Work

Chk1 inhibition potentiates the therapeutic efficacy of PARP inhibitor BMN673 in gastric cancer.

Year: 2017

Type: article

Abstract: experiments using a gastric cancer PDx model. The synergy between LY2606368 and PARP1 was likely caused by impaired the G2M checkpoint due to LY2606368 treatment, which forced mitotic entry and cell death in the presence of BMN673. In conclusion, we propose that Chk1 is a valued target for gastric cancer treatment, especially Chk1 inhibitor combined with PARP inhibitor may be a more effective therapeutic strategy in gastric cancer.

Source: PubMed Central

Authors: Yuping Yin, Qian Shen, Peng Zhang, Ruikang Tao, Weilong Chang, Ruidong Li, Gengchen Xie, Weizhen Liu, Lihong Zhang, Prabodh Kapoor, Shumei Song, Jaffer Ajani, Gordon B Mills, Jianying Chen, Kaixiong Tao, Guang Peng

Institutions: The University of Texas MD Anderson Cancer Center, Wuhan Union Hospital, Huazhong University of Science and Technology, The University of Texas at Austin, Tongji Hospital, University of California, Santa Cruz, The University of Texas Health Science Center at Tyler

Language: English

Topic: PARP inhibition in cancer therapy

Subfield: Oncology

Field: Medicine

Domain: Health Sciences

SDG: Good health and well-being

Open Access status: green

Funder: National Cancer Institute

Award: U.T. M. D. Anderson Cancer Center SPORE in Ovarian Cancer

OpenAlex ID: W2611411691

FWCI: 3.135

Cites: 26

Cited by: 52

Related to: 10