The deregulation of several signal transduction pathways is integral to the onset ofcancer. These pathways involve both tumor promoters (the "gas pedals") and tumorsuppressors (the "brake pedals").Which would be a more effective treatment for cancer: A small molecule inhibitorthat targets a tumor suppressor or one that targets a tumor promoter? Brieflyexplain your choice. (THIS CAN BE DONE IN LESS THAN TWO SENTENCES, ANDMINIMALLY IN ABOUT EIGHT WORDS.)Edit View. Insert Format Tools Table12pt vParagraph BI UAV 2VT² V| :

Cancer is most commonly caused by genetic alterations (mutations) affecting the genes involved in…

Answered: Which would be a more effective…

Human Heredity: Principles and Issues (MindTap Course List)

11th Edition

ISBN:9781305251052

Author:Michael Cummings

Publisher:Michael Cummings

Chapter12: Genes And Cancer

Section12.10: Genomics, Epigenetics,and Cancer

Problem 2GR: Another model, the random model, proposes that any cell in a malignant tumor has the potential to...

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Describe the general process of cell signalling pathways: what events take place for a signal to cause cellular changes? Provide examples and how perturbation of these events can result in “cancer pathways”. In addition, describe in detail a typical cancer pathway and its strategy to activate gene expression. What is the origin of many cancer pathways, i.e., during which stage of an organism’s live process(es) are they physiologically activated? Why is this important for cancer development?
The best strategy for treating a specific type of human tumor can depend on identifying the type of cell that became cancerous to give rise to the tumor. For some tumors that have colonized a distant location (metastasized), identifying the parental cell type can be difficult. Because the type of IF protein expressed is cell-type-specific, using monoclonal antibodies that react with only one type of IF protein can help in this identification. What IF proteins would you produce monoclonal antibodies against to identify (a) a sarcoma of muscle cell origin, (b) an epithelial cell carcinoma, and (c) an astrocytoma (glial cell tumor)?
Can restoring tumor suppressor function, such as mutant p53 or pRb, be used to cure cancer? If that's the case, how is it possible?
What would be the effect of a mutation that inactivates the p14ARF tumor suppressor upon p53 functions?
Cancer is caused by many different types of gene mutations. Some mutations are in proto-oncogenes, which lead to overexpression of the genes, and other mutations are in tumor suppressor genes, which lead to under expression or no expression in these genes. Which kinds of gene mutations would RNA interference (RNAi) be better at treating? Explain.
p53 is a tumor suppressor gene in human cells. Transcription of this gene leads to the production of the p53 protein in cells which modulates many signal pathways that lead to anti-tumor effects. The strength of anti-tumor effects is directly porportional to the accumulation of the protein within the cells of the person. Suppose a pediatric patient was recently admitted for a rare lung cancer related to p53 deficiencies (although the p53 itself is not mutated). Armed with your knowledge about the different mechanisms which govern transcription and translation, what are some potential reasons for the deficiency in p53 levels and how can you restore them if the reason you assumed for the deficiency is not directly reparable (i.e if you assume that protein degradation is too fast, you cannot directly repair protein degradation but you may want to increase transcription & translation rates to compensate)? Will your hypothesized repair(s) cause negative impacts to the cell? Why?
For many years, targeted therapies for cancer treatment continue to be developed, however more and more patients are developing resistance to targeted therapies. Discuss one mechanism of resistance to targeted therapies for cancer and provide an example of how might creatively combat it using clinical concepts.
The normal function of one tumor-suppressor gene acting at the G1 checkpoint is to prevent cells with damaged chromosomes and DNA from “progressing from G1 to S.” Another tumor-suppressor gene, acting at the G2/M checkpoint, prevents “passage from G2 to M.” When these tumor-suppressor genes fail to work, cancer can result. Explain what the phrases in quotations mean.
Studies suggest that the presence of oncogenic Ras is not sufficient to drive tumorigenesis. Instead, the activity of Ras needs to be amplified and sustained to induce pathological consequences. Recent studies have suggested a role for inflammatory stimuli on tumor development in the context of oncogenic Ras. Is the presence of oncogenic Ras necessary for transient inflammatory stimulation to induce chronic pathologies (such as cancer) OR is chronic inflammation essential for oncogenic Ras to induce tumorigenesis?
What is the most likely outcome is we lose the tumor suppressor proteins, cyclin- dependent kinase inhibitors. Select one: o a. Cyclin-cylin dependent kinases will phosphorylate retinoblastoma protein and cell- cycle will not proceed. o b. Cyclin-cylin dependent kinase complex will not phosphorylate retinoblastoma protein and cell-cycle will not proceed. o c. Cyclin-cylin dependent kinase complex will not phosphorylate retinoblastoma protein and cell-cycle will proceed. o d. Cyclin-cylin dependent kinases will phosphorylate retinoblastoma protein and cell- cycle will proceed.
Cancer is driven by alterations in the expression of critical genes, namely tumour suppressors, which play a growth-regulatory role, and proto-oncogenes, which promote the growth and survival of the cell. For both classes of cancer-related gene, suggest a likely mechanism of alteration and sketch the consequence for the gene and protein. Tumour suppressor gene (i.e. TP53, PTEN or APC) Oncogene (i.e. RAS, MYC)
Which of the following steps are correct about multistep tumorigenesis (select all that apply)? A. Mutations in progenitor cells are more likely to develop a neoplastic state compared to mutations in stem cells B. Driver mutations give a cell clone a proliferative advanage C. The rate of mutation /genetic change is constant during tumor progression D. Nutrition/diet may effect rate of tumorigenesis E. All cells within a tumor are biologically equivalent and equally capable of high levels proliferation

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