Compare and contrast the roles of oncogenes and tumor suppressors in oncogenesis. How were each discovered and studied? What is unusual about p53 in terms of being a tumor suppressor?
The oncogenes are genes which induces the formation of the tumor because of its potential to proliferate and become cancerous. The oncogenes are majorly present in the tumor cells and are expressed at a very high rate. The proto-oncogenes are activated when there is a mutation and it starts to multiply and produce multiple copies forming the oncogenes. The tumor suppressor genes are those which helps in slowing down mistakes during DNA replication, slow down cell division and signals apoptosis and hence helps in suppressing formation of tumor. The tumor suppressor genes when are inactivated through mutation causes cancer and oncogenes when activated causes cancer.
The first oncogene that was discovered with confirmation was in the year 1970 and was called sarcom and it was found within the chicken retrovirus. The tumor suppressor gene was found after the two hit hypothesis that was given by A.G Knudson and it was found in the retinoblastoma.
The p53 is a tumor suppressor gene but its activity depends on what is being inherited. If a person inherits one copy of the p53 that is function, it has predisposition to cancer formation and may form independent tumors. When it contains both copy, it helps in suppressing the tumor formation.
Compare and contrast the roles of oncogenes and tumor suppressors in oncogenesis. How were each discovered...
Compare and contrast proto-oncogenes and tumor suppressor genes with respect to modes of action and examples
Contrast what tumor suppressor genes and proto-oncogenes do in their normal and cancer-promoting states. Normal Cancer-promoting Tumor suppressor gene (Proto-)oncogene
PATH370 2018 - risk factors/predisposing factors for carcinogenesis: tobacco, nutrition, genetics (proto-oncogenes, oncogenes, tumor suppressor genes), viruses - role of p53 and Rb carcinogenesis: what is initiation, promotion, progression? - carcinogen vs mutagen vs teratogen - metastasis: define/describe, pattern of spread, tumor markers, angiogenesis, grading/staging, most common organs where metastasis occurs, first place of metastasis for many cancers - TNM system: what does each letter represent, are low or high number more severe? - generalized effects of cancer on the...
Compare and contrast a contractile ring and a sarcomere. Focus on function, structure, and mechanisms of operation. Compare and contrast CDK and cyclin. Focus on function, stability/levels of molecules in cells Compare and contrast tumor suppressor proteins and proto-oncoproteins. Describe a protein that fits each category, and discuss how that protein functions.
Directions: You have been studying various oncogenes and tumor suppressor genes in tumor cell lines in vitro, but would now like to address certain questions in mouse models in vivo. For each of the questions below, briefly describe the type of mouse model you would use. For xenograft/allograft experiments, briefly describe the type of cell lines you might use and the experimental end points you would be looking at. For GEMs, briefly describe the type of mouse you would make...
help me with that please this question is cery important i have a final , 7. Loss-of-function mutations in p53 typify the ajority of human cancers Discovery of the roles for p53 in the DNA damage checkpoint and in apoptosis helps to explain its potency as a tumor suppressor protein. Recent studies suggest that p53 may possess an additional anti-tumor function: preventing telomerase activity. In one such study by Ogawa and colleagues, a human pancreatic cell line called MIA PaCa-2,...
You are an oncologist (cancer doctor) who specializes in pioneering new advances in cancer therapies. You have been given an exciting new gene therapy treatment that aims at increasing the levels of the p53 protein in tumor cells that have lost all functional p53. You have a cancer patient who is going to be one of the first people ever to receive this treatment since their tumor cells have mutated versions of p53. But they have many questions about the...
Please answer the following questions: 1. Compare and contrast the roles and responsibilities of Health Education Specialists working in schools, public and community health agencies, worksites, and healthcare facilities. How are all of these settings similar? How are they different? 2. If you were in a position to hire a new Health Education Specialist, what qualities, traits, and experiences would you look for in making your hiring decision? And explain as to why.
Negative and positive feedback systems both have their roles in physiology. Compare and contrast these two types of feedback systems and provide a biological example of each, illustrating how it works. Which, if any, of these two types of feedback are involved in the maintenance of homeostasis? Explain.
1. Damaged DNA is discovered during the G1 checkpoint. How does p53 react, and what are the possible results? 2. If S phase checkpoints detect nucleotides deficit, what happens to the dividing cell and the cell cycle? 3. What three conditions may be detected during the G2 checkpoints, and what are the two possible results if there is inadequate DNA or spindle fibers? 4. What two conditions are checked during the metaphase checkpoint? What happens if the cell “passes” the...