If not apoptosis, then what? Treatment-induced senescence and mitotic catastrophe in tumor cells.
By I. Roninson, E. Broude, B. Chang. Drug resistance updates, 2001
765 citations recorded by the source corpus.
Subfields: Molecular Biology, Oncology, Physiology
View Paper: https://www.semanticscholar.org/paper/04f9f655431d5a9df121cedae8a4776dec4f484c
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In Molecular Biology
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In Oncology
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In Physiology
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Citations in the corpus
- beta4 integrin-dependent formation of polarized three-dimensional architecture confers resistance to apoptosis in normal and malignant mammary epithelium. (2002, background): “BM-induced tissue polarity is necessary for apoptosis resistance regardless of growth status Cytotoxic drugs induce apoptosis in target cells based upon their capacity to promote cell-cycle arrest (Roninson et al., 2001; Hurley, 2002).”
- Pathways of apoptotic and non-apoptotic death in tumour cells (2004, background): “Importantly, the fraction of tumour cells that undergo non-apoptotic death increases if apoptosis is inhibited in response to anticancer agents or radiatio”
- Mitotic catastrophe: a mechanism for avoiding genomic instability (2011, background): “In this case, cell death can occur quickly, within hours after mitotic exit, or in a delayed fashion, as exemplified by the 'delayed radio-induced cell death' that can occur years after radiotherapy in human tissue”
- Molecular definitions of cell death subroutines: recommendations of the Nomenclature Committee on Cell Death 2012 (2011, methodology): “employ the term ‘mitotic catastrophe’ for cell death occurring in mitosis.(106,107) More frequently, mitotic catastrophe refers to cases of cell death that are triggered by aberrant mitosis and”
- Cell death by mitotic catastrophe: a molecular definition (2004, background): “…microtubule-hyperpolymerizing agents (taxanes, elutherobins, epothilones, laulimalide, sarcodictyins, docodermolide) and by microtubule-depolymerizing agents (such as the Vinca alkaloids, cryptophyscins, halichondrins, estramustine and colchicine) as well as by DNA damage (Roninson et al., 2001).”
- Radiation-induced cell death mechanisms (2010, background): “Aberrant mitosis produce an atypical chromosome segregation and cell division and leads to the formation of giant cells with aberrant nuclear morphology [71, 72, 74], multiple nuclei [72, 75], and/or several micronuclei [ 68 ] (Fig. 3). Two important mechanisms for the induction of the mitotic catas”
- The role of p53 in determining sensitivity to radiotherapy (2003, background): “Mitotic catastrophe is a significant cause of cell death in different tumour cell lines after treatment with DNA-damaging agents, including I”