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Cited by 562

The DOI matches its Crossref record; 1 of the 1 references it cites were found in a registry or an index.

Aberrant Activation of Notch Signaling in Human Breast Cancer

Stylianou, Spyros, Clarke, Rob B., Brennan, Keith·2006·Cancer Research

Abstract

A role for Notch signaling in human breast cancer has been suggested by both the development of adenocarcinomas in the murine mammary gland following pathway activation and the loss of Numb expression, a negative regulator of the Notch pathway, in a large proportion of breast carcinomas. However, it is not clear currently whether Notch signaling is frequently activated in breast tumors, and how it causes cellular transformation. Here, we show accumulation of the intracellular domain of Notch1 and hence increased Notch signaling in a wide variety of human breast carcinomas. In addition, we show that increased RBP-Jκ–dependent Notch signaling is sufficient to transform normal breast epithelial cells and that the mechanism of transformation is most likely through the suppression of apoptosis. More significantly, we show that attenuation of Notch signaling reverts the transformed phenotype of human breast cancer cell lines, suggesting that inhibition of Notch signaling may be a therapeutic strategy for this disease. (Cancer Res 2006; 66(3): 1517-25)

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Metadata

Authors
Stylianou, S., Clarke, R. B., & Brennan, K.
Venue
Cancer Research
Published
2006-02-01
Volume
66
Issue
3
Pages
1517-1525
ISSN
  • 0008-5472 (ISSN-L)
  • 1538-7445
OpenAlex
W2001780798
Cited by
562
References
1
FWCI
12.89
Type
journal article
Language
en
Open access
closed

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CoChat. (2026). Citation check: Aberrant Activation of Notch Signaling in Human Breast Cancer. https://app.cochat.ai/papers/10.1158/0008-5472.can-05-3054
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Stylianou, S., Clarke, R. B., & Brennan, K. (2006). Aberrant Activation of Notch Signaling in Human Breast Cancer. Cancer Research. https://doi.org/10.1158/0008-5472.can-05-3054

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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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