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Apoptosis is a multi-step, multi-pathway cell-death programme that is inherent in every cell of the body. In cancer, the apoptosis cell-division ratio is altered. Cancer treatment by chemotherapy and irradiation kills target cells primarily by inducing apoptosis. [98]
Many tumor suppressor genes effect signal transduction pathways that regulate apoptosis, also known as "programmed cell death". Tumor suppressor genes code for anti-proliferation signals and proteins that suppress mitosis and cell growth. Generally, tumor suppressors are transcription factors that are activated by cellular stress or DNA
Older hypotheses such as the Warburg hypothesis suggest the Warburg effect may simply be a consequence of damage to the mitochondria in cancer. It may also be an adaptation to low-oxygen environments within tumors, or a result of cancer genes shutting down the mitochondria, which are involved in the cell's apoptosis program that kills cancer cells.
PUMA has been shown to be active in inducing apoptosis in hematopoietic and intestinal tissue following γ-irradiation. [12] [55] Since inhibition of PUMA does not directly cause spontaneous malignancies, therapeutics to inhibit PUMA function in healthy tissue could lessen or eliminate the side effects of traditional cancer therapies. [7]
malignant melanoma, papillary thyroid cancer, colorectal cancer, and ovarian cancer [31] involved in organism development, cell cycle regulation, cell proliferation, differentiation, cells survival, and apoptosis [32] Regulatory GTPases: Ras protein: adenocarcinomas of the pancreas and colon, thyroid tumors, and myeloid leukemia [33]
Anti-cancer drugs and radiation, for example, work by triggering apoptosis in diseased cells. Many diseases and disorders are linked with the life and death of cells—increased apoptosis is a characteristic of AIDS, Alzheimer's, and Parkinson's disease, while decreased apoptosis can signal lupus or cancer.