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Cellular calcium dynamics in lactation and breast cancer: from physiology to pathology.

Authors
  • Cross, Brandie M
  • Breitwieser, Gerda E
  • Reinhardt, Timothy A
  • Rao, Rajini
Type
Published Article
Journal
AJP Cell Physiology
Publisher
American Physiological Society
Publication Date
Mar 15, 2014
Volume
306
Issue
6
Identifiers
DOI: 10.1152/ajpcell.00330.2013
PMID: 24225884
Source
Medline
Keywords
License
Unknown

Abstract

Breast cancer is the second leading cause of cancer mortality in women, estimated at nearly 40,000 deaths and more than 230,000 new cases diagnosed in the U.S. this year alone. One of the defining characteristics of breast cancer is the radiographic presence of microcalcifications. These palpable mineral precipitates are commonly found in the breast after formation of a tumor. Since free Ca(2+) plays a crucial role as a second messenger inside cells, we hypothesize that these chelated precipitates may be a result of dysregulated Ca(2+) secretion associated with tumorigenesis. Transient and sustained elevations of intracellular Ca(2+) regulate cell proliferation, apoptosis and cell migration, and offer numerous therapeutic possibilities in controlling tumor growth and metastasis. During lactation, a developmentally determined program of gene expression controls the massive transcellular mobilization of Ca(2+) from the blood into milk by the coordinated action of calcium transporters, including pumps, channels, sensors and buffers, in a functional module that we term CALTRANS. Here we assess the evidence implicating genes that regulate free and buffered Ca(2+) in normal breast epithelium and cancer cells and discuss mechanisms that are likely to contribute to the pathological characteristics of breast cancer.

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