Humans are integrated with the environment where they live. Gravitational force plays an important role in shaping the universe, lives, and even cellular biological processes. Research in the last 40 years has shown how exposure to microgravity changes biological processes. Microgravity has been shown to have significant effects on cellular proliferation, invasion, apoptosis, migration, and gene expression, specifically in tumor cells, and these effects may also exist in stem and cancer stem cells. It has also been shown that microgravity changes the effects of chemotherapeutic drugs. Although studies have been carried out in a simulated microgravity environment in cell culture lines, there are few animal experiments or true microgravity studies. Cancer remains one of the most significant problems worldwide. Despite advances in medical science, no definitive strategies have been found for the prevention of cancer formation or to inform treatment. Thus, the microgravity environment is a potential new therapeutic strategy for future cancer treatment. This review will focus on current knowledge on the impact of the microgravity environment on cancer cells, stem cells, and the biological behavior of cancer stem cells.
The most frequently diagnosed endocrine cancer, which causes more deaths than any other endocrine cancer, is thyroid cancer. Cancer stem cells are rare cells found in tumors that can regenerate themselves, phenotypically leads to various tumor cell populations and trigger tumorigenesis. Cancer stem cells have been identified in many cancers, including thyroid cancer. Having an understanding of the molecular mechanisms which control the biology of cancer stem cells and the disease processes will help us in designing more rational targeted therapies for aggressive thyroid cancers. In this review, we aimed to present the current accepted knowledge about thyroid stem cells, information regarding the cellular origin of thyroid cancer stem cells, and the clinical results of cancer stem cells present in the thyroid gland.
Decitabine (5-aza-2p-deoxycytidine) is a hypomethylation agent with a double-action mechanism, these are the reactivation of silenced genes; exhibiting differentiation at low doses and showing cytotoxicity at high doses. Decitabine was used as a classic anticancer drug in the original studies in the 1980s, 1500 to 2500 mg/m2 per cycle was the maximum clinically tolerated dose. The dosage was reassessed after a better understanding of epigenetics in cancer and the role of decitabine in epigenetic (hypomethylation) therapy was obtained, in about 1/20th of the previous doses (i.e., 'optimal biological' doses modulating hypomethylation). It has been found that decitabine (100 to 150 mg / m2 per cycle) can be used in patients with myelodysplastic syndromes (MDS) and other myeloid tumors, with manageable side effects. Combination therapies which amplify the epigenetic effect of decitabine will most likely improve the patient responses and allow it to be used in the treatment of other malignancies.
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