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If a drug can inhibit telomerase in cancer cells, the telomeres of successive generations will progressively shorten, limiting tumor growth. [56] Telomerase is a good biomarker for cancer detection because most human cancer cells express high levels of it. Telomerase activity can be identified by its catalytic protein domain .
To measure the concentrations of TRF1 and the relationships among telomere length, telomerase activity, and TRF1 levels in tumor and normal colorectal mucosa, from normal and tumoral samples of patients who underwent surgery for colorectal cancer we analyzed TRF1 protein concentration, and telomerase activity were analysed.
Two concerns with applying telomerase inhibitors in cancer treatment are that effective treatment requires continuous, long-term drug application and that off-target effects are common. [30] For example, the telomerase inhibitor imetelstat, first proposed in 2003, [31] [32] has been held up in clinical trials due to hematological toxicity. [30]
In most multicellular eukaryotic organisms, telomerase is active only in germ cells, some types of stem cells such as embryonic stem cells, and certain white blood cells. [9] Telomerase can be reactivated and telomeres restored to the embryonic state by somatic cell nuclear transfer. [18]
90% of cancers are characterized by increased telomerase activity. [28] Lung cancer is the most well characterized type of cancer associated with telomerase. [29] There is a lack of substantial telomerase activity in some cell types such as primary human fibroblasts, which become senescent after about 30–50 population doublings. [28]
A comparison of two chemotherapy regimens for advanced Hodgkin lymphoma found the less intensive treatment was more effective for the blood cancer and caused fewer side effects.
The FDA approval is based on data from a mid-stage study that showed that 58% of patients treated with Pfizer's therapy had no signs of cancer or had seen a significant decrease in cancer cells in ...
Response to treatment is thus associated with reduced levels of S100-beta in the blood of such individuals. [ 37 ] [ 38 ] Similarly, additional laboratory research has shown that tumor cells undergoing apoptosis can release cellular components such as cytochrome c , nucleosomes , cleaved cytokeratin-18 , and E-cadherin .