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Cited by 202

The DOI matches its Crossref record; 9 of the 9 references it cites were found in a registry or an index.

The rise and fall of apoptosis during multistage tumorigenesis: down-modulation contributes to tumor progression from angiogenic progenitors.

Open access
Naik, P, Karrim, J, Hanahan, D·1996·Genes & Development

Abstract

In a mouse model of multistage tumorigenesis of islet beta-cells, apoptosis was activated concomitant with T-antigen oncogene-induced cell proliferation, further increased in the angiogenic stage, and markedly reduced in solid tumors. Crosses to p53-null mice confirmed this stage-specific variation as a p53-independent apoptotic process. Several apoptosis regulators were expressed, of which bcl-xL was up-regulated in tumors. When overexpressed throughout the pathway, bcl-xL protected most oncogene-expressing cells from apoptosis, enhancing progression from angiogenic progenitor to tumor without affecting earlier transitions. Further, two classes of solid tumor are described, distinguished by size and apoptotic incidence, implicating apoptosis regulation in expansive tumor growth. Thus, down-modulation of apoptosis selectively contributes to late steps in a tumorigenesis pathway.

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Metadata

Authors
Naik, P., Karrim, J., & Hanahan, D.
Venue
Genes & Development
Published
1996-09-01
Volume
10
Issue
17
Pages
2105-2116
ISSN
  • 0890-9369 (ISSN-L)
  • 1549-5477
OpenAlex
W2059928759
Cited by
202
References
9
Type
posted content
Language
en
Open access
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CoChat. (2026). Citation check: The rise and fall of apoptosis during multistage tumorigenesis: down-modulation contributes to tumor progression from angiogenic progenitors. https://app.cochat.ai/papers/10.1101/gad.10.17.2105
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Naik, P., Karrim, J., & Hanahan, D. (1996). The rise and fall of apoptosis during multistage tumorigenesis: down-modulation contributes to tumor progression from angiogenic progenitors. Genes & Development. https://doi.org/10.1101/gad.10.17.2105

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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).

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