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Articles by Ryma Benayed
Cancer type-specific variation in patterns of driver alterations across 50,000 tumors
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.
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
TRK-rearranged spindle cell neoplasm: Initial observation of imaging appearance and clinicopathologic correlation
To explore pre-treatment imaging findings of neurotrophic tyrosine receptor kinase (NTRK)-rearranged spindle cell neoplasm, an emerging group of molecularly defined soft tissue tumors and summarize the clinical course, including TRK inhibitor therapy response. This retrospective study included 8 women and 4 men with NTRK-rearranged spindle cell neoplasm (median age, 35.5 years, range, 0–66). Available pre-treatment MRI, CT, PET, and US imaging were reviewed.
Overall survival with circulating tumor DNA-guided therapy in advanced non-small-cell lung cancer - Nature Medicine
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Abstract Circulating tumor DNA (ctDNA) sequencing guides therapy decisions but has been studied mostly in small cohorts without sufficient follow-up to determine its influence on overall survival. We prospectively followed an international cohort of 1,127 patients with non-small-cell lung cancer and ctDNA-guided therapy.
By Justin Jee, Jamie E. Chaft, A. Rose Brannon, Ryma Benayed, Ahmet Zehir, Nikolaus Schultz, Debyani Chakravarty, Ritika Kundra, Chong-Rui Xu, Helena A. Yu, Michael Offin, Piro Lito, Kathryn C. Arbour, Marjorie G. Zauderer, Daniela Molena, Stephen Clarke, David B. Solit, Andreas Rimner, Alexander Drilon, Sohrab P. Shah, Michael Berger, Ross Levine, Ronglai Shen, Pedram Razavi, Jorge S. Reis-Filho, David Jones, Charles M. Rudin, James M. Isbell, Randy Yeh, Candace Tong-Li
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Nature
Verified
Structure-function analysis of oncogenic EGFR Kinase Domain Duplication reveals insights into activation and a potential approach for therapeutic targeting | Nature Communications
Abstract Mechanistic understanding of oncogenic variants facilitates the development and optimization of treatment strategies. We recently identified in-frame, tandem duplication of EGFR exons 18 - 25, which causes EGFR Kinase Domain Duplication (EGFR-KDD). Here, we characterize the prevalence of ERBB family KDDs across multiple human cancers and evaluate the functional biochemistry of EGFR-KDD as it relates to pathogenesis and potential therapeutic intervention.
Pan-Trk Immunohistochemistry Is an Efficient and Reliable Screen for the Detection of NTRK Fusions
INTRODUCTION Neurotrophic tyrosine kinase receptor (NTRK) is a family of 3 proto-oncogenes including NTRK1, NTRK2, and NTRK3 which encode Trk A, Trk B, and Trk C proteins, respectively. The latter are involved in biological processes such as neuronal survival, differentiation, and plasticity under physiological circumstances. In various cancers, oncogenic fusions involving the kinase domain of NTRK1, 2, or 3 are present.
Diagnosis of known sarcoma fusions and novel fusion partners by targeted RNA sequencing with identification of a recurrent ACTB-FOSB fusion in pseudomyogenic hemangioendothelioma | Modern Pathology
1. Fletcher CDM, Gronchi A, Singer S, et al. Tumours of soft tissue: introduction. In: Fletcher CDM, Bridge JA, Hogendoorn PCW, Mertens F, (eds). World Health Organization., International Agency for Research on Cancer. WHO classification of tumours of soft tissue and bone. 4th ed. Lyon: International Agency for Research on Cancer (IARC); 2013. p. 10–18. 2. Taylor BS, Barretina J, Maki RG, Antonescu CR, Singer S, Ladanyi M. Advances in sarcoma genomics and new therapeutic targets. Nat Rev Cancer.
Erratum: Mutational landscape of metastatic cancer revealed from prospective clinical sequencing of 10,000 patients
In the version of this article initially published online, the top value in the y axis of the Kaplan–Meier plots in Figure 3c was incorrectly denoted as 0.1. The correct value is 1. The error has been corrected in the HTML and PDF versions of the article.
Mutational landscape of metastatic cancer revealed from prospective clinical sequencing of 10,000 patients
Tumor molecular profiling is a fundamental component of precision oncology, enabling the identification of genomic alterations in genes and pathways that can be targeted therapeutically. The existence of recurrent targetable alterations across distinct histologically defined tumor types, coupled with an expanding portfolio of molecularly targeted therapies, demands flexible and comprehensive approaches to profile clinically relevant genes across the full spectrum of cancers.
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