Breast Cancer Patients Treated With Endocrine Therapy

1592 WordsMay 2, 20177 Pages
When it is assumed that 40 % of breast cancer patients treated with endocrine therapy are resistant to this therapy it becomes a problem within the health world, because that such a larger number of patients are not being cured from this treatment. Researchers have studied the Cyclin D1 (CCND1) amplification for being the possible cause for tamoxifen resistance. Cyclin D1 is found within 10-20% of breast cancer patients making it a prime suspect too why patients are becoming resistant to treatment procedures. Not only does CCND1 amplification preferentially occurs in ER positive breast cancer patients, but also eight different studies have shown data linking poor response of tamoxifen therapy too CCND1. FISH (Fluorescence in situ…show more content…
This means the average number of tumor blocks per breast cancer was 6.0 in this study. All in all the results show that the CCND1 amplifications is rarely heterogeneous in breast cancer. The high degree of homogeneity seen for CCND1 amplification suggests that this alteration represents an early event in breast cancer development in a small subset of breast cancers and that the CCND1 amplification status determined in a core biopsy will be highly representative of the entire tumor and appropriate for predicting treatment outcome if applicable. (CDKs) cyclin-dependent kinases are a family of serine/threonine kinases that are controlling progression throughout the cell cycle. In this review the main focus is going to be on cyclin D1 and other similar manner of functions. Cyclin D1 plays one of the most important roles in the cell cycle, because it will lead to progression through association with CDK4 and CDK6. The problem discussed is that within Cyclin D1 the DNA damage response and repairs alarms the chromosome stability. Metastasis has become a major cause of death in cancer patients that resulted in studies of cellular migration making it essential for tumor metastasis. Scientist have figured out that cyclin D1 binding of pk27 contributed to cellular migration. The review very comprehensive it is 9 pages of solid information even though 4 of the 9 pages are references. No, all the references are not related to the problem under

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