Breast cancer family

Martino S, Disch D, Dowsett S, Mershon J (2005b) Raloxifene and Breast Cancer Risk Reduction based on Breast Cancer Family History. Abstract. ASCO, San Francisco... 

Other examples of single-gene diseases with delayed age of onset include familial breast cancer, familial colon cancer, adult polycystic kidney disease, and hemochromatosis. 

The two-hit model applies to a number of other inherited neoplasias, including familial breast cancer, familial colon cancer, familial melanoma, and neurofibromatosis. 

Germline alterations In the CLSPN gene in breast cancer families. 

Ikeda N, Miyoshi Y, Yoneda K, Shiba E, Sekihara Y, Moritoshi K, et al. Frequency of BRCAl and BRCA2 germline mutations in Japanese breast cancer families. Int J Cancer 2001 91 83-8. 

Meiser B, Butow P, Friedlander M, Barratt A, Schnieden V, Watson M, et al. Psychological impact of genetic testing in women from high-risk breast cancer families. Eur J Cancer 2002 38 2025-31. 

Scott CL, Jenkins MA, Southey M, Davis TA, Leary JA, Easton DF, et al. Average age-specific cumulative risk of breast cancer according to type and site of germline mutations in BRCAl and BRCA2 estimated from multiple-case breast cancer families attending Australian family cancer clinics. Hum Genet 2003 112 542-51. 

Vehmanen P, Friedman LS, Eerola H, McClure M, Ward B, Sarantaus L, et al. Low proportion of BRCAl and BRCA2 mutations in Finnish breast cancer families evidence for additional susceptibility genes. Hum Molec Genet 1997 6 2309-15. 

Zhi X, Szabo C, Chopin S, Suter N, Wang QS, Ostrander EA, et al. BRCAl and BRCA2 sequence variants in Chinese breast cancer families. Hum Mut 2002 554 online,... 

The breast cancer resistance protein (BCRP) belongs to the G-branch of the ABC-transporter family (ABCG2). In contrast to most other ABC-proteins, BCRP consists of only one transmembrane domain (TDM) with one nucleotide binding fold (NBF) at its C-terminus. Because of this structural characteristic BCRP as well as other ABC-transporters with only one TMD are termed half transporters. To achieve functional activity these transporters have to form hetero- or homodimers. BCRP is involved in the multidrug resistance of certain tumors and transports endogenous compounds like cholesterol and steroid hormones. 

Because the WHI is the best evidence to date linking HRT with breast cancer, women with a personal history of breast cancer and possibly even a strong family history of breast cancer should avoid the use of HRT and consider non-hormonal alternatives for the treatment of vasomotor symptoms. 

Both personal and family histories influence a woman s risk of developing breast cancer. A past medical history for breast cancer is associated with about a fivefold increased risk of... 

It has been recognized for some time that a family history of breast cancer is associated rather strongly with a woman s own risk for developing the disease. The percentage of all breast cancers in the population that can be attributed to family history range between 6% and 12%.8 Empirical estimates of the risks associated with particular patterns of family history of breast cancer indicate the following 8... 

Voskuil, DW, A Vrieling, CM Korse et al. 2008. Effects of lycopene on the insulin-like growth factor (IGF) system in premenopausal breast cancer surviviors and women at high familial breast cancer risk. Nutr Cancer 60(3) 342-353. 

Garber, J. (1999), A 40-year-old woman with a strong family history of breast cancer ,/ Am. Med. Assoc., 282, 1953-1960. 

Rohlfs EM, Puget N, Graham ML et al. An Alu-mediated 7.1 kb deletion of BRCA1 exons 8 and 9 in breast and ovarian cancer families that results in alternative splicing of exon 10. Genes Chromosomes Cancer 2000 28[3] 300—307. 

The choice to use CHCs should not be affected by the presence of benign breast disease or a family history of breast cancer with either mutation. The WHO precautions state that women with recent personal history of breast cancer should not use CHCs, but that CHCs can be considered in women without evidence of disease for 5 years. 

Miproxifene (TAT-59) is a prodrug of 4-hydroxy-tamoxifen that has been developed for tamoxifen-resistant carcinoma, but relatively little information has been published on this drug. Compared with tamoxifen, miproxifene inhibits estradiol-stimulated proliferation of MCF-7 cells at a threefold lower dose than that of tamoxifen, and of dimethyl-benzanthracene (DMBA)-induced rat mammary tumors at a dose tenfold lower than tamoxifen (Toko et al. 1990). In any event, in preclinical castrated rat models, it shows an endometrial stimulation activity that is similar to that of tamoxifen, which means it has limited potential use in the prevention or treatment of osteoporosis or cardiovascular disease (Shibata et al. 2000). Similarly, considering the preclinical findings of endometrial stimulation reported on GW5638 (Willson et al. 1997), it is likely that this new SERM belonging to the triphenylethylene family will be limited in clinical use to the treatment of advanced tamoxifen-resistant breast cancer once its efficacy is demonstrated in human clinical trials. 

Until recently tamoxifen has been the gold standard for adjuvant therapy in ER(+) early breast cancer. Recent information from controlled trials comparing tamoxifen to aromatase inhibitors has challenged this idea. More research is needed to establish the respective roles of the two families of substances in the hormonal management of breast cancer (Chlebowski et al. 2002). 

Three other studies were conducted to investigate the preventive potential of tamoxifen. One in Italy (Veronesi et al. 1998), one at the Royal Marsden Hospital, United Kingdom (Powles et al. 1998), and a multicentric international study (IBIS 2002). The British study was the smallest in size (2471 participants) but concentrated on women with a high incidence of family history and consequently presented a higher number of breast cancers. The Italian trial included only women with previous hysterectomy and, accordingly, around 50% had also undergone bilateral oophorectomy. The family risk was low only 15% had a first-degree relative affected by breast cancer. Both European studies permitted concurrent HRT, and 26% of the participants in the British trial received HRT while on study and 42% had ever received HT for menopausal symptoms. Neither of the studies showed any positive effect of the treatment with tamoxifen on the incidence of breast cancer. Reasons for this lack of effect can be different for each trial. 

The IBIS-I study was promoted by the UK Coordinating Committee for Cancer Research and supported by the Imperial Cancer Research Fund. A group of 7152 high-risk women were selected according to criteria related to familial cases of breast cancer, previous atypical biopsies, and parity. The most important group was that of women with two or more first- or second-degree relatives with breast cancer. For this group the yearly frequency of breast cancer, in the absence of any intervention, was calculated to be 7.50 per 1000 women. This proved to be accurate since the actual frequency in the placebo... 

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