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Breast Cancer Development (breast + cancer_development)
Selected AbstractsTransforming properties of TC-1 in human breast cancer: Interaction with FGFR2 and ,-catenin signaling pathwaysINTERNATIONAL JOURNAL OF CANCER, Issue 6 2007Zeng-Quan Yang Abstract Breast cancer development is associated with gene amplification and over expression that is believed to have a causative role in oncogenesis. Previous studies have demonstrated that over expression of TC-1(C8orf4) mRNA occurs in ,50% of breast cancer cell lines and primary tumor specimens. Here, we show that TC-1 has transforming properties in human mammary epithelial (HME) cells and its expression is mechanistically linked to FGFR signaling cascades. In vitro experiments demonstrate that TC-1 over expression mediates both anchorage-independent and growth factor-independent proliferation of HME cells. TC-1 was down regulated by the FGFR inhibitor PD173074 in the breast cancer cell line SUM-52 that also has an FGFR2 gene amplification and over expression. Furthermore, forced expression of FGFR2 in HME cells increased the level of expression of endogenous TC-1 mRNA. TC-1 has been implicated as a modulator of Wnt/,-catenin signaling in 293 cells and in gastric cancer cells. However, while we did find increased expression of a subset of ,-catenin target genes in TC-1 over expressing cells, we did not find an association of TC-1 with global expression of ,-catenin target genes in our cells. Taken together, our data suggest that TC-1 over expression is transforming and may link with the FGFR pathway in a subset of breast cancer. © 2007 Wiley-Liss, Inc. [source] PPFIA1 and CCND1 are frequently coamplified in breast cancerGENES, CHROMOSOMES AND CANCER, Issue 1 2010Ana-Maria Dancau Recently, amplification of PPFIA1, encoding a member of the liprin family located about 600 kb telomeric to CCND1 on chromosome band 11q13, was described in squamous cell carcinoma of head and neck. Because 11q13 amplification is frequent in breast cancer, and PPFIA1 has been suggested to contribute to mammary gland development, we hypothesized that PPFIA1 might also be involved in the 11q13 amplicon in breast cancer and contribute to breast cancer development. A tissue microarray containing more than 2000 human breast cancers was analyzed for gene copy numbers of PPFIA1 and CCND1 by means of fluorescence in situ hybridization. PPFIA1 amplification was found in 248/1583 (15.4%) of breast cancers. Coamplification with CCND1 was found in all (248/248, 100%) PPFIA1 -amplified cancers. CCND1 amplification without PPFIA1 coamplification was found in additional 117 (4.7%) tumors. Amplification of both PPFIA1 and CCND1 were significantly associated with high-grade phenotype (P = 0.0002) but were unrelated to tumor stage (P = 0.7066) or nodal stage (P = 0.5807). No difference in patient prognosis was found between 248 CCND1/PPFIA1 coamplified tumors and 117 tumors with CCND1 amplification alone (P = 0.6419). These data show that PPFIA1 amplification occurs frequently in breast cancer. The higher incidence of CCND1 amplification when compared with PPFIA1, the lack of prognostic relevance of coamplifications, and the fact that PPFIA1 amplification was found exclusively in CCND1 -amplified cancers suggest that PPFIA1 gene copy number changes represent concurrent events of CCND1 amplification rather than specific biological incidents. © 2009 Wiley-Liss, Inc. [source] De novo breast cancer in patients with liver transplantation: University of Pittsburgh's experience and review of the literatureLIVER TRANSPLANTATION, Issue 1 2004M.Tahir Oruc De novo malignancies are one of the current problems in patients with organ transplantation. The incidence has been considered to be higher as a result of increases of oncogenic viruses in immunosuppressed organ recipients. Published reports have shown increased incidence of de novo tumors such as malignant lymphomas and cutaneous neoplasms but decreased incidence of breast cancer. A variety of factors affect de novo breast cancer development in organ recipients, including immunosuppression, viruses, and underlying disease. The aims of this review are to evaluate the incidence and management of patients with de novo breast cancer by giving the University of Pittsburgh's data, and to evaluate the incidence of de novo breast cancer in published reports in light of an age-adjusted rate. According to age-adjusted rates presented by the National Cancer Institute's Surveillance, Epidemiology and End Results data, we found increased incidence rate of de novo breast cancer in the previously published series. The University of Pittsburgh's incidence rate of de novo breast cancer was determined in a fashion similar to that for the Surveillance, Epidemiology and End Results data. Eighty-three percent of all patients were diagnosed at early stages, and it appeared to take longer for de novo breast cancer to develop in patients treated with tacrolimus than in patients treated with cyclosporine. In conclusion, surgical treatment of breast cancer in liver recipients is the same as treatment of breast cancer in patients without transplantation. However, the effects of chemotherapy, radiotherapy, and/or tamoxifen remain unclear in transplanted patients and need to be evaluated in larger studies. (Liver Transpl 2004;10:1,6.) [source] Risk of breast cancer in association with exposure to two different groups of tricyclic antidepressants,PHARMACOEPIDEMIOLOGY AND DRUG SAFETY, Issue 10 2006Hani Tamim PhD Abstract Purpose In 2002, we reported an epidemiological study in which we found that some tricyclic antidepressants (identified as genotoxic in Drosophila Melanogaster) were associated with an increased risk of breast cancer, when exposure took place 11,15 years before the date of diagnosis. The implications of the results found lead us to carry out a separate case-control study, using the same source population, to validate the conclusions drawn from our previous study. Methods We accrued 7330 breast cancer cases, diagnosed between 1981 and 2000, and 29,320 controls matched on age and time. Results The association between exposure to genotoxic TCAs 11,15 years before diagnosis and the risk of breast cancer development was much weaker, as compared to what was reported in our previous study. The relative risk of breast cancer in women exposed to high doses of genotoxic TCAs 11,15 years before diagnosis was 1.17 (95%CI: 0.79,1.74), while in women exposed to high levels of non-genotoxic TCAs during the same period it was 0.95 (95%CI: 0.61,1.48). Conclusion In conclusion, we did not find supporting evidence for an increased risk of breast cancer among women exposed to TCAs up to 20 years in the past. Copyright © 2006 John Wiley & Sons, Ltd. [source] Estrogen signaling pathway and its imaging in human breast cancerCANCER SCIENCE, Issue 10 2009Shin-ichi Hayashi Recent remarkable progress in hormonal therapy has provided great benefit to breast cancer patients, but it also evokes novel issues: how accurately can the efficacy of each hormonal therapy be predicted and how can hormonal therapy,resistant patients be treated? These clinically important issues must be closely related to the biological events in each cancer, such as the alteration of intracellular multiple estrogen signaling pathways and the estrogen-related cancer microenvironment, which has recently revealed by molecular biological studies on estrogen and its receptors. However, the estrogen signaling status in individual breast cancers has not been clarified yet. Here we present the context of these issues and introduce our study of new tools which enable the visualization of estrogen signals in individual cancers. The assessment of estrogen receptor (ER)-, activity in individual cancers or ER-activating ability of the cancer microenvironment in each breast cancer patient revealed several new findings and interesting observations. We hope that these approaches provide new clues about the estrogen-dependent mechanisms of breast cancer development, and will be useful to advance the diagnosis and treatment of breast cancer patients. (Cancer Sci 2009; 100: 1773,1778) [source] | ||||||||||