Functional interrogation of DNA damage response variants with base editing screens DOI
Raquel Cuella-Martin, Samuel B. Hayward, Xiao Fan

et al.

Cell, Journal Year: 2021, Volume and Issue: 184(4), P. 1081 - 1097.e19

Published: Feb. 1, 2021

Language: Английский

Shieldin complex promotes DNA end-joining and counters homologous recombination in BRCA1-null cells DOI
Harveer Dev,

Ting-Wei Chiang,

Chloé Lescale

et al.

Nature Cell Biology, Journal Year: 2018, Volume and Issue: 20(8), P. 954 - 965

Published: July 17, 2018

Language: Английский

Citations

365

Fanconi anaemia and cancer: an intricate relationship DOI
Grzegorz Nalepa,

D. Wade Clapp

Nature reviews. Cancer, Journal Year: 2018, Volume and Issue: 18(3), P. 168 - 185

Published: Jan. 29, 2018

Language: Английский

Citations

337

The antitumorigenic roles of BRCA1–BARD1 in DNA repair and replication DOI
Madalena Tarsounas, Patrick Sung

Nature Reviews Molecular Cell Biology, Journal Year: 2020, Volume and Issue: 21(5), P. 284 - 299

Published: Feb. 24, 2020

Language: Английский

Citations

276

The Roles of Histone Deacetylases and Their Inhibitors in Cancer Therapy DOI Creative Commons
Li Guo, Yuan Tian, Wei‐Guo Zhu

et al.

Frontiers in Cell and Developmental Biology, Journal Year: 2020, Volume and Issue: 8

Published: Sept. 29, 2020

Genetic mutations and abnormal gene regulation are key mechanisms underlying tumorigenesis. Nucleosomes, which consist of DNA wrapped around histone cores, represent the basic units chromatin. The fifth amino group (Nε) lysine residues is a common site for post-translational modifications (PTMs), these, acetylation second most common. Histone modulated by acetyltransferases (HATs) deacetylases (HDACs), involved in expression. Over past two decades, numerous studies characterizing HDACs HDAC inhibitors (HDACi) have provided novel exciting insights concerning their biological potential anti-cancer treatments. In this review, we detail diverse structures functions, including transcriptional regulation, metabolism, angiogenesis, damage response, cell cycle, apoptosis, protein degradation, immunity other several physiological processes. We also highlight avenues to use HDACi as novel, precision cancer

Language: Английский

Citations

269

Cellular Stress Responses in Radiotherapy DOI Creative Commons
Wanyeon Kim, Sungmin Lee, Danbi Seo

et al.

Cells, Journal Year: 2019, Volume and Issue: 8(9), P. 1105 - 1105

Published: Sept. 18, 2019

Radiotherapy is one of the major cancer treatment strategies. Exposure to penetrating radiation causes cellular stress, directly or indirectly, due generation reactive oxygen species, DNA damage, and subcellular organelle damage autophagy. These radiation-induced responses cooperatively contribute cell death, but paradoxically, radiotherapy also activation damage-repair survival signaling alleviate cytotoxic effects in a small percentage cells, these activations are responsible for tumor radio-resistance. The present study describes molecular mechanisms stress response radioresistance, therapeutic approaches used overcome radioresistance.

Language: Английский

Citations

264

DNA damage kinase signaling: checkpoint and repair at 30 years DOI Open Access
Michael C. Lanz, Diego Dibitetto, Marcus B. Smolka

et al.

The EMBO Journal, Journal Year: 2019, Volume and Issue: 38(18)

Published: Aug. 8, 2019

Language: Английский

Citations

243

DNA Damage and Cancer Immunotherapy: A STING in the Tale DOI Creative Commons
Timo Reisländer, Florian J. Groelly, Madalena Tarsounas

et al.

Molecular Cell, Journal Year: 2020, Volume and Issue: 80(1), P. 21 - 28

Published: Aug. 17, 2020

Language: Английский

Citations

243

Oxidative stress and DNA damage after cerebral ischemia: Potential therapeutic targets to repair the genome and improve stroke recovery DOI
Peiying Li, R. Anne Stetler, Rehana K. Leak

et al.

Neuropharmacology, Journal Year: 2017, Volume and Issue: 134, P. 208 - 217

Published: Nov. 8, 2017

Language: Английский

Citations

236

DNA damage checkpoint kinases in cancer DOI
Hannah L. Smith, Harriet Southgate, Deborah A. Tweddle

et al.

Expert Reviews in Molecular Medicine, Journal Year: 2020, Volume and Issue: 22

Published: Jan. 1, 2020

Abstract DNA damage response (DDR) pathway prevents high level endogenous and environmental being replicated passed on to the next generation of cells via an orchestrated integrated network cell cycle checkpoint signalling repair pathways. Depending type damage, where in it occurs different pathways are involved, with ATM-CHK2-p53 controlling G1 or ATR-CHK1-Wee1 S G2/M checkpoints. Loss control is common cancer through TP53, ATM mutations, Rb loss cyclin E overexpression, providing a stronger rationale for targeting S/G2 This review will focus ATM-CHK2-p53-p21 ATR-CHK1-WEE1 ongoing efforts target these patient benefit.

Language: Английский

Citations

232

Therapeutic Targeting of CDK12/CDK13 in Triple-Negative Breast Cancer DOI Creative Commons
Víctor Quereda,

Simon Bayle,

Francesca Vena

et al.

Cancer Cell, Journal Year: 2019, Volume and Issue: 36(5), P. 545 - 558.e7

Published: Oct. 24, 2019

Language: Английский

Citations

231