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3D chromatin remodeling potentiates transcriptional programs driving cell invasion.
Proc Natl Acad Sci U S A
September 2022
Department of Experimental Medicine, Faculty of Medicine, McGill University, Montréal, QC H4A 3J1, Canada.
Article Synopsis
- Deregulated chromatin architecture, particularly due to the loss of CTCF, plays a significant role in cancer progression, especially in breast cancer.
- Loss of a single CTCF allele disrupts chromatin insulation, leading to enhanced cell invasion and altered chromatin structure, affecting oncogene expression.
- This reorganization creates new promoter-enhancer interactions that make cancer cells more sensitive to mTOR inhibitors, indicating a potential therapeutic target.
Whole-Genome Duplication Shapes the Aneuploidy Landscape of Human Cancers.
Cancer Res
May 2022
Department of Human Molecular Genetics and Biochemistry, Faculty of Medicine, School of Medicine, Tel Aviv University, Tel Aviv, Israel.
Unlabelled: Aneuploidy is a hallmark of cancer with tissue-specific prevalence patterns that suggest it plays a driving role in cancer initiation and progression. However, the contribution of aneuploidy to tumorigenesis depends on both cellular and genomic contexts. Whole-genome duplication (WGD) is a common macroevolutionary event that occurs in more than 30% of human tumors early in tumorigenesis.
View Article and Find Full Text PDFNon-genetic and genetic rewiring underlie adaptation to hypomorphic alleles of an essential gene.
EMBO J
November 2021
Institute of Medical Biology (IMB), Agency for Science, Technology and Research (A*STAR), Singapore, Singapore.
Adaptive evolution to cellular stress is a process implicated in a wide range of biological and clinical phenomena. Two major routes of adaptation have been identified: non-genetic changes, which allow expression of different phenotypes in novel environments, and genetic variation achieved by selection of fitter phenotypes. While these processes are broadly accepted, their temporal and epistatic features in the context of cellular evolution and emerging drug resistance are contentious.
View Article and Find Full Text PDFCENP-A chromatin prevents replication stress at centromeres to avoid structural aneuploidy.
Proc Natl Acad Sci U S A
March 2021
Institut Curie, PSL Research University, CNRS, UMR 144, F-75005 Paris, France;
Chromosome segregation relies on centromeres, yet their repetitive DNA is often prone to aberrant rearrangements under pathological conditions. Factors that maintain centromere integrity to prevent centromere-associated chromosome translocations are unknown. Here, we demonstrate the importance of the centromere-specific histone H3 variant CENP-A in safeguarding DNA replication of alpha-satellite repeats to prevent structural aneuploidy.
View Article and Find Full Text PDFP53 induces senescence in the unstable progeny of aneuploid cells.
Cell Cycle
December 2020
nstitute of Medical Biology (IMB), Agency for Science, Technology and Research (A*STAR), Singapore 138648, Singapore.
Aneuploidy is the condition of having an imbalanced karyotype, which is associated with tumor initiation, evolution, and acquisition of drug-resistant features, possibly by generating heterogeneous populations of cells with distinct genotypes and phenotypes. Multicellular eukaryotes have therefore evolved a range of extrinsic and cell-autonomous mechanisms for restraining proliferation of aneuploid cells, including activation of the tumor suppressor protein p53. However, accumulating evidence indicates that a subset of aneuploid cells can escape p53-mediated growth restriction and continue proliferating .
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