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Cited by 411

The DOI matches its Crossref record; 97 of the 97 references it cites were found in a registry or an index.

Cyclin D1 in Breast Cancer Pathogenesis

Arnold, Andrew, Papanikolaou, Alexandros·2005·Journal of Clinical Oncology

Abstract

Taking a perspective on available evidence that emphasizes relevance to human disease, cyclin D1 is solidly established as an oncogene with an important pathogenetic role in breast cancer and other human tumors. However, the precise cellular mechanisms through which aberrant cyclin D1 expression drives human neoplasia are less well established. Indeed, emerging evidence suggests that cyclin D1 might act, predominantly or at least in part, through pathways that do not involve its widely accepted function as a cell cycle regulator. Although therapeutic exploitation of the role of cyclin D1 as a molecular driver of breast cancer carries great promise, it is also suggested that direct targeting of the cyclin D1 gene or gene products may prove more successful than approaches that rely on arguably incomplete knowledge of the oncogenic mechanisms of cyclin D1.

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Crossref · 10.1200/jco.2005.05.064

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Metadata

Authors
Arnold, A., & Papanikolaou, A.
Venue
Journal of Clinical Oncology
Published
2005-06-20
Volume
23
Issue
18
Pages
4215-4224
ISSN
  • 0732-183X (ISSN-L)
  • 1527-7755
OpenAlex
W2111369086
Cited by
411
References
97
FWCI
7.77
Type
journal article
Language
en
Open access
closed

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CoChat. (2026). Citation check: Cyclin D1 in Breast Cancer Pathogenesis. https://app.cochat.ai/papers/10.1200/jco.2005.05.064
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Arnold, A., & Papanikolaou, A. (2005). Cyclin D1 in Breast Cancer Pathogenesis. Journal of Clinical Oncology. https://doi.org/10.1200/jco.2005.05.064

Data sources

Bibliographic data: Semantic Scholar, OpenAlex, Crossref.

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

Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.