Upon DNA breakage, a genomic locus undergoes alterations in three-dimensional chromatin architecture to facilitate signaling and repair. Although cells possess mechanisms to repair damaged DNA, it is ...

Cells generate purine nucleotides through de novo purine biosynthesis (DNPB) and purine salvage. Purine salvage represses DNPB to prevent excessive purine nucleotide synthesis through mechanisms that ...

Statistical thinking is a core part of solid, trustworthy biology. However, many studies still include insufficient sample sizes, have poor experimental design or select an incorrect statistical metho...

The Curie Institute Research CenterThe Institut Curie is a major player in the research and fight against cancer. It consists of a hospital and a Research Center of more than 1000 employees with a str...

Chromosomal instability (CIN) is a hallmark of cancer, and a primary cause of genetic heterogeneity in tumors. Depending on the degree of CIN and the affected tissue, CIN can promote or suppress tumor...

To study pathways that lead to aneuploidy during aging, the authors provide a system that enables cohesion protein depletion in mouse oocytes, mimicking effects that occur during aging. They uncover a...

Telomerase counteracts telomere shortening by repeatedly adding DNA repeats to chromosome ends. We identified the replication protein A (RPA) heterotrimer as a telomerase processivity factor critical ...

Homologous recombination (HR) deficiency upon Breast Cancer Gene 2 (BRCA2) loss arises from defects in the formation of RAD51 nucleoprotein filaments. We demonstrate that loss of the anti-recombinase ...

Mutations in the ATRX chromatin remodeller predispose to a developmental genetic disorder and cancer, but how it safeguards genome and telomere stability remains unresolved. Here, we uncover critical ...

The analysis of DNA sequence outcomes provides molecular insights into double-strand break (DSB) repair mechanisms. Using parallel in-pool profiling of Cas9-induced insertions and deletions (indels) w...

Department of Biochemistry, School of Medicine—Basic Sciences

The cell cycle is governed by tightly regulated checkpoints and proteogenomic oscillations that ensure genomic fidelity during cell proliferation. Dysregulation of the cell cycle can drive oncogenic transformation, and this positions it as a pivotal target in precision oncology. Recent advances reveal how proteomic and post-translational dynamics orchestrate cell-cycle phase transitions that are aberrantly disrupted in cancers. Therapeutic targeting of the CDK4/6 represents a cornerstone of cancer therapy, but resistance mechanisms limit its clinical efficacy. Emerging strategies such as targeted protein degradation, synthetic lethality, and combination immunotherapies further expand the therapeutic window. These innovations, coupled with biomarker-driven precision medicine, exploit cell-cycle vulnerabilities and transform them into an active tool to combat human cancers more effectively. This review highlights emerging mechanistic insights underlying tumorigenesis driven by an aberrant cell cycle and proposes potential therapeutics aimed at cell-cycle machinery-relevant targets.

YouTube video by Stowers Institute for Medical Research