Paclitaxel-induced mitotic arrest results in a convergence of apoptotic dependencies that can be safely exploited by BCL-XL degradation to overcome cancer chemoresistance.

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Title: Paclitaxel-induced mitotic arrest results in a convergence of apoptotic dependencies that can be safely exploited by BCL-XL degradation to overcome cancer chemoresistance.
Authors: Qin X; John B. Little Center for Radiation Sciences, Harvard T.H. Chan School of Public Health, Boston, MA.; Laboratory of Systems Pharmacology, Harvard Program in Therapeutic Science, Department of Systems Biology, Harvard Medical School, Boston, MA.; Molecular and Integrative Physiological Sciences Program, Harvard T.H. Chan School of Public Health; Boston MA., Presser A; John B. Little Center for Radiation Sciences, Harvard T.H. Chan School of Public Health, Boston, MA.; Laboratory of Systems Pharmacology, Harvard Program in Therapeutic Science, Department of Systems Biology, Harvard Medical School, Boston, MA.; Molecular and Integrative Physiological Sciences Program, Harvard T.H. Chan School of Public Health; Boston MA., Johnson L; John B. Little Center for Radiation Sciences, Harvard T.H. Chan School of Public Health, Boston, MA.; Laboratory of Systems Pharmacology, Harvard Program in Therapeutic Science, Department of Systems Biology, Harvard Medical School, Boston, MA.; Molecular and Integrative Physiological Sciences Program, Harvard T.H. Chan School of Public Health; Boston MA., Matoba Y; Vincent Center for Reproductive Biology, Department of Obstetrics and Gynecology, Massachusetts General Hospital, Boston, MA.; Obstetrics, Gynecology and Reproductive Biology, Harvard Medical School, Boston, MA., Shay BS; Department of Cell Biology, Harvard Medical School, Boston, MA.; Ludwig Center at Harvard, Harvard Medical School Boston, Boston, Ma., Xu W; Department of Cell Biology, Harvard Medical School, Boston, MA.; Ludwig Center at Harvard, Harvard Medical School Boston, Boston, Ma., Choiniere J; John B. Little Center for Radiation Sciences, Harvard T.H. Chan School of Public Health, Boston, MA.; Laboratory of Systems Pharmacology, Harvard Program in Therapeutic Science, Department of Systems Biology, Harvard Medical School, Boston, MA.; Molecular and Integrative Physiological Sciences Program, Harvard T.H. Chan School of Public Health; Boston MA., Fraser C; John B. Little Center for Radiation Sciences, Harvard T.H. Chan School of Public Health, Boston, MA.; Laboratory of Systems Pharmacology, Harvard Program in Therapeutic Science, Department of Systems Biology, Harvard Medical School, Boston, MA.; Molecular and Integrative Physiological Sciences Program, Harvard T.H. Chan School of Public Health; Boston MA., Garbicz F; Department of Pathology, Dana-Farber Cancer Institute, Boston, MA.; Department of Immunology, Medical University of Warsaw, Poland., Spetz J; John B. Little Center for Radiation Sciences, Harvard T.H. Chan School of Public Health, Boston, MA.; Laboratory of Systems Pharmacology, Harvard Program in Therapeutic Science, Department of Systems Biology, Harvard Medical School, Boston, MA.; Molecular and Integrative Physiological Sciences Program, Harvard T.H. Chan School of Public Health; Boston MA., Yu S; John B. Little Center for Radiation Sciences, Harvard T.H. Chan School of Public Health, Boston, MA.; Laboratory of Systems Pharmacology, Harvard Program in Therapeutic Science, Department of Systems Biology, Harvard Medical School, Boston, MA.; Molecular and Integrative Physiological Sciences Program, Harvard T.H. Chan School of Public Health; Boston MA., Florido MHC; John B. Little Center for Radiation Sciences, Harvard T.H. Chan School of Public Health, Boston, MA.; Laboratory of Systems Pharmacology, Harvard Program in Therapeutic Science, Department of Systems Biology, Harvard Medical School, Boston, MA.; Molecular and Integrative Physiological Sciences Program, Harvard T.H. Chan School of Public Health; Boston MA., Picucci F; John B. Little Center for Radiation Sciences, Harvard T.H. Chan School of Public Health, Boston, MA.; Laboratory of Systems Pharmacology, Harvard Program in Therapeutic Science, Department of Systems Biology, Harvard Medical School, Boston, MA.; Molecular and Integrative Physiological Sciences Program, Harvard T.H. Chan School of Public Health; Boston MA., Yang Y; University of Texas San Antonio, San Antonio, TX., Drapkin R; Penn Ovarian Cancer Research Center, Department of Obstetrics and Gynecology, University of Pennsylvania Perelman School of Medicine, Philadelphia, PA.; Basser Center for BRCA, Abramson Cancer Center, University of Pennsylvania Perelman School of Medicine, Philadelphia, PA., Carrasco R; Department of Pathology, Dana-Farber Cancer Institute, Boston, MA.; Department of Pathology, Brigham and Women's Hospital, Harvard Medical School, Boston, MA., Hill SJ; Department of Medical Oncology, Dana-Farber Cancer Institute, Boston MA.; Department of Medicine, Harvard Medical School, Boston MA., Liu J; Department of Medical Oncology, Dana-Farber Cancer Institute, Boston MA.; Department of Medicine, Harvard Medical School, Boston MA., Matulonis U; Department of Medical Oncology, Dana-Farber Cancer Institute, Boston MA.; Department of Medicine, Harvard Medical School, Boston MA., Brugge J; Department of Cell Biology, Harvard Medical School, Boston, MA.; Ludwig Center at Harvard, Harvard Medical School Boston, Boston, Ma., Rueda BR; Vincent Center for Reproductive Biology, Department of Obstetrics and Gynecology, Massachusetts General Hospital, Boston, MA.; Obstetrics, Gynecology and Reproductive Biology, Harvard Medical School, Boston, MA., Zhou D; University of Texas San Antonio, San Antonio, TX., Stover EH; Department of Medical Oncology, Dana-Farber Cancer Institute, Boston MA.; Department of Medicine, Harvard Medical School, Boston MA., Sarosiek KA; John B. Little Center for Radiation Sciences, Harvard T.H. Chan School of Public Health, Boston, MA.; Laboratory of Systems Pharmacology, Harvard Program in Therapeutic Science, Department of Systems Biology, Harvard Medical School, Boston, MA.; Molecular and Integrative Physiological Sciences Program, Harvard T.H. Chan School of Public Health; Boston MA.; Department of Medical Oncology, Dana-Farber Cancer Institute, Boston MA.
Source: BioRxiv : the preprint server for biology [bioRxiv] 2025 Jun 26. Date of Electronic Publication: 2025 Jun 26.
Publication Type: Journal Article; Preprint
Journal Info: Country of Publication: United States NLM ID: 101680187 Publication Model: Electronic Cited Medium: Internet ISSN: 2692-8205 (Electronic) Linking ISSN: 26928205 NLM ISO Abbreviation: bioRxiv Subsets: PubMed not MEDLINE
Database: MEDLINE Ultimate
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  Data: Paclitaxel-induced mitotic arrest results in a convergence of apoptotic dependencies that can be safely exploited by BCL-X<subscript>L</subscript> degradation to overcome cancer chemoresistance.
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