TY - JOUR
T1 - The biology of breast cancer
AU - Nass, S. J.
AU - Davidson, N. E.
N1 - Funding Information:
Part of this work was supported by the National Cancer Institute, the United States Army Research and Materiel Command, and the Susan G. Komen Breast Cancer Foundation.
PY - 1999
Y1 - 1999
N2 - This article focuses on the major hormones and growth factors for which a critical role in normal mammary growth has been clearly defined. Certainly other hormonal systems and growth factors could also affect breast cancer initiation and progression, but their exact contribution to normal and/or malignant breast cell growth is poorly delineated. Examples of such factors include somatostatin, mammostatin, mammary-derived growth inhibitor (MDGI), mammary-derived growth factor-1 (MDGF-1), inhibins, activins, androgens, glucocorticoids, vitamin D, thyroid hormones, ecosinoids, and oxytocin. Clearly, the hormonal regulation of breast cancer cell growth and survival is multifaceted and very complex. In particular, the effects of estrogens and anti-estrogens on breast cells may depend on their interaction with a wide variety of other pathways. In addition, these interactions may vary among individual breast tumors depending on other genetic changes in the tumor cells that have not been discussed here, such as oncogene activation and loss of tumor suppressors. A more detailed understanding of how cells circumvent a dependency on these pathways is greatly needed in order to identify new biological targets and to design novel therapies for breast cancers that are resistant to antiestrogen therapy. Such agents could be used alone or in combination with anti-estrogens to improve response to a second course of hormonal therapy.
AB - This article focuses on the major hormones and growth factors for which a critical role in normal mammary growth has been clearly defined. Certainly other hormonal systems and growth factors could also affect breast cancer initiation and progression, but their exact contribution to normal and/or malignant breast cell growth is poorly delineated. Examples of such factors include somatostatin, mammostatin, mammary-derived growth inhibitor (MDGI), mammary-derived growth factor-1 (MDGF-1), inhibins, activins, androgens, glucocorticoids, vitamin D, thyroid hormones, ecosinoids, and oxytocin. Clearly, the hormonal regulation of breast cancer cell growth and survival is multifaceted and very complex. In particular, the effects of estrogens and anti-estrogens on breast cells may depend on their interaction with a wide variety of other pathways. In addition, these interactions may vary among individual breast tumors depending on other genetic changes in the tumor cells that have not been discussed here, such as oncogene activation and loss of tumor suppressors. A more detailed understanding of how cells circumvent a dependency on these pathways is greatly needed in order to identify new biological targets and to design novel therapies for breast cancers that are resistant to antiestrogen therapy. Such agents could be used alone or in combination with anti-estrogens to improve response to a second course of hormonal therapy.
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U2 - 10.1016/S0889-8588(05)70058-7
DO - 10.1016/S0889-8588(05)70058-7
M3 - Article
C2 - 10363133
AN - SCOPUS:0032987987
VL - 13
SP - 311
EP - 332
JO - Hematology/Oncology Clinics of North America
JF - Hematology/Oncology Clinics of North America
SN - 0889-8588
IS - 2
ER -