancers. Recurrent BRAF alterations in NSCLC adenocarcinoma are comparable to the frequency of other NSCLC oncogenic drivers, such as ALK, and exceed that of ROS1 or RET. This work supports a broad profiling approach in lung cancers and suggests that non-V600E BRAF alterations represent a subgroup of lung cancers in which targeted therapy should be considered.

Published
2018

13. Recurrence‐free survival dynamics following adjuvant chemotherapy for resected colorectal cancer: A systematic review of randomized controlled trials

Author

Vail, Emma, primary, Choubey, Ankur P., additional, Alexander, H. Richard, additional, August, David A., additional, Berry, Abril, additional, Boland, Patrick M., additional, Eskander, Mariam F., additional, Grandhi, Miral S., additional, Haliani, Brittany, additional, In, Haejin, additional, Kennedy, Timothy J., additional, Langan, Russell C., additional, Maggi, Jason C., additional, Pitt, Henry A., additional, Ganesan, Shridar, additional, and Ecker, Brett L., additional

Published
2024
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19. Impact of Environmental Temperature on Clinical Outcomes and Tumor Microenvironment of Early-Stage Breast Cancer

Author

Roy, Arya M, primary, Rosario, Spencer, additional, George, Anthony, additional, Hu, Qiang, additional, Czerniecki, Brian, additional, Carpten, John, additional, Borges, Virginia F, additional, Schneider, Bryan, additional, Kolesar, Jill, additional, Moskaluk, Christopher, additional, Shriver, Craig, additional, Matsen, Cindy, additional, Ganesan, Shridar, additional, Phadke, Sneha, additional, Razaq, Wajeeha, additional, Attwood, Kristopher, additional, and Gandhi, Shipra, additional

Published
2023
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24. Breaking satellite silence: human satellite II RNA expression in ovarian cancer

Author

Ganesan, Shridar

Subjects
Immune response -- Genetic aspects -- Health aspects, RNA -- Physiological aspects -- Health aspects, Ovarian cancer -- Genetic aspects -- Development and progression, Health care industry
Abstract

Multiple cancer types demonstrate abnormal expression of repetitive RNA sequences as a form of epigenetic instability. There is growing interest in understanding the role of repetitive RNAs in cancer pathogenesis and immunogenicity and in their potential role as diagnostic or therapeutic biomarkers. In this issue of the JCI, Porter and colleagues report on satellite RNA in a subset of ovarian cancers. The authors found that high expression of human satellite (HSAT) repeats--but not other families of repeats--was associated with an immunosuppressive phenotype in ovarian cancer cell lines and tumor samples. Further induction of HSAT RNA levels in vitro, surprisingly, leads to innate immune activation, suggesting a potential therapeutic strategy. This work highlights the expanding role of repetitive RNAs in tumor biology and the need to better define specific classes of repetitive elements expressed in cancer--as well as their role in tumorigenesis, tumor immunity, and the host response to cancer., Repetitive elements in the genome Repetitive elements constitute a substantial proportion (more than 50%) of the human genome and include interspersed repeats and tandem repeats (1, 2). Interspersed repeats include [...]

Published
2022
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25. Publisher Correction: Truncated FGFR2 is a clinically actionable oncogene in multiple cancers

Author

Zingg, Daniel, Bhin, Jinhyuk, Yemelyanenko, Julia, Kas, Sjors M., Rolfs, Frank, Lutz, Catrin, Lee, Jessica K., Klarenbeek, Sjoerd, Silverman, Ian M., Annunziato, Stefano, Chan, Chang S., Piersma, Sander R., Eijkman, Timo, Badoux, Madelon, Gogola, Ewa, Siteur, Bjørn, Sprengers, Justin, de Klein, Bim, de Goeij-de Haas, Richard R., Riedlinger, Gregory M., Ke, Hua, Madison, Russell, Drenth, Anne Paulien, van der Burg, Eline, Schut, Eva, Henneman, Linda, van Miltenburg, Martine H., Proost, Natalie, Zhen, Huiling, Wientjens, Ellen, de Bruijn, Roebi, de Ruiter, Julian R., Boon, Ute, de Korte-Grimmerink, Renske, van Gerwen, Bastiaan, Féliz, Luis, Abou-Alfa, Ghassan K., Ross, Jeffrey S., van de Ven, Marieke, Rottenberg, Sven, Cuppen, Edwin, Chessex, Anne Vaslin, Ali, Siraj M., Burn, Timothy C., Jimenez, Connie R., Ganesan, Shridar, Wessels, Lodewyk F. A., and Jonkers, Jos

Published
2022
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33. A phase I trial of riluzole and sorafenib in patients with advanced solid tumors: CTEP #8850

Author

Spencer, Kristen R., primary, Portal, Daniella E., additional, Aisner, Joseph, additional, Stein, Mark N., additional, Malhotra, Jyoti, additional, Shih, Weichung, additional, Chan, Nancy, additional, Silk, Ann W., additional, Ganesan, Shridar, additional, Goodin, Susan, additional, Gounder, Murugesan, additional, Lin, Hongxia, additional, Li, Jiadong, additional, Cerchio, Robert, additional, Marinaro, Christina, additional, Chen, Suzie, additional, and Mehnert, Janice M., additional

Published
2023
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34. Abstract 3488: Truncated FGFR2 - a clinically actionable oncogene in multiple cancers

Author

Zingg, Daniel Kaspar, primary, Bhin, Jinhyuk, additional, Yemelyanenko, Julia, additional, Kas, Sjors M., additional, Lutz, Catrin, additional, Lin, Chi-Chuan, additional, Klarenbeek, Sjoerd, additional, Lee, Jessica K., additional, Silverman, Ian M., additional, Annunziato, Stefano, additional, Ven, Marieke van de, additional, Ali, Siraj M., additional, Burn, Timothy C., additional, Ganesan, Shridar, additional, Wessels, Lodewyk F., additional, and Jonkers, Jos, additional

Published
2023
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35. Supplementary Tables 1-2 from Loss of 53BP1 Causes PARP Inhibitor Resistance in Brca1-Mutated Mouse Mammary Tumors

Author

Jaspers, Janneke E., primary, Kersbergen, Ariena, primary, Boon, Ute, primary, Sol, Wendy, primary, van Deemter, Liesbeth, primary, Zander, Serge A., primary, Drost, Rinske, primary, Wientjens, Ellen, primary, Ji, Jiuping, primary, Aly, Amal, primary, Doroshow, James H., primary, Cranston, Aaron, primary, Martin, Niall M.B., primary, Lau, Alan, primary, O'Connor, Mark J., primary, Ganesan, Shridar, primary, Borst, Piet, primary, Jonkers, Jos, primary, and Rottenberg, Sven, primary

Published
2023
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37. Supplementary Figures 1-10 from Loss of 53BP1 Causes PARP Inhibitor Resistance in Brca1-Mutated Mouse Mammary Tumors

Author

Jaspers, Janneke E., primary, Kersbergen, Ariena, primary, Boon, Ute, primary, Sol, Wendy, primary, van Deemter, Liesbeth, primary, Zander, Serge A., primary, Drost, Rinske, primary, Wientjens, Ellen, primary, Ji, Jiuping, primary, Aly, Amal, primary, Doroshow, James H., primary, Cranston, Aaron, primary, Martin, Niall M.B., primary, Lau, Alan, primary, O'Connor, Mark J., primary, Ganesan, Shridar, primary, Borst, Piet, primary, Jonkers, Jos, primary, and Rottenberg, Sven, primary

Published
2023
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46. Supplementary Figure Legends 1-10 from Loss of 53BP1 Causes PARP Inhibitor Resistance in Brca1-Mutated Mouse Mammary Tumors

Author

Jaspers, Janneke E., primary, Kersbergen, Ariena, primary, Boon, Ute, primary, Sol, Wendy, primary, van Deemter, Liesbeth, primary, Zander, Serge A., primary, Drost, Rinske, primary, Wientjens, Ellen, primary, Ji, Jiuping, primary, Aly, Amal, primary, Doroshow, James H., primary, Cranston, Aaron, primary, Martin, Niall M.B., primary, Lau, Alan, primary, O'Connor, Mark J., primary, Ganesan, Shridar, primary, Borst, Piet, primary, Jonkers, Jos, primary, and Rottenberg, Sven, primary

Published
2023
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50. Immunohistochemical analysis of adipokine and adipokine receptor expression in the breast tumor microenvironment: associations of lower leptin receptor expression with estrogen receptor-negative status and triple-negative subtype

Author

Llanos, Adana A. M., Lin, Yong, Chen, Wenjin, Yao, Song, Norin, Jorden, Chekmareva, Marina A., Omene, Coral, Cong, Lei, Omilian, Angela R., Khoury, Thaer, Hong, Chi-Chen, Ganesan, Shridar, Foran, David J., Higgins, Michael, Ambrosone, Christine B., Bandera, Elisa V., and Demissie, Kitaw

Published
2020
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