Tolerance of Oncogene-Induced Replication Stress: A Fuel for Genomic Instability DOI Open Access
Taichi Igarashi,

Kimiyoshi Yano,

Satoshi Endo

et al.

Cancers, Journal Year: 2024, Volume and Issue: 16(20), P. 3507 - 3507

Published: Oct. 17, 2024

Activation of oncogenes disturbs a wide variety cellular processes and induces physiological dysregulation DNA replication, widely referred to as replication stress (RS). Oncogene-induced RS can cause forks stall or collapse, thereby leading damage. While the damage response (DDR) provoke an anti-tumor barrier prevent development cancer, small subset cells triggers tolerance (RST), allowing precancerous survive, promoting clonal expansion genomic instability (GIN). Genomic (GIN) is hallmark driving genetic alterations ranging from nucleotide changes aneuploidy. These increase probability oncogenic events create heterogeneous cell population with enhanced ability evolve. This review explores how major such RAS, cyclin E, MYC induce through diverse mechanisms. Additionally, we delve into strategies employed by normal cancer tolerate promote GIN. Understanding intricate relationship between oncogene activation, RS, GIN crucial better understand emerge develop potential therapies that target these vulnerabilities.

Language: Английский

The RB protein: more than a sentry of cell cycle entry DOI
Pulari U. Thangavelu, Cheng-Yu Lin, Farzaneh Forouz

et al.

Trends in Molecular Medicine, Journal Year: 2025, Volume and Issue: unknown

Published: April 1, 2025

Language: Английский

Citations

0
Tolerance of Oncogene-Induced Replication Stress: A Fuel for Genomic Instability DOI Open Access
Taichi Igarashi,

Kimiyoshi Yano,

Satoshi Endo

et al.

Cancers, Journal Year: 2024, Volume and Issue: 16(20), P. 3507 - 3507

Published: Oct. 17, 2024

Activation of oncogenes disturbs a wide variety cellular processes and induces physiological dysregulation DNA replication, widely referred to as replication stress (RS). Oncogene-induced RS can cause forks stall or collapse, thereby leading damage. While the damage response (DDR) provoke an anti-tumor barrier prevent development cancer, small subset cells triggers tolerance (RST), allowing precancerous survive, promoting clonal expansion genomic instability (GIN). Genomic (GIN) is hallmark driving genetic alterations ranging from nucleotide changes aneuploidy. These increase probability oncogenic events create heterogeneous cell population with enhanced ability evolve. This review explores how major such RAS, cyclin E, MYC induce through diverse mechanisms. Additionally, we delve into strategies employed by normal cancer tolerate promote GIN. Understanding intricate relationship between oncogene activation, RS, GIN crucial better understand emerge develop potential therapies that target these vulnerabilities.

Language: Английский

Citations

0