Please describe one well-studied example of a tumor suppressor gene, and highlight its normal function and how it might play a role in cancer.
Tumor suppressor genes are the genes that regulate cell cycle
during the normal cell development.
The mutation of this gene causes the cell to undergo uncontrollable
division leading to the formation of tumors.
Examples include p53, BCL2, pRB, etc.
p53 is a tumor suppressor gene that encodes for a protein known
as p53 which protects the genome of the cell.
This protein is mainly involved in apoptosis, DNA repair,
transcription and maintaining cell cycle. This protein mainly
prevents tumor formation and functions as a tumor suppressor. In
normal cells, p53 is in the inactive state, when there is a
damage then p53 gets dissociated with mdm2 complex and gets
activated and induces cell cycle arrest and either
repair the cell or induces apoptosis.
If p53 is mutated, then whenever a cell undergoes damage, the p53
does not perform its function.
As a result, the cells might divide abnormally without undergoing
repair or apoptosis .
The accumulated effect leads to the development of the tumor.
Which of the following is a false statements about tumor suppressor genes? Gene amplification (duplication) of a tumor suppressor gene is less likely to result in cancer than gene amplification of a proto-onocogene. Individuals with a single normal copy of a tumor suppressor gene are more prone to cancer than those with two normal copies. Inactivation of tumor suppressor genes can lead to enhanced cell survival and cell proliferation. Epigenetic changes that silence tumor suppressor genes would not lead to...
Given that TP53 is a recessive gene and is not located on the X chromosome, why would people who inherit just one mutant copy of a recessive tumor-suppressor gene be at higher risk of developing cancer than those without the recessive gene? Given that is a recessive gene and is not located on the X chromosome, why would people who inherit just one mutant copy of a recessive tumor-suppressor gene be at higher risk of developing cancer than those without...
Describe two potential observations or scientific strategies in which the role of a tumor suppressor could be determined. You can provide an example.
Retinoblastoma (resulting in eye tumor) results from inactivation of Rb gene, a tumor suppressor. A).List the molecular events that lead to the development of hereditary retinoblastoma? ________________________________________________________________________________________________________________________________________________________________________________________________ B). How the development of sporadic retinoblastoma will be different from the hereditary one? Mention the molecular steps that will be unique for the sporadic retinoblastoma? _________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________ C). Is the loss of Rb function dominant or recessive and why? ________________________________________________________________________________________________________________________________________________________________________________________________ D). Knowing the Rb binds to E2F, which is transcription factor activating expression...
Differentiate between the normal cellular actions / functions of a tumor suppressor and a protooncogene. Using p53 and Ras as specific examples, describe one of the pathways each are involved in (can be a specific pathway or a more general type of pathway). Explain what type of mutation, for each protein, would lead to disruption of the pathway. Finally, explain how disruption of this pathway could lead to cancer. You can use the chart below to answer the question tumor...
Using one example of each class of gene, explain how mutations in tumour suppressor genes and oncogenes can lead to alterations in cell signalling pathways, and contribute to cancer development.
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...
Consider a spontaneous mutation in the gene HER2, a tumor suppressor involved in cell cycle control Mutations happen at a rate of about 1 error per 109 bases per generation. A spontaneous deleterious mutation must occur in HER2 specifically, and not in another gene. The likelihood that a spontaneous mutation is deleterious and could lead to cancer depends on the number of mutable bases in HER2, the fraction of bases that will affect the function of HER2, and that both...
please help me with this genetics question! thank you! TS =Tumor Suppressor genes O = Oncogenes 5A. (12pts) Cancer is a genetic disease. Some of the causative mutations are Tumor Suppressor genes, and others convert proto-oncogenes into Oncogenes. In the list of properties below, mark an X in the column for TS, O, or both. TS O both Causes of inherited elevated cancer risk. Leads to uncontrolled cell growth. Typically, spontaneous, gain-of-function mutations. Can cause increased DNA damage. Dominant in...
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...