This is a commentary on 'Virtual diversity: Resolving the tension between the wider culture and the institution of science', by Harry Collins, Robert Evans, Luis Reyes-Galindo.
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http://dx.doi.org/10.1177/03063127251314452 | DOI Listing |
This is a commentary on 'Virtual diversity: Resolving the tension between the wider culture and the institution of science', by Harry Collins, Robert Evans, Luis Reyes-Galindo.
View Article and Find Full Text PDFPathol Res Pract
November 2024
School of Bioengineering and Biosciences, Lovely Professional University, Jalandhar, Punjab 144411, India. Electronic address:
Non-coding RNAs have gathered significant attention for their unique roles in biological regulation. Across a broad spectrum of developmental processes and diseases, particularly in human malignancies, ncRNAs play pivotal roles in regulatory mechanisms. MicroRNAs, long noncoding RNAs, and small nucleolar RNAs stand out among the diverse forms of ncRNAs that have been implicated in cancer.
View Article and Find Full Text PDFCell Rep Med
December 2024
Department of Epigenetics and Molecular Carcinogenesis, The University of Texas MD Anderson Cancer Center, Houston, TX, USA; Department of Bioinformatics and Computational Biology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA; Quantitative and Computational Biosciences Program, Baylor College of Medicine, Houston, TX, USA.
Therapeutic strategies targeting the DNA damage response, such as poly (ADP-ribose) polymerase (PARP) inhibitors (PARPi), have revolutionized cancer treatment in tumors deficient in homologous recombination (HR). However, overcoming innate and acquired resistance to PARPi remains a significant challenge. Here, we employ a genome-wide CRISPR knockout screen and discover that the depletion of ubiquitin-activating enzyme E1 (UBA1) enhances sensitivity to PARPi in HR-proficient ovarian cancer cells.
View Article and Find Full Text PDFCancer Res
January 2025
Institute for Research in Biomedicine (IRB Barcelona), Barcelona Institute of Science and Technology (BIST), Barcelona, Spain.
Anticancer therapies can induce cellular senescence or drug-tolerant persistence, two types of proliferative arrest that differ in their stability. While senescence is highly stable, persister cells efficiently resume proliferation upon therapy termination, resulting in tumor relapse. Here, we used an ATP-competitive mTOR inhibitor to induce and characterize persistence in human cancer cells of various origins.
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