Replication stress is a major cause of genomic instability and a crucial vulnerability of
cancer cells. This vulnerability can be therapeutically targeted by inhibiting kinases that …

Normal cells explore multiple states to survive stresses encountered during development
and self-renewal as well as environmental stresses such as starvation, DNA damage, toxins …

Uterine fibroid (UF) driver mutations in Mediator complex subunit 12 (MED12) trigger
genomic instability and tumor development through unknown mechanisms. Herein, we show …

Simple Summary Chemotherapeutic DNA-damaging agents targeting replication are widely
used but predictive rationales for drug combinations and patient selection still need clinical …

Background The microbiota inhabits the epithelial surfaces of hosts, which influences
physiological functions from helping digest food and acquiring nutrition to regulate …

DNA replication stress is a major source of DNA damage, including double-stranded breaks
that promote DNA damage response (DDR) signaling. Inefficient repair of such lesions can …

Purpose: Combining gemcitabine with CHK1 inhibition has shown promise in preclinical
models of pancreatic ductal adenocarcinoma (PDAC). Here, we report the findings from a …

In preparation for cell division, the genome must be copied with high fidelity. However,
replisomes often encounter obstacles, including bulky DNA lesions caused by reactive …

Head and neck squamous cell carcinoma (HNSCC) poses significant treatment challenges,
with high recurrence rates for locally advanced disease despite aggressive therapy typically …

Late‐stage colorectal cancer (CRC) is still a clinically challenging problem. The activity of
the tumor suppressor p53 is regulated via post‐translational modifications (PTMs). While the …