Yasir Elamin
University of Texas MD Anderson Cancer Center
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Featured researches published by Yasir Elamin.
Cold Spring Harb Mol Case Stud | 2017
Vijaykumar Holla; Yasir Elamin; Ann M. Bailey; Amber Johnson; Beate C. Litzenburger; Yekaterina B. Khotskaya; Nora Sanchez; Jia Zeng; Abu Shufean; Kenna R. Shaw; John Mendelsohn; Gordon B. Mills; Funda Meric-Bernstam; George R. Simon
The anaplastic lymphoma kinase (ALK) gene plays an important physiologic role in the development of the brain and can be oncogenically altered in several malignancies, including non-small-cell lung cancer (NSCLC) and anaplastic large cell lymphomas (ALCL). Most prevalent ALK alterations are chromosomal rearrangements resulting in fusion genes, as seen in ALCL and NSCLC. In other tumors, ALK copy-number gains and activating ALK mutations have been described. Dramatic and often prolonged responses are seen in patients with ALK alterations when treated with ALK inhibitors. Three of these—crizotinib, ceritinib, and alectinib—are now FDA approved for the treatment of metastatic NSCLC positive for ALK fusions. However, the emergence of resistance is universal. Newer ALK inhibitors and other targeting strategies are being developed to counteract the newly emergent mechanism(s) of ALK inhibitor resistance. This review outlines the recent developments in our understanding and treatment of tumors with ALK alterations.
Cancer Discovery | 2018
Ferdinandos Skoulidis; Michael E. Goldberg; Danielle Greenawalt; Matthew D. Hellmann; Mark M. Awad; Justin F. Gainor; Alexa B. Schrock; Ryan J. Hartmaier; Sally E. Trabucco; Siraj M. Ali; Julia A. Elvin; Gaurav Singal; Jeffrey S. Ross; David Fabrizio; Peter Szabo; Han Chang; Ariella Sasson; Sujaya Srinivasan; Stefan Kirov; Joseph D. Szustakowski; Patrik Vitazka; Robin Edwards; Jose A. Bufill; Neelesh Sharma; Sai-Hong Ignatius Ou; Nir Peled; David R. Spigel; Hira Rizvi; Elizabeth Jimenez Aguilar; Brett W. Carter
KRAS is the most common oncogenic driver in lung adenocarcinoma (LUAC). We previously reported that STK11/LKB1 (KL) or TP53 (KP) comutations define distinct subgroups of KRAS-mutant LUAC. Here, we examine the efficacy of PD-1 inhibitors in these subgroups. Objective response rates to PD-1 blockade differed significantly among KL (7.4%), KP (35.7%), and K-only (28.6%) subgroups (P < 0.001) in the Stand Up To Cancer (SU2C) cohort (174 patients) with KRAS-mutant LUAC and in patients treated with nivolumab in the CheckMate-057 phase III trial (0% vs. 57.1% vs. 18.2%; P = 0.047). In the SU2C cohort, KL LUAC exhibited shorter progression-free (P < 0.001) and overall (P = 0.0015) survival compared with KRASMUT;STK11/LKB1WT LUAC. Among 924 LUACs, STK11/LKB1 alterations were the only marker significantly associated with PD-L1 negativity in TMBIntermediate/High LUAC. The impact of STK11/LKB1 alterations on clinical outcomes with PD-1/PD-L1 inhibitors extended to PD-L1-positive non-small cell lung cancer. In Kras-mutant murine LUAC models, Stk11/Lkb1 loss promoted PD-1/PD-L1 inhibitor resistance, suggesting a causal role. Our results identify STK11/LKB1 alterations as a major driver of primary resistance to PD-1 blockade in KRAS-mutant LUAC.Significance: This work identifies STK11/LKB1 alterations as the most prevalent genomic driver of primary resistance to PD-1 axis inhibitors in KRAS-mutant lung adenocarcinoma. Genomic profiling may enhance the predictive utility of PD-L1 expression and tumor mutation burden and facilitate establishment of personalized combination immunotherapy approaches for genomically defined LUAC subsets. Cancer Discov; 8(7); 822-35. ©2018 AACR.See related commentary by Etxeberria et al., p. 794This article is highlighted in the In This Issue feature, p. 781.
Nature Medicine | 2018
Jacqulyne P. Robichaux; Yasir Elamin; Zhi Tan; Brett W. Carter; Shuxing Zhang; Shengwu Liu; Shuai Li; Ting Chen; Alissa Poteete; Adriana Estrada-Bernal; Anh T. Le; Anna Truini; Monique B. Nilsson; Huiying Sun; Emily Roarty; Sarah B. Goldberg; Julie R. Brahmer; Mehmet Altan; Charles Lu; Vassiliki Papadimitrakopoulou; Katerina Politi; Robert C. Doebele; Kwok-Kin Wong; John V. Heymach
Although most activating mutations of epidermal growth factor receptor (EGFR)-mutant non–small cell lung cancers (NSCLCs) are sensitive to available EGFR tyrosine kinase inhibitors (TKIs), a subset with alterations in exon 20 of EGFR and HER2 are intrinsically resistant and lack an effective therapy. We used in silico, in vitro, and in vivo testing to model structural alterations induced by exon 20 mutations and to identify effective inhibitors. 3D modeling indicated alterations restricted the size of the drug-binding pocket, limiting the binding of large, rigid inhibitors. We found that poziotinib, owing to its small size and flexibility, can circumvent these steric changes and is a potent inhibitor of the most common EGFR and HER2 exon 20 mutants. Poziotinib demonstrated greater activity than approved EGFR TKIs in vitro and in patient-derived xenograft models of EGFR or HER2 exon 20 mutant NSCLC and in genetically engineered mouse models of NSCLC. In a phase 2 trial, the first 11 patients with NSCLC with EGFR exon 20 mutations receiving poziotinib had a confirmed objective response rate of 64%. These data identify poziotinib as a potent, clinically active inhibitor of EGFR and HER2 exon 20 mutations and illuminate the molecular features of TKIs that may circumvent steric changes induced by these mutations.Poziotinib is a candidate inhibitor for a subset of EGFR or HER2 mutant non–small cell lung cancers that lack effective therapy.
Clinical Lung Cancer | 2018
Yasir Elamin; Daniel R. Gomez; Mara B. Antonoff; Jacqulyne P. Robichaux; Hai T. Tran; Melissa K. Shorter; Jadi M. Bohac; Marcelo Vailati Negrao; Xiuning Le; Waree Rinsurogkawong; Jeff Lewis; Lara Lacerda; Emily Roarty; Stephen G. Swisher; Jack A. Roth; Jianjun Zhang; Vassiliki Papadimitrakopoulou; John V. Heymach
Introduction: Although most NSCLC patients with sensitizing epidermal growth factor receptor (EGFR) mutations have an impressive initial response, the vast majority has residual disease and develops acquired resistance after 9 to 14 months of EGFR tyrosine kinase (TKI) therapy. We recently reported a phase II trial showing that, for patients with molecularly unselected oligometastatic NSCLC who did not progress after first‐line systemic therapy, local consolidation therapy (LCT) with surgery or radiation improved progression‐free survival (PFS), compared with maintenance therapy alone. Herein, we report a retrospective analysis of LCT after TKI in patients with metastatic EGFR mutant NSCLC. Patients and Methods: We identified patients with metastatic EGFR mutant NSCLC treated with TKI plus LCT or with TKI alone in the MD Anderson GEMINI (Genomic Marker‐Guided Therapy Initiative) database and in our recently published LCT trial. PFS was compared between LCT plus TKI and TKI only treated patients using the log‐rank test. Results: We identified 129 patients with EGFR mutant NSCLC who were treated with first‐line TKI and 12 that were treated with TKI followed by LCT. Among the 12 patients treated with TKI plus LCT, 8 patients had oligometastatic disease (defined as ≤ 3 metastases), and 4 patients had > 3 metastases. LCT regimens were hypofractionated radiotherapy or stereotactic ablative body radiotherapy for 11 patients and surgery for 1 patient. TKI followed by LCT resulted in a significantly longer PFS (36 months) compared with TKI alone (PFS, 14 months; log‐rank P = .0024). Conclusions: Our data suggests that first‐line TKI plus LCT is a promising therapeutic strategy for patients with EGFR mutant NSCLC that merits further investigation.
Journal of Clinical Oncology | 2017
Ferdinandos Skoulidis; Matthew D. Hellmann; Mark M. Awad; Hira Rizvi; Brett W. Carter; Warren Denning; Yasir Elamin; Jianjun Zhang; Giulia Costanza Leonardi; Darragh Halpenny; Andrew J. Plodkowski; Niamh Long; Jeremy J. Erasmus; Vassiliki Papadimitrakopoulou; Kwok-Kin Wong; Ignacio I. Wistuba; Pasi A. Jänne; Charles M. Rudin; John V. Heymach
Journal of Thoracic Oncology | 2017
Ferdinandos Skoulidis; Yasir Elamin; Vassiliki Papadimitrakopoulou; Pan Tong; Jing Wang; Jeff Lewis; Waree Rinsurongkawong; Caleb T. Chu; Emily Roarty; Jianjun Zhang; Hai T. Tran; Jaime Rodriguez-Canales; Edwin R. Parra; Carmen Behrens; Humam Kadara; Ignacio I. Wistuba; John V. Heymach
Journal of Thoracic Oncology | 2017
Yasir Elamin; Jacqulyne P. Robichaux; V. Lam; Anne Tsao; Charles Lu; George R. Blumenschein; J. Kurie; Julie R. Brahmer; Sigui Li; Ting Chen; A. Estrada-Bernal; Anna Truini; Monique B. Nilsson; Anh T. Le; Zhi Tan; Shuxing Zhang; Robert C. Doebele; Katerina Politi; Z. Yang; Shengwu Liu; Kwok-Kin Wong; John V. Heymach
Journal of Thoracic Oncology | 2017
Hai T. Tran; Jianjun Zhang; Marya Vasquez; Frank V. Fossella; George R. Simon; Anne Tsao; Don L. Gibbons; Yasir Elamin; Kimberly C. Banks; Richard B. Lanman; Vassiliki Papadimitrakopoulou; John V. Heymach
Journal of Thoracic Oncology | 2017
Yasir Elamin; Jacqulyne P. Robichaux; John V. Heymach
Ophthalmic Plastic and Reconstructive Surgery | 2018
Oded Sagiv; Stephanie Ding; Renata Ferrarotto; Bonnie S. Glisson; Mehmet Altan; Faye M. Johnson; Yasir Elamin; Sudip D. Thakar; Priyadharsini Nagarajan; Bita Esmaeli