How might the loss of components of the apoptosis
machinery render cancer cells more susceptible than normal cells to
certain types of cell death?
Defects in programmed apoptosis mechanisms play important roles in tumor pathogenesis, allowing neoplastic cells to survive over intended lifespans, subverting the need for exogenous survival factors and providing protection from oxidative stress and hypoxia as the tumor mass expands. That gives time for accumulation of genetic alterations that deregulate cell proliferation, interfere with differentiation, promote angiogenesis, and increase invasiveness during tumor progression . Apoptosis defects are now considered an important complement of protooncogene activation, as many deregulated oncoproteins that drive cell division also trigger apoptosis (e.g., Myc, E1a, and Cyclin-D1) . On the other hand, the noncancerous cells have a DNA repair machinery. Defects in DNA repair and/or chromosome segregation normally trigger cell suicide as a defense mechanism for eradicating genetically unstable cells and thus such suicide mechanism
How might the loss of components of the apoptosis machinery render cancer cells more susceptible than...
13. Which of these statements is TRUE? a. Cancer cells usually have more than one mutation. . Proto-oncogenes are normal genes that code for proteins that cause cells to undergo apoptosis (programmed cell death) c. Cancer usually involves a gain-of-function mutation in a tumor suppressor gene d. Cancer usually involves a loss-of-function mutation proto-oncogene
Depletion of cholesterol in the cell membrane using a drug (mevastatin) has been associated with apoptosis in cancer cells. a. What effect would cholesterol depletion have on the integrity of lipid rafts in the membrane? b. Researchers found that FAS death receptor was activated in cholesterol depleted cancer cells. Explain how activation of this receptor activates killer caspases. c. When a caspase is converted from its inactive to its active form there are changes in the primary and tertiary structure...
Cancer cells often lack normal DNA damage response and cell-cycle control mechanisms. Why does this make them more susceptible to DNA-damaging chemotherapies? O Cancer cells will arrest in the cycle and will not grow further O Cancer cells with activating mutations in Ras will amplify the damage through the Ras signaling pathway Cancer cells might ignore the normal mechanisms that halt the cell cycle in response to damage, and subsequent division with damage leads to death, O Cancer cells have...
Cancer cells typically have less cholesterol and more phospholipid in their cell membranes. This phenotype is also associated with resistance to apoptosis. The FAS death receptor is localized to lipid rafts. Using this information to explain why increased phospholipid and increased cholesterol could inhibit the initiation of apoptosis. Rubric (2): Plausible link between increased change in membrane composition, effect on lipid raft formation and lack of FAS receptor activation.
Why might inhibition of LDH in cancer cells lead to cancer cell death? Explain why conjugating an LDH inhibitor to glucose leads to preferential targeting of cancer cells?
Customary treatment for metastatic cancer, chemotherapy and radiation, execute growth cells by inciting apoptosis. Be that as it may, disease cells get to be safe in view of numerous systems in particular, multidrug resistance pumps, temperamental genomes, changes, and so on. Propose elective medications that might be more fruitful against tumors and that don't include the apoptotic pathway (caspase-autonomous pathways). please include the page where you got it from.
QUESTION 1 Match the following terms pertaining to cancer treatment with the correct descriptions/definitions. A apoptosis B differentiation C. fractionation D metastasis E morbidity F. radiosensitizer G.anaplasia H fibrosarcoma L pedunculated J. angiogenesis K oncogene L alkylating agents M.laparoscopy N en bloc resection o pleomorphic P carcinoma in situ a cachexia R adenocarcinoma s exfoliative cytology T mutagenic Malnutrition associated with chronic disease (such as malignancy) and ill health Region of DNA found in tumor cells, examples are abl, ras,...
1. Why do cancer cells spread throughout the body? Select all that apply (Think: how are cancer cells different than normal cells?) __________ a. They enrich nutrients at the original site b. They have loose adherence c. They travel through blood vessels d. They do not respond to contact inhibition e. They are fragile and damage easily f. They readily respond to signals for apoptosis 2. Benign cells have which characteristics? Select all that...
Describe the potential mechanisms that are thought to be involved in how stems cells might ‘work’. Your ‘list’ may not be relevant to all stem cell types, or therapies, but you need to consider them all. (Hint: there are more than 3!)
Cancer biologists use principles of evolution to understand the development of tumors. A population of cells can obtain a mutation after exposure to a carcinogen. In some of the cells, the mutation is not repaired by the cell’s DNA repair machinery and is retained in the genotype. Only a fraction of the cells retaining the mutation become cancerous and only a fraction of those cells have the ability to form a tumor – cells that grow much faster than normal...