Recruitment of KMT2C/MLL3 to DNA Damage Sites Mediates DNA Damage Responses and Regulates PARP Inhibitor Sensitivity in Cancer-Reference-Cited by-同舟云学术

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Recruitment of KMT2C/MLL3 to DNA Damage Sites Mediates DNA Damage Responses and Regulates PARP Inhibitor Sensitivity in Cancer

Published:2021-04-14 Issue:12 Volume:81 Page:3358-3373
ISSN:0008-5472
Container-title:Cancer Research
language:en
Short-container-title:Cancer Res

Author:

Chang Antao,Liu Liang^ORCID,Ashby Justin M.,Wu Dan,Chen Yanan,O'Neill Stacey S.,Huang Shan,Wang Juan,Wang Guanwen,Cheng Dongmei,Tan Xiaoming,Petty W.J.,Pasche Boris C.^ORCID,Xiang Rong,Zhang Wei,Sun Peiqing

Funder

NIHNCINCI

China National Science Foundation

Publisher

American Association for Cancer Research (AACR)

Subject

Cancer Research,Oncology

Cited by 42 articles. 订阅此论文施引文献订阅此论文施引文献，注册后可以免费订阅5篇论文的施引文献，订阅后可以查看论文全部施引文献

1. A pan-cancer interrogation of intronic polyadenylation and its association with cancer characteristics;Briefings in Bioinformatics;2024-07-25

2. Pan‑cancer analysis on the role of KMT2C expression in tumor progression and immunotherapy;Oncology Letters;2024-07-19

3. Loss of Kmt2c or Kmt2d drives brain metastasis via KDM6A-dependent upregulation of MMP3;Nature Cell Biology;2024-06-26

4. Clinical, pathological and gene expression profiling of estrogen receptor discordance in breast cancer;Clinical and Translational Oncology;2024-06-26

5. The tumor-maintaining function of UTX/KDM6A in DNA replication and the PARP1-dependent repair pathway;2024-06-03

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