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Benjamin H. Lok
Researcher at Princess Margaret Cancer Centre
Publications - 69
Citations - 2163
Benjamin H. Lok is an academic researcher from Princess Margaret Cancer Centre. The author has contributed to research in topics: Radiation therapy & Medicine. The author has an hindex of 19, co-authored 58 publications receiving 1460 citations. Previous affiliations of Benjamin H. Lok include University of York & University of Toronto.
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Journal ArticleDOI
Chemosensitive Relapse in Small Cell Lung Cancer Proceeds through an EZH2-SLFN11 Axis
Eric E. Gardner,Eric E. Gardner,Benjamin H. Lok,Valentina E. Schneeberger,Patrice Desmeules,Linde A. Miles,Paige K. Arnold,Andy Ni,Inna Khodos,Elisa de Stanchina,Thuyen Nguyen,Julien Sage,John Campbell,Scott Ribich,Natasha Rekhtman,Afshin Dowlati,Pierre P. Massion,Charles M. Rudin,Charles M. Rudin,John T. Poirier +19 more
TL;DR: Inclusion of an EZH2 inhibitor with standard cytotoxic therapies prevented emergence of acquired resistance and augmented chemotherapeutic efficacy in both chemosensitive and chemoresistant models of small cell lung cancer.
Journal ArticleDOI
Unravelling the biology of SCLC: implications for therapy
Joshua K. Sabari,Benjamin H. Lok,James Laird,John T. Poirier,Charles M. Rudin,Charles M. Rudin +5 more
TL;DR: Progress made in uncovering aspects of the biology of SCLC and its microenvironment that are defining new therapeutic strategies and offering renewed hope for patients are reviewed.
Journal ArticleDOI
PARP Inhibitor Activity Correlates with SLFN11 Expression and Demonstrates Synergy with Temozolomide in Small Cell Lung Cancer.
Benjamin H. Lok,Eric E. Gardner,Eric E. Gardner,Valentina E. Schneeberger,Andy Ni,Patrice Desmeules,Natasha Rekhtman,Elisa de Stanchina,Beverly A. Teicher,Nadeem Riaz,S.N. Powell,S.N. Powell,John T. Poirier,John T. Poirier,Charles M. Rudin,Charles M. Rudin +15 more
TL;DR: SLFN11 is a relevant predictive biomarker of sensitivity to PARP inhibitor monotherapy in SCLC and combinatorial therapy with TMZ is identified as a particularly promising therapeutic strategy that warrants further clinical investigation.
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RAD52 inactivation is synthetically lethal with deficiencies in BRCA1 and PALB2 in addition to BRCA2 through RAD51-mediated homologous recombination.
TL;DR: Findings suggest that RAD52 is an alternative repair pathway of RAD51-mediated HR, and a target for therapy in cells deficient in the BRCA1–PALB2–BRCA2 repair pathway.
Journal ArticleDOI
Molecular pathways: understanding the role of Rad52 in homologous recombination for therapeutic advancement
Benjamin H. Lok,Simon N. Powell +1 more
TL;DR: Screening for ways to inhibit Rad52 would potentially provide a complementary strategy for targeting BRCA-deficient cancers in addition to poly (ADP-ribose) polymerase (PARP) inhibitors.