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Articles by Ping Chi
Fibroblast growth factor receptor inhibition for succinate dehydrogenase-deficient gastrointestinal stromal tumors: a phase 2 trial
Abstract While most gastrointestinal stromal tumors are driven by oncogenic mutations in KIT or PDGFRA, 10–15% exhibit functional loss of the succinate dehydrogenase (SDH) complex and genome-wide DNA hypermethylation. Excess methylation in SDH-deficient gastrointestinal stromal tumors disrupts genomic insulators, inducing aberrant expression of oncogenic ligands FGF3, FGF4, and activating an autocrine signaling loop mediated through FGFR1.
Cancer type-specific variation in patterns of driver alterations across 50,000 tumors
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Main text (Cancer Cell , 1–18, May 11, 2026) Due to a typesetting error, this article was initially published online with an incorrect Received date of March 4, 2025. The manuscript was originally submitted to on April 26, 2024, and subsequently transferred to on January 7, 2026. The Received date should have reflected the original submission date of April 26, 2024. The journal has now corrected the Received date online and apologizes to the authors and readers for the confusion.
By Chaitanya Bandlamudi, Daniel Muldoon, Ino de Bruijn, Mingxuan Zhang, Michael V. Gormally, Emily Harrold, Subhiksha Nandakumar, Shaleigh A. Smith, Mark Jeng, Sydney Woods, Kanika Arora, Walid K. Chatila, Bastien Nguyen, Henry Walch, Jun Woo, Craig M. Bielski, Christopher H Fong, Thinh Tran, Gaofei Zhao, Miika Mehine, Sam E. Tischfield, Allison Richards, Suraj Rajendran, Hongxin Zhang, Christoph K. Kreitzer, Ronak Shah, Risha Huq, Jesse Galle, Tina Alano, Ramyasree Madupuri, Ritika Kundra, Justin Jee, Karl Pichotta, Michele Waters, Richard A. Hickman, Josephine K. Dermawan, Jie-Fu Chen, Anton Safonov, Konrad H. Stopsack, Ritesh R. Kotecha, Hira Rizvi, Claire F. Friedman, Pedram Razavi, Ezra Y Rosen, Yonina R. Murciano-Goroff, Luc G.T. Morris, James A. Fagin, Ingo K. Mellinghoff, Ping Chi, Neerav Shukla, Adam Schoenfeld, Gregory J Riely, Charles M. Rudin, Alexander Drilon, Jake Lee, Hikmat Al-Ahmadie, Gopa Iyer, Anna Varghese, Eileen M. O’Reilly, Zsofia K. Stadler, Mark E. Robson, Ed Reznik, Jianjiong Gao, Diana Mandelker, Irina Ostrovnaya, Satshil Rana, Gowtham Jayakumaran, Anita S. Bowman, Abhinita S Mohanty, Anoop Rema Balakrishnan, Aijazuddin Syed, Ryan N. Ptashkin, Jacklyn Casanova-Murphy, Debyani Chakravarty, Ryma Benayed, Maria E. Arcila, Sarat Chandarlapaty, Helena A. Yu, Neal Rosen, Mark T.A. Donoghue, Christopher A Klebanoff, Rona Yaeger, A. Rose Brannon, Ahmet Zehir, Marc Ladanyi, Nikolaus Schultz, David B. Solit, Michael Berger Verified
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Cell Press
Verified
Cancer type-specific variation in patterns of driver alterations across 50,000 tumors
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Refers to: Keywords cancer type-specific tissue-specific driver alterations hotspots precision oncology clinical sequencing age of cancer diagnosis HLA genotype neoantigen-directed TCR therapies HLA loss of heterozygosity Introduction Cancer is a genetic disease defined by the serial acquisition of cell fitness-promoting mutations, referred to as “drivers.”1 Characterization of driver alterations is fundamental to understanding cancer pathogenesis, molecular classification of tumors, and...
By Chaitanya Bandlamudi, Daniel Muldoon, Ino de Bruijn, Mingxuan Zhang, Michael V. Gormally, Emily Harrold, Subhiksha Nandakumar, Shaleigh A. Smith, Mark Jeng, Sydney Woods, Kanika Arora, Walid K. Chatila, Bastien Nguyen, Henry Walch, Jun Woo, Craig M. Bielski, Christopher H Fong, Thinh Tran, Gaofei Zhao, Miika Mehine, Sam E. Tischfield, Allison Richards, Suraj Rajendran, Hongxin Zhang, Christoph K. Kreitzer, Ronak Shah, Risha Huq, Jesse Galle, Tina Alano, Ramyasree Madupuri, Ritika Kundra, Justin Jee, Karl Pichotta, Michele Waters, Richard A. Hickman, Josephine K. Dermawan, Jie-Fu Chen, Anton Safonov, Konrad H. Stopsack, Ritesh R. Kotecha, Hira Rizvi, Claire F. Friedman, Pedram Razavi, Ezra Y Rosen, Yonina R. Murciano-Goroff, Luc G.T. Morris, James A. Fagin, Ingo K. Mellinghoff, Ping Chi, Neerav Shukla, Adam Schoenfeld, Gregory J Riely, Charles M. Rudin, Alexander Drilon, Jake Lee, Hikmat Al-Ahmadie, Gopa Iyer, Anna Varghese, Eileen M. O'Reilly, Zsofia K. Stadler, Mark E. Robson, Ed Reznik, Jianjiong Gao, Diana Mandelker, Irina Ostrovnaya, Satshil Rana, Gowtham Jayakumaran, Anita S. Bowman, Abhinita S Mohanty, Anoop Rema Balakrishnan, Aijazuddin Syed, Ryan N. Ptashkin, Jacklyn Casanova-Murphy, Debyani Chakravarty, Ryma Benayed, Maria E. Arcila, Sarat Chandarlapaty, Helena A. Yu, Neal Rosen, Mark T.A. Donoghue, Christopher A Klebanoff, Rona Yaeger, A. Rose Brannon, Ahmet Zehir, Marc Ladanyi, Nikolaus Schultz, David B. Solit, Michael Berger Verified
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Cell Press
Verified
Loss of Kmt2c or Kmt2d primes urothelium for tumorigenesis and redistributes KMT2A–menin to bivalent promoters - Nature Genetics
Abstract Members of the KMT2C/D–KDM6A complex are recurrently mutated in urothelial carcinoma and in histologically normal urothelium. Here, using genetically engineered mouse models, we demonstrate that Kmt2c/d knockout in the urothelium led to impaired differentiation, augmented responses to growth and inflammatory stimuli and sensitization to oncogenic transformation by carcinogen and oncogenes.
Distinct genomic landscapes in radiation‐associated angiosarcoma compared with other radiation‐associated sarcoma histologies
Abstract MYC amplifications have been frequently detected in radiation (RT)-associated angiosarcomas (ASs) by low-resolution molecular methods. However, large-scale next-generation sequencing (NGS) studies to investigate the genomic landscape of RT-AS are scarce, particularly compared with other RT-associated sarcomas. We performed a detailed comparative genomic investigation of RT-AS versus other RT-associated histotypes, as well as sporadic sarcomas with similar histologies.
Phase II Trial of Imatinib Plus Binimetinib in Patients With Treatment-Naive Advanced Gastrointestinal Stromal Tumor
Abstract Dual targeting of the gastrointestinal stromal tumor (GIST) lineage-specific master regulators, ETV1 and KIT, by MEK and KIT inhibitors were synergistic preclinically and may enhance clinical efficacy. This trial was designed to test the efficacy and safety of imatinib plus binimetinib in first-line treatment of GIST.
Phase II Trial of Imatinib Plus Binimetinib in Patients With Treatment-Naive Advanced Gastrointestinal Stromal Tumor
Ping Chi, MD, PhD1,2,3; Li-Xuan Qin, PhD4; Bastien Nguyen, PhD1,5; Ciara M. Kelly, MD2,3; Sandra P. D'Angelo, MD2,3; Mark A. Dickson, MD2,3; Mrinal M. Gounder, MD2,3; Mary L. Keohan, MD2,3; Sujana Movva, MD2,3; Benjamin A. Nacev, MD, PhD2,3; Evan Rosenbaum, MD2,3; Katherine A. Thornton, MD2,3; Aimee M. Crago, MD, PhD6,7; Sam Yoon, MD6,7; Gary Ulaner, MD, PhD8,9; Randy Yeh, MD9; Moriah Martindale, BS2; Haley T. Phelan, RN2; Matthew D. Biniakewitz, RN2; Sarah Warda, BS1; Cindy J. Lee, MS1; Michael F.
Ripretinib intrapatient dose escalation after disease progression provides clinically meaningful outcomes in advanced gastrointestinal stromal tumour
Highlights • Treatment options are limited for advanced gastrointestinal stromal tumour (GIST). • Ripretinib is a novel oral switch-control tyrosine kinase inhibitor. • Ripretinib is approved for patients with advanced GIST in the fourth line and beyond. • Ripretinib dose escalation at progression provides clinical benefit in advanced GIST.
Switch Control Inhibition of KIT and PDGFRA in Patients With Advanced Gastrointestinal Stromal Tumor: A Phase I Study of Ripretinib
Activating genomic alterations in KIT or PDGFRA drive cellular growth in most gastrointestinal stromal tumors (GISTs) and other cancer types, including systemic mastocytosis and some glioblastomas.1-4 There is no curative therapy for metastatic GIST.
Expanding the Molecular Characterization of Thoracic Inflammatory Myofibroblastic Tumors beyond ALK Gene Rearrangements
Introduction Inflammatory myofibroblastic tumors (IMTs) display a wide morphologic spectrum, ranging from a predominantly inflammatory lesion with a paucity of spindle cells and prominent chronic inflammation and/or hyalinized stroma to a highly cellular myofibroblastic proliferation and occasionally frankly sarcomatous neoplasm lacking a significant inflammatory and/or stromal component.
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