Jeffrey Li

University of California, Los Angeles

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Sentai Ding

Shandong Provincial Hospital

Kangling Xu

Shenzhen University

Xiangyi Li

Shanghai Jiao Tong University

Sam Ding

The University of Texas Southwestern Medical Center

Scott M. Dehm

University of Minnesota

Sandeep Burma

The University of Texas Health Science Center at San Antonio

Johann S. de Bono

Institute of Cancer Research

Felix Y. Feng

University of California, San Francisco

Ram S. Mani

The University of Texas Southwestern Medical Center

Ryan Hutchinson

The University of Texas Southwestern Medical Center

Cooperative Institutions

The University of Texas Southwestern Medical Center

University of California, Berkeley

Southwestern Medical Center

University of Michigan–Ann Arbor

University of California, Los Angeles

Los Angeles Medical Center

University of California, San Francisco

Shanghai Jiao Tong University

University of California, San Diego

Washtenaw Community College

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Figure S1 from Androgen Receptor Variants Mediate DNA Repair after Prostate Cancer Irradiation

Yi Yin Rui Li Kangling Xu Sentai Ding Jeffrey Li

ADT increases the ARV expression in ex vivo cultures of primary PCa tissues

Ex vivo

10.1158/0008-5472.22414328

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S2955 A Rare Case of an Asymptomatic Solitary Colonic Ganglioneuroma Found on Screening Colonoscopy

The American Journal of Gastroenterology (2024)

Sameeha Rau Jeffrey Li Mark Baniqued Bita Shahrvini Vismaya S. Bachu

10.14309/01.ajg.0001041188.02648.cf

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Structural basis for antibody inhibition of flavivirus NS1–triggered endothelial dysfunction

Science (2021)

Scott B. Biering David L. Akey Marcus P. Wong William Clay Brown Nicholas T. N. Lo

Two antibodies against flaviviruses Flaviviruses are a group of RNA viruses that include the human pathogens dengue virus, Zika virus, and West Nile virus. The envelope protein (E) on the virus surface has been the target of vaccine development, but problems have arisen with antibodies against E, leading to enhanced infection. Now, Modhiran et al. and Biering et al. describe two different antibodies that bind to the flavivirus NS1 protein and prevent it from disrupting epithelial cells, which is associated with severe disease. Both antibodies cross-react with multiple flavivirus NS1 proteins. The antibodies reduce viremia and increase survival in mouse models of flavivirus disease. Both papers include structures of NS1 bound to an antibody, which give insight into the protective mechanism. Science , this issue p. 190 , p. 194

Flavivirus

Viremia

Zika Virus

Antibody-dependent enhancement

10.1126/science.abc0476

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Figure S6 from Androgen Receptor Variants Mediate DNA Repair after Prostate Cancer Irradiation

Yi Yin Rui Li Kangling Xu Sentai Ding Jeffrey Li

Differential IR-induced interactions between ARfl and ARVs with DNA-PKc.

10.1158/0008-5472.22414313

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Figure S3 from Androgen Receptor Variants Mediate DNA Repair after Prostate Cancer Irradiation

Yi Yin Rui Li Kangling Xu Sentai Ding Jeffrey Li

Response profile of subcutaneous PCa xenografts to RT

10.1158/0008-5472.22414322

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Figure S3 from Androgen Receptor Variants Mediate DNA Repair after Prostate Cancer Irradiation

Yi Yin Rui Li Kangling Xu Sentai Ding Jeffrey Li

Response profile of subcutaneous PCa xenografts to RT

10.1158/0008-5472.22414322.v1

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Evaluating the Public Perception of Trees: How Do Residents in the Greendale and Burncoat Neighborhoods of Worcester, Massachusetts Value Trees in Their Neighborhoods.

Jeffrey Li Jeffrey Russell Robinson Kyle James Diaz

Value (mathematics)

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Data from Androgen Receptor Variants Mediate DNA Repair after Prostate Cancer Irradiation

Yi Yin Rui Li Kangling Xu Sentai Ding Jeffrey Li

<div>AbstractIn prostate cancer, androgen deprivation therapy (ADT) enhances the cytotoxic effects of radiotherapy. This effect is associated with weakening of the DNA damage response (DDR) normally supported by the androgen receptor. As a significant number of patients will fail combined ADT and radiotherapy, we hypothesized that DDR may be driven by androgen receptor splice variants (ARV) induced by ADT. Investigating this hypothesis, we found that ARVs increase the clonogenic survival of prostate cancer cells after irradiation in an ADT-independent manner. Notably, prostate cancer cell irradiation triggers binding of ARV to the catalytic subunit of the critical DNA repair kinase DNA-PK. Pharmacologic inhibition of DNA-PKc blocked this interaction, increased DNA damage, and elevated prostate cancer cell death after irradiation. Our findings provide a mechanistic rationale for therapeutic targeting of DNA-PK in the context of combined ADT and radiotherapy as a strategy to radiosensitize clinically localized prostate cancer. Cancer Res; 77(18); 4745–54. ©2017 AACR.</div>

10.1158/0008-5472.c.6508943

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Figure S2 from Androgen Receptor Variants Mediate DNA Repair after Prostate Cancer Irradiation

Yi Yin Rui Li Kangling Xu Sentai Ding Jeffrey Li

ARV mediates DDR and clonogenic survival.

10.1158/0008-5472.22414325

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Figure S2 from Androgen Receptor Variants Mediate DNA Repair after Prostate Cancer Irradiation

Yi Yin Rui Li Kangling Xu Sentai Ding Jeffrey Li

ARV mediates DDR and clonogenic survival.

10.1158/0008-5472.22414325.v1

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