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An elevated mitotic index indicates more cells are dividing. In cancer cells, the mitotic index may be elevated compared to normal growth of tissues or cellular repair of the site of an injury. [2] The mitotic index is therefore an important prognostic factor predicting both overall survival and response to chemotherapy in most types of cancer ...
Prophase II of meiosis is very similar to prophase of mitosis. The most noticeable difference is that prophase II occurs with a haploid number of chromosomes as opposed to the diploid number in mitotic prophase. [12] [10] In both animal and plant cells chromosomes may de-condense during telophase I requiring them to re-condense in prophase II.
The intracellular concentration can have important implications for cancer prognosis. High levels of nuclear cyclin B1 is associated with high tumor grade, larger tumor size and higher metastasis probability, therefore a high level of cyclin B1 is a predictor of poor prognosis. [26]
[4] [5] A tumor suppressor would trigger an apoptotic pathway in a cancer cell if there were DNA damage, polyploidy, or uncontrolled cell growth. Simultaneously, tumor cells need to upregulate oncogenes , which promote or cause downstream activation of growth factors and cell survival signals such as RAS, [ 6 ] Mitogen-activated protein kinase ...
A panel of epigenetic methylation marker has been explored for prognosis of ovarian cancer, and it is reported that the panel exhibited high specificity and sensitivity (both above 70%) as a screen marker. [5] Epigenetic markers have also shown promising potential as prognostic markers for bladder cancer. [6]
Similar studies have correlated low levels of p27 with a worse prognosis in breast cancer. [35] Colorectal carcinomas that lacked p27 were shown to have increased p27-specific proteolysis and a median survival of only 69 months compared to 151 months for patients with high or normal levels of p27. [36]
Cancer cells have been observed to divide in multiple directions by evading the spindle assembly checkpoint resulting in multipolar mitoses. [78] The multipolar metaphase-anaphase transition occurs through an incomplete separase cycle that results in frequent nondisjunction events which amplify aneuploidy in cancer cells.
Cyclin A2 regulates homologous recombinational DNA repair in human breast cancer cells [21] Loss of cyclin A2 causes high rates of double-strand breaks in DNA. The increase in double-strand breaks is a consequence of defective homologous recombinational repair of the breaks resulting from reduced MRE11 and RAD51 DNA repair proteins. [21]