Cellular immortalization and neoplastic transformation
نویسندگان
چکیده
منابع مشابه
Telomerase: cellular immortalization and neoplastic transformation. Multiple functions of a multifaceted complex.
The telomerase complex allows telomere length maintenance, which is required for an unlimited cellular proliferation. Telomerase is virtually absent in normal human somatic cells, which are characterized by a definite proliferation potential, while it is present in the vast majority of tumors (around 90%). Restoring telomerase activity in normal somatic cells can indefinitely prolong cellular l...
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A comparison was made of the competence for neoplastic transformation in three different sublines of NIH 3T3 cells and multiple clonal derivatives of each. Over 90% of the neoplastic foci produced by an uncloned transformed (t-SA') subline on a confluent background of nontransformed cells were of the dense, multilayered type, but about half of the t-SA' clones produced only light foci in assays...
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The disruption of homeostatic mechanisms that regulate normal cell growth and proliferation is a hallmark of cancer. Experimentally, many of the same genetic changes that lead to abnormal cell proliferation conspire to confer replicative immortality upon cells in culture. Correspondingly, several lines of evidence implicate cellular immortalization as a prerequisite for cell transformation. Rec...
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The unique ability of tumour cells to proliferate indefinitely is crucial to neoplastic progression as it allows these cells to express the aggressive properties of cancer without the censure of physiological ageing. This is in contrast to normal somatic cells which are subject to a "mitotic clock," a phenomenon that has been linked to telomeric shortening after each round of cell replication, ...
متن کاملdeltaNp73 facilitates cell immortalization and cooperates with oncogenic Ras in cellular transformation in vivo.
TP73, despite significant homology to TP53, is not a classic tumor suppressor gene, since it exhibits upregulation of nonmutated products in human tumors and lacks a tumor phenotype in p73-deficient mice. We recently reported that an N-terminally truncated isoform, DeltaNp73, is upregulated in breast and gynecological cancers. We further showed that DeltaNp73 is a potent transdominant inhibitor...
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ژورنال
عنوان ژورنال: Cell Cycle
سال: 2013
ISSN: 1538-4101,1551-4005
DOI: 10.4161/cc.24940