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CORE BREAST CANCER ASSOCIATED MOLECULES: The Essence |
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| รหัสดีโอไอ | |
| Creator | 1. Moltira Promkan 2. Pimpicha Patmasiriwat |
| Title | CORE BREAST CANCER ASSOCIATED MOLECULES: The Essence |
| Publisher | Genetics Society of Thailand |
| Publication Year | 2556 |
| Journal Title | Thai Journal of Genetics |
| Journal Vol. | 6 |
| Journal No. | 2 |
| Page no. | 128-140 |
| Keyword | BRCA1, c-Myc, CyclinD1, ER-related molecules, survivin |
| ISSN | 8578664 |
| Abstract | Driving of cell cycle and proliferation in normal mammary epithelial and breast cancer cells appears to have similar pattern but they are different in the expression of responsible genes. Various cellular factors in which their proliferative functions are inter-related (i.e., genes, proteins, miRNA) have been increasingly reported, both in normal and cancer cells. Increase in cellular proliferative rate in cancer is attributed to deregulation of mechanisms related to cell cycle, tumor suppressor and apoptotic control pathways. In this regard, there must be some errors occurring within the functional molecules in one or more of these pathways. For instances, gene mutation or amplification, chromosome aberration, epigenetic change, abnormal increase or decrease of some miRNA or derangement of interacting proteins. In breast cancer, like other cancers, cell cycle driving genes and genes involved in cellular proliferation, sometimes known as "proliferative or cancer signature" genes, usually are expressed at the level higher than normal. Noteworthy, some cancer-associated genes expressed at a low level in cancer cells are not recognized as the proliferative or cancer signature in spite of their obvious roles on tumorigenesis. These genes include those known to encode for cell cycle inhibitors, intercellular adhesive molecules, proteins which function for DNA repairing and genome stability and molecules that contribute in apoptosis. This review gathers and concludes the roles of key molecules believed to be associated with breast cancer to date. Cumulative knowledge of molecular crosstalk signals in normal mammary epithelium could help in understanding how deviated molecules and distorted regulations occur in breast cancer. In addition, no single molecule can provide full cellular proliferative function and this is also true in cancer. Hence, cancer therapy with highly specific inhibitor targeting a single molecule is generally not guaranteed of the therapeutic success, and should be performed with careful consideration. |
