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cscs are a small population of cells within the tumor. the cscs are characterized by their self-renewal and differentiation abilities, and are able to generate tumors from serial transplantation. the cscs are involved in the initiation and progression of various types of cancer and are considered to be the primary source of tumor resistance to conventional therapies and tumor relapse [ 58 ].cscs generally exist in a few subpopulations of the whole tumor mass. cscs are often identified by the expression of stem cell markers. in the csc model, the cscs can be isolated and cultured in vitro as well as in vivo, thereby providing an in vitro model to study cscs. cscs have been identified in many types of cancers. the first identified csc in the breast cancer was the aldehyde dehydrogenase (aldh)1(+) cscs [ 59 ], which can be identified by the aldh1 enzyme that participates in the oxidation of intracellular aldehydes. another identified cscs is cd44(+)cd24(−) cells in the human breast cancer cell line mcf-7 [ 60 ], which are able to grow as mammospheres in serum-free medium [ 61 ] and can initiate tumors in scid mice [ 62 ].research has also shown that some of the cscs are able to migrate to distant sites, invade into adjacent tissues and form metastatic tumors. this process is known as metastasis. cscs in the cca are considered to be the main source of metastasis [ 63 ]. cscs are able to proliferate and self-renew by asymmetric cell division. the asymmetric cell division is mediated by the localization of spindle assembly checkpoint proteins such as pard6b and pard3, which prevent cell cycle arrest and apoptosis in daughter cells with damaged dna [ 64 ]. therefore, the cscs can repair dna damage and escape the apoptosis of cancer cells, which further allows them to survive the chemotherapy and radiotherapy. in addition, many researchers have reported that the cscs from pancreatic cancer cells are able to generate tumors in mice [ 65, 66 ].
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