ArticleOncogene1999
Loss of anti-mitotic effects of Bcl-2 with retention of anti-apoptotic activity during tumor progression in a mouse model.
Article in Oncogene, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
24 citing papers in PubMed, 54 citations in OpenAlex.
- Targeting the Pro-survival Protein BCL-2 to Prevent Breast Cancer.Cancer prevention research (Philadelphia, Pa.) · 2022Article
- miR-424(322)/503 is a breast cancer tumor suppressor whose loss promotes resistance to chemotherapy.Genes & development · 2017Article
- Targeting BCL-2 to enhance vulnerability to therapy in estrogen receptor-positive breast cancer.Oncogene · 2016Review
- Bcl-2 family proteins in breast development and cancer: could Mcl-1 targeting overcome therapeutic resistance?Oncotarget · 2015Review
- Removal of the BH4 domain from Bcl-2 protein triggers an autophagic process that impairs tumor growth.Neoplasia (New York, N.Y.) · 2013Article
- Forced involution of the functionally differentiated mammary gland by overexpression of the pro-apoptotic protein bax.Genesis (New York, N.Y. : 2000) · 2011Article
- Mammary involution and breast cancer risk: transgenic models and clinical studies.Journal of mammary gland biology and neoplasia · 2009Review
- G0 function of BCL2 and BCL-xL requires BAX, BAK, and p27 phosphorylation by Mirk, revealing a novel role of BAX and BAK in quiescence regulation.The Journal of biological chemistry · 2008Article
- Loss of Bcl-x in Ph+ B-ALL increases cellular proliferation and does not inhibit leukemogenesis.Blood · 2008Article
- Absence of Bcl-2 and Fas/CD95/APO-1 predicts the response to immunotherapy in metastatic renal cell carcinoma.British journal of cancer · 2006Article
- Loss of BCL-2 in the progression of oral cancer is not attributable to mutations.Journal of clinical pathology · 2005Article
- A cytoskeleton-based functional genetic screen identifies Bcl-xL as an enhancer of metastasis, but not primary tumor growth.Oncogene · 2004Article
- Bcl-xL/Bcl-2 coordinately regulates apoptosis, cell cycle arrest and cell cycle entry.The EMBO journal · 2003Article
- Bcl-2 activates a programme of premature senescence in human carcinoma cells.The Biochemical journal · 2003Article
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- Bcl-2 expression inhibits liver carcinogenesis and delays the development of proliferating foci.The American journal of pathology · 2002Article
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- Transgenic mouse models of human breast cancer.Oncogene · 2000Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 4 institutions in 2 countries.
Funding
Abstract
Bcl-2 is an anti-apoptotic and anti-proliferative protein over-expressed in several different human cancers including breast. Gain of Bcl-2 function in mammary epithelial cells was superimposed on the WAP-TAg transgenic mouse model of breast cancer progression to determine its effect on epithelial cell survival and proliferation at three key stages in oncogenesis: the initial proliferative process, hyperplasia, and cancer. During the initial proliferative process, Bcl-2 strongly inhibited both apoptosis and mitotic activity. However as tumorigenesis progressed to hyperplasia and adenocarcinoma, the inhibitory effects on mitotic activity were lost. In contrast, anti-apoptotic activity persisted in both hyperplasias and adenocarcinomas. These results demonstrate that the inhibitory effect of Bcl-2 on epithelial cell proliferation and apoptosis can separate during cancer progression. In this model, retention of anti-apoptotic activity with loss of anti-proliferative action resulted in earlier tumor presentation.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.