Hormones[edit]
Birth control[edit]
In breast cancer survivors, non-hormonal birth control methods should be used as first-line options. Progestogen-based methods such as depot medroxyprogesterone acetate,IUD with progestogen or progestogen only pills have a poorly investigated but possible increased risk of cancer recurrence, but may be used if positive effects outweigh this possible risk.[174]
Menopausal hormone replacement[edit]
In breast cancer survivors, it is recommended to first consider non-hormonal options for menopausal effects, such as bisphosphonates or selective estrogen receptor modulators(SERMs) for osteoporosis, and vaginal estrogen for local symptoms. Observational studies of systemic hormone replacement therapy after breast cancer are generally reassuring. If hormone replacement is necessary after breast cancer, estrogen only therapy or estrogen therapy with an intrauterine device with progestogen may be safer options than combined systemic therapy.[175]
Research[edit]
Treatments are constantly evaluated in randomized, controlled trials, to evaluate and compare individual drugs, combinations of drugs, and surgical and radiation techniques. Investigations include new types of targeted therapy as well as cancer vaccines.
The latest research is reported annually at scientific meetings such as that of the American Society of Clinical Oncology, San Antonio Breast Cancer Symposium,[176] and the St. Gallen Oncology Conference in St. Gallen, Switzerland.[177] These studies are reviewed by professional societies and other organizations, and formulated into guidelines for specific treatment groups and risk category.
Fenretinide, a retinoid, is also being studied as a way to reduce the risk of breast cancer (retinoids are drugs related to vitamin A).[178][179]
Cryoablation[edit]
As of 2014 cryoablation is being studied to see if it could be a substitute for a lumpectomy in small cancers.[180] There is tentative evidence in those with tumors less than 2 centimeters.[181] It may also be used in those in who surgery is not possible.[181] Another reviews states that cryoablation looks promising for early breast cancer of small size.[182]
Breast cancer cell lines[edit]
See also: List of breast cancer cell lines
A considerable part of the current knowledge on breast carcinomas is based on in vivo and in vitro studies performed with cell lines derived from breast cancers. These provide an unlimited source of homogenous self-replicating material, free of contaminating stromal cells, and often easily cultured in simple standard media. The first breast cancer cell line described, BT-20, was established in 1958. Since then, and despite sustained work in this area, the number of permanent lines obtained has been strikingly low (about 100). Indeed, attempts to culture breast cancer cell lines from primary tumors have been largely unsuccessful. This poor efficiency was often due to technical difficulties associated with the extraction of viable tumor cells from their surrounding stroma. Most of the available breast cancer cell lines issued from metastatic tumors, mainly from pleural effusions. Effusions provided generally large numbers of dissociated, viable tumor cells with little or no contamination by fibroblasts and other tumor stroma cells. Many of the currently used BCC lines were established in the late 1970s. A very few of them, namely MCF-7, T-47D, and MDA-MB-231, account for more than two-thirds of all abstracts reporting studies on mentioned breast cancer cell lines, as concluded from a Medline-based survey.
Molecular markers[edit]
Transcription factors[edit]
NFAT transcription factors are implicated in breast cancer, more specifically in the process of cell motility at the basis of metastasis formation. Indeed, NFAT1 (NFATC2) and NFAT5 are pro-invasive and pro-migratory in breast carcinoma[183][184] and NFAT3 (NFATc4) is an inhibitor of cell motility.[185] NFAT1 regulates the expression of the TWEAKR and its ligand TWEAK with the Lipocalin 2 to increase breast cancer cell invasion[186] and NFAT3 inhibits Lipocalin 2 expression to blunt the cell invasion.[185]
Metabolic markers[edit]
Clinically, the most useful metabolic markers in breast cancer are the estrogen and progesterone receptors that are used to predict response to hormone therapy. New or potentially new markers for breast cancer include BRCA1 and BRCA2[187] to identify patients at high risk of developing breast cancer, HER-2[188] and SCD1[189] for predicting response to therapeutic regimens, and urokinase plasminogen activator, PA1-1[190] and SCD1[191] for assessing prognosis.
Other animals[edit]
- Mammary tumor for breast cancer in other animals
- Mouse models of breast cancer metastasis
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