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      Mammary stem cell number as a determinate of breast cancer risk

      editorial
      Author(s): 1 , 1 ,
      Publication date (Electronic):
      Journal: Breast cancer research : BCR
      Publisher: BioMed Central

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          Abstract

          The 'cancer stem cell hypothesis' posits that cancers, including breast cancer, arise in tissue stem or progenitor cells. If this is the case, then it follows that the risk for developing breast cancer may be determined in part by the number of breast stem/progenitor cells that can serve as targets for transformation. Stem cell number may be set during critical windows of development, including in utero, adolescence, and pregnancy. The growth hormone/insulin-like growth factor-1 axis may play an important role in regulating breast stem cell number during these developmental windows, suggesting an important link between this signaling pathway and breast cancer risk.

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          Growth patterns and the risk of breast cancer in women.

          Martin Ahlgren, Mads Melbye, Jan Wohlfahrt … (2004)
          Adult height and body-mass index influence the risk of breast cancer in women. Whether these associations reflect growth patterns of the fetus or growth during childhood and adolescence is unknown. We investigated the association between growth during childhood and the risk of breast cancer in a cohort of 117,415 Danish women. Birth weight, age at menarche, and annual measurements of height and weight were obtained from school health records. We used the data to model individual growth curves. Information on vital status, age at first childbirth, parity, and diagnosis of breast cancer was obtained through linkages to national registries. During 3,333,359 person-years of follow-up, 3340 cases of breast cancer were diagnosed. High birth weight, high stature at 14 years of age, low body-mass index (BMI) at 14 years of age, and peak growth at an early age were independent risk factors for breast cancer. Height at 8 years of age and the increase in height during puberty (8 to 14 years of age) were also associated with breast cancer. The attributable risks of birth weight, height at 14 years of age, BMI at 14 years of age, and age at peak growth were 7 percent, 15 percent, 15 percent, and 9 percent, respectively. No effect of adjusting for age at menarche, age at first childbirth, and parity was observed. Birth weight and growth during childhood and adolescence influence the risk of breast cancer. Copyright 2004 Massachusetts Medical Society.
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            Correlation of umbilical cord blood hormones and growth factors with stem cell potential: implications for the prenatal origin of breast cancer hypothesis

            Todd Savarese, William C Strohsnitter, Hoi Pang Low … (2007)
            Introduction Prenatal levels of mitogens may influence the lifetime breast cancer risk by driving stem cell proliferation and increasing the number of target cells, and thereby increasing the chance of mutation events that initiate oncogenesis. We examined in umbilical cord blood the correlation of potential breast epithelial mitogens, including hormones and growth factors, with hematopoietic stem cell concentrations serving as surrogates of overall stem cell potential. Methods We analyzed cord blood samples from 289 deliveries. Levels of hormones and growth factors were correlated with concentrations of stem cell and progenitor populations (CD34+ cells, CD34+CD38- cells, CD34+c-kit+ cells, and granulocyte–macrophage colony-forming units). Changes in stem cell concentration associated with each standard deviation change in mitogens and the associated 95% confidence intervals were calculated from multiple regression analysis. Results Cord blood plasma levels of insulin-like growth factor-1 (IGF-1) were strongly correlated with all the hematopoietic stem and progenitor concentrations examined (one standard-deviation increase in IGF-1 being associated with a 15–19% increase in stem/progenitor concentrations, all P < 0.02). Estriol and insulin-like growth factor binding protein-3 levels were positively and significantly correlated with some of these cell populations. Sex hormone-binding globulin levels were negatively correlated with these stem/progenitor pools. These relationships were stronger in Caucasians and Hispanics and were weaker or not present in Asian-Americans and African-Americans. Conclusion Our data support the concept that in utero mitogens may drive the expansion of stem cell populations. The correlations with IGF-1 and estrogen are noteworthy, as both are crucial for mammary gland development.
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              The GH-IGF-I axis and breast cancer.

              P. Jenkins, Stephen A. Bustin, C Laban (2002)
              The growth hormone-insulin-like growth factor-I (GH-IGF-I) axis plays a fundamental role in the development of the breast. The maintenance of breast tissue architecture is aided by its effect on proliferation, differentiation and apoptosis. There has been increasing recognition of its role as a major determinant of breast cancer and, more recently, its involvement in the development of resistance to both tamoxifen and an important novel therapy for advanced disease, trastuzumab (Herceptin). Here, we discuss the influence of the GH-IGF-I axis in normal mammary development and homeostasis, its putative role in breast tumorigenesis and its interactions with estrogen signalling.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Breast Cancer Res
                Title: Breast cancer research : BCR
                Publisher: BioMed Central
                ISSN (Print): 1465-5411
                ISSN (Electronic): 1465-542X
                Publication date (Print): 2007
                Publication date (Electronic): 31 July 2007
                Volume: 9
                Issue: 4
                Page: 109
                Affiliations
                [1 ]Comprehensive Cancer Center, Department of Internal Medicine, University of Michigan, 1500 E. Medical Center Drive, Ann Arbor, Michigan 48109, USA
                Article
                Publisher ID: bcr1741
                DOI: 10.1186/bcr1741
                PMC ID: 2206714
                PubMed ID: 17688678
                SO-VID: 66d69f4a-5b9b-4f4d-9693-5279cc987aab
                Copyright © Copyright © 2007 BioMed Central Ltd
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                Subject: Editorial

                ScienceOpen disciplines: Oncology & Radiotherapy
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                ScienceOpen disciplines: Oncology & Radiotherapy

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