F
Francisco Sanchez-Vega
Researcher at Memorial Sloan Kettering Cancer Center
Publications - 115
Citations - 20975
Francisco Sanchez-Vega is an academic researcher from Memorial Sloan Kettering Cancer Center. The author has contributed to research in topics: Cancer & Medicine. The author has an hindex of 36, co-authored 84 publications receiving 13474 citations. Previous affiliations of Francisco Sanchez-Vega include Washington University in St. Louis & National Institutes of Health.
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Journal ArticleDOI
Conditional Selection of Genomic Alterations Dictates Cancer Evolution and Oncogenic Dependencies.
Marco Mina,Marco Mina,Franck Raynaud,Franck Raynaud,Daniele Tavernari,Daniele Tavernari,Elena Battistello,Elena Battistello,Elena Battistello,Stephanie Sungalee,Sadegh Saghafinia,Sadegh Saghafinia,Sadegh Saghafinia,Titouan Laessle,Francisco Sanchez-Vega,Nikolaus Schultz,Elisa Oricchio,Giovanni Ciriello,Giovanni Ciriello +18 more
TL;DR: This work designed SELECT, an algorithmic approach to systematically identify evolutionary dependencies from alteration patterns, which provides a framework for the design of strategies to predict cancer progression and therapeutic response.
Journal ArticleDOI
KMT2C mediates the estrogen dependence of breast cancer through regulation of ERα enhancer function.
Kinisha Gala,Qing X. Li,Amit U. Sinha,Pedram Razavi,Madeline Dorso,Francisco Sanchez-Vega,Young Rock Chung,Ronald C. Hendrickson,James J. Hsieh,Michael F. Berger,Nikolaus Schultz,Alessandro Pastore,Omar Abdel-Wahab,Sarat Chandarlapaty,Sarat Chandarlapaty +14 more
TL;DR: KMT2C is a key regulator of ERα activity whose loss uncouples breast cancer proliferation from hormone abundance, and from a therapeutic standpoint, KMT-depleted cells that develop hormone-independence retain their dependence on ERα, displaying ongoing sensitivity to ERα antagonists.
Journal ArticleDOI
Mismatch Repair-Deficient Rectal Cancer and Resistance to Neoadjuvant Chemotherapy.
Andrea Cercek,Gustavo Dos Santos Fernandes,Campbell S.D. Roxburgh,Karuna Ganesh,S.Y. Ng,Francisco Sanchez-Vega,Rona Yaeger,Neil H. Segal,Diane Reidy-Lagunes,Anna M. Varghese,Arnold J. Markowitz,Chao Wu,Bryan C. Szeglin,Charles-Etienne Gabriel Sauve,Erin E. Salo-Mullen,Christina Tran,Zalak Patel,Asha Krishnan,Kaitlyn Tkachuk,Garrett M. Nash,Jose G. Guillem,Philip B. Paty,Jinru Shia,Nikolaus Schultz,Julio Garcia-Aguilar,Luis A. Diaz,Karyn A. Goodman,Leonard B. Saltz,Martin R. Weiser,J. Joshua Smith,Zsofia K. Stadler +30 more
Abstract: Purpose: Evaluate response of mismatch repair–deficient (dMMR) rectal cancer to neoadjuvant chemotherapy. Experimental Design: dMMR rectal tumors at Memorial Sloan Kettering Cancer Center (New York, NY) were retrospectively reviewed for characteristics, treatment, and outcomes. Fifty patients with dMMR rectal cancer were identified by IHC and/or microsatellite instability analysis, with initial treatment response compared with a matched MMR-proficient (pMMR) rectal cancer cohort. Germline and somatic mutation analyses were evaluated. Patient-derived dMMR rectal tumoroids were assessed for chemotherapy sensitivity. Results: Of 21 patients receiving neoadjuvant chemotherapy (fluorouracil/oxaliplatin), six (29%) had progression of disease. In comparison, no progression was noted in 63 pMMR rectal tumors (P = 0.0001). Rectal cancer dMMR tumoroids reflected this resistance to chemotherapy. No genomic predictors of chemotherapy response were identified. Of 16 patients receiving chemoradiation, 13 (93%) experienced tumor downstaging; one patient had stable disease, comparable with 48 pMMR rectal cancers. Of 13 patients undergoing surgery, 12 (92%) had early-stage disease. Forty-two (84%) of the 50 patients tested positive for Lynch syndrome with enrichment of germline MSH2 and MSH6 mutations when compared with 193 patients with Lynch syndrome–associated colon cancer (MSH2, 57% vs 36%; MSH6, 17% vs 9%; P Conclusions: Over one-fourth of dMMR rectal tumors treated with neoadjuvant chemotherapy exhibited disease progression. Conversely, dMMR rectal tumors were sensitive to chemoradiation. MMR status should be performed upfront in all locally advanced rectal tumors with careful monitoring for response on neoadjuvant chemotherapy and genetic testing for Lynch syndrome in patients with dMMR rectal cancer.
Journal ArticleDOI
The Underlying Tumor Genomics of Predominant Histologic Subtypes in Lung Adenocarcinoma.
Raul Caso,Francisco Sanchez-Vega,Kay See Tan,Brooke Mastrogiacomo,Jian Zhou,Gregory D. Jones,Bastien Nguyen,Nikolaus Schultz,James G. Connolly,Whitney S. Brandt,Matthew J. Bott,Gaetano Rocco,Daniela Molena,James M. Isbell,Yuan Liu,Marty W. Mayo,Prasad S. Adusumilli,William D. Travis,David R. Jones +18 more
TL;DR: These results provide the first in-depth assessment of tumor genomic profiling of predominant LUAD histologic subtypes, their associations with recurrence, and their correlation with targetable driver alterations in patients with surgically resected LUAD.
Journal ArticleDOI
Harmonization of Tumor Mutational Burden Quantification and Association With Response to Immune Checkpoint Blockade in Non-Small-Cell Lung Cancer.
Natalie I. Vokes,Natalie I. Vokes,David Liu,David Liu,Biagio Ricciuti,Elizabeth Jimenez-Aguilar,Hira Rizvi,Felix Dietlein,Felix Dietlein,Meng Xiao He,Claire A. Margolis,Claire A. Margolis,Haitham Elmarakeby,Haitham Elmarakeby,Jeffrey Girshman,Anika E. Adeni,Francisco Sanchez-Vega,Nikolaus Schultz,Suzanne E. Dahlberg,Ahmet Zehir,Pasi A. Jänne,Pasi A. Jänne,Mizuki Nishino,Mizuki Nishino,Renato Umeton,Renato Umeton,Lynette M. Sholl,Eliezer M. Van Allen,Eliezer M. Van Allen,Matthew D. Hellmann,Matthew D. Hellmann,Mark M. Awad +31 more
TL;DR: Heterogeneity in tumor mutational burden quantification across sequencing platforms limits the application and further study of this potential biomarker of response to immune checkpoint inhibitors (ICI), but z-score conversion harmonizes TMB values and enables integration of datasets derived from different sequencing panels.