» Articles » PMID: 9679488

A Developmental Hypothesis to Explain the Multicentricity of Breast Cancer

Overview
Journal CMAJ
Date 1998 Jul 29
PMID 9679488
Citations 3
Authors
Affiliations
Soon will be listed here.
Abstract

In this article the author proposes that the multicentricity of breast cancer might be explained by a developmental hypothesis. Genetic alterations ("hits") occurring in epithelial stem cells during the development of the breast may be transmitted to populations of daughter cells during growth. As a result, areas of the breast may be predisposed to malignant transformation with the occurrence of further genetic hits. Areas with the same predisposition should be anatomically connected, and earlier hits during breast development should result in larger areas of predisposition. The multicentricity of breast cancer would be explained if multiple lesions--monoclonal for the predisposing genetic hit and polyclonal for subsequent hits--developed within a predisposed area. Multiple lesions arising from the spread of disease by extension would be expected to share many genetic hits. The author discusses the implications that further evidence supporting the developmental hypothesis would have for the prevention and treatment of breast cancer.

Citing Articles

Oncotype dx results in multiple primary breast cancers.

Toole M, Kidwell K, Van Poznak C Breast Cancer (Auckl). 2014; 8:1-6.

PMID: 24453493 PMC: 3891573. DOI: 10.4137/BCBCR.S13727.


In vivo biosafety model to assess the risk of adverse events from retroviral and lentiviral vectors.

Bauer G, Dao M, Case S, Meyerrose T, Wirthlin L, Zhou P Mol Ther. 2008; 16(7):1308-15.

PMID: 18461052 PMC: 3013368. DOI: 10.1038/mt.2008.93.


Rating the risk factors for breast cancer.

Singletary S Ann Surg. 2003; 237(4):474-82.

PMID: 12677142 PMC: 1514477. DOI: 10.1097/01.SLA.0000059969.64262.87.

References
1.
Mohrenweiser H, Zingg B . Mosaicism: the embryo as a target for induction of mutations leading to cancer and genetic disease. Environ Mol Mutagen. 1995; 25 Suppl 26:21-9. DOI: 10.1002/em.2850250606. View

2.
LAGIOS M, WESTDAHL P, Margolin F, Rose M . Duct carcinoma in situ. Relationship of extent of noninvasive disease to the frequency of occult invasion, multicentricity, lymph node metastases, and short-term treatment failures. Cancer. 1982; 50(7):1309-14. DOI: 10.1002/1097-0142(19821001)50:7<1309::aid-cncr2820500716>3.0.co;2-#. View

3.
Thilly W . Looking ahead: algebraic thinking about genetics, cell kinetics and cancer. IARC Sci Publ. 1988; (89):486-92. View

4.
Cohen S, Ellwein L . Cell proliferation in carcinogenesis. Science. 1990; 249(4972):1007-11. DOI: 10.1126/science.2204108. View

5.
Moolgavkar S, Day N, Stevens R . Two-stage model for carcinogenesis: Epidemiology of breast cancer in females. J Natl Cancer Inst. 1980; 65(3):559-69. View