Mutations in the BRCA genes have been shown to be related to a higher incidence of breast cancer in humans, and genetic tests are available that enable women to discover whether they carry versions of the gene associated with high risk. However, even early detection of breast cancer does not guarantee a cure. What considerations can you think of for and against advising women to take the tests? ·
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- Distinguish between What is known of CD105 (endoglin) as an hepatcellular carcinoma marker and it’s potential as a drug target. Discuss: - Is anything known about its biology? E.g does it have known ligands and normal functions? - if you were to target it would you just use it to get growth inhibiting compound into the new blood vessels or is CD105 required for neovascularization?The decision by some high-risk women to have their breasts removed to prevent the possibility of developing cancer could be a truly life-altering decision. At first glance, this decision could make sense for those women who are at elevated risk due to genetic or family history factors. Counter that with living in a society that seems to be moving toward even greater obsession with female breasts at earlier ages (e.g., breast implants for 16th birthdays!) Learn more about oncogenes and breast cancer.: What are the benefits of learning you have a gene that may lead to cancer? What are the disadvantages of receiving such knowledge?Skin cancer carries a lifetime risk nearly equal to that of allother cancers combined. Following is a graph [modified fromK. H. Kraemer (1997). Proc. Natl. Acad. Sci. (USA) 94:11–14]depicting the age of onset of skin cancers in patients with orwithout XP, where the cumulative percentage of skin cancer is plotted against age. The non-XP curve is based on 29,757 cancerssurveyed by the National Cancer Institute, and the curverepresenting those with XP is based on 63 skin cancers from theXeroderma Pigmentosum Registry.
- Genetic tests that detect mutations in the BRCA1 and BRCA2 oncogenes are widely available. These tests reveal a number of mutations in these genes—mutations that have been linked to familial breast cancer. Assume that a young woman in a suspected breast cancer family takes the BRCA1 and BRCA2 genetic tests and receives negative results. That is, she does not test positive for the mutant alleles of BRCA1 or BRCA2. Can she consider herself free of risk for breast cancer?Identify two genetic mechanisms whereby proto-oncogenes can become overexpressed. Select the two mechanisms. Identify two genetic mechanisms whereby proto-oncogenes can become overexpressed.Select the two mechanisms. 1) alterations in chromatin structure 2) a gain-of-function alteration 3)modification of proto-oncogenes products 4)mutations that result in an abnormal protein product 5)mutations within gene-regulatory regionsIn Metastatic Breast Cancer [such as in Breast Invasive Ductal Carcinoma; Breast Invasive Carcinoma, NOS; Breast Invasive Cancer, NOS; Invasive Breast Carcinoma; Breast Invasive Lobular Carcinoma; Breast Mixed Ductal and Lobular Carcinoma] what role does the genes Tp53 and Tp63 have? Would one of them affect the other (i.e. mutation, etc) or there is not relationship among the two genes at all.
- 5) Briefly explain why the formation of a tumour can pose a risk to a person's homeostasis. 6) The functioning of the "Ras/MAPK" signal transduction pathway is absolutely essential in order for cells to grow, divide, and migrate. One important protein that is part of this pathway is BRAF. This protein is a kind of enzyme called a "kinase" – an enzyme that transfers a phosphate group onto another protein. In some melanomas, a mutated form of BRAF called BRAF Val600AGlu drives the progression of the cancer. The drug "vemurafenib" slows the progression of the cancer by slowing the production of the mutant BRAF protein. (National Cancer Institute. 2019. Types of Cancer Treatment. Retrieved from: https://www.cancer.gov/about-cancer/treatment/types/ Is this an example of a traditional cancer therapy or a targeted therapy? Briefly explain your reasoning in the space provided, using information provided in the text to support your answer. Type of therapy (traditional or targeted)?: Brief…Plasma PDGF levels can be a diagnostic marker for severity and progression of breast cancer. The assay data below shows the plasma levels of PDGF in normal individuals, Stage II and Stage IV (More severe). You are treating a patient with breast cancer and assay indicates that their plasma PDGF level 6 fmoles/ 100 uL.Based on this info, in which stages has this patient's cancer progressed? Explain what process this patient's tumor has likely undergone and which cell types you would expect to now be associated with this tumor.Our government has finite funds to devote to cancer research.Discuss which of the following areas of research you think shouldreceive the most funding.A. Identifying and characterizing oncogenes and tumorsuppressorgenesB. Identifying agents in our environment that cause cancerC. Identifying viruses that cause cancer D. Devising methods aimed at killing cancer cells in the bodyE. Informing the public of the risks involved in exposure tocarcinogensIn the long run, in which of these areas would you expect successfulresearch to be the most effective in decreasing human mortalitydue to cancer?
- Link: Lack of RAC1 in macrophages protects against atherosclerosis - PMC (nih.gov) Could somone explain exactly what this means below? NOT HW just trying to get a better understanding on what this experiment is about. To produce mice that are deficient for RAC1 in macrophages, female C57BL/6 mice homozygously expressing the floxed Rac1 gene (Rac1fl/fl) [6] were crossbred with male mice homozygously expressing Cre under the monocyte-specific lysozyme M promoter (LC) [12]. Mice were genotyped for Rac1 deficiency as previously describedTumor suppressor genes and oncogenes are implicated in carcinogenesis. However, one can predict whether a gene potentially encodes for a protein that influences carcinogenesis by examining their mutational profile. You sequence the genome of 4 cancers and identify 3 genes of interest. Which of the following genes has the best potential to an oncogene? Tumor 1 Tumor 2 Tumor 3 Tumor 4 Gene A S24F, N465T R33T T345S, G366R P367E, P368Y Gene B S34R, F360I S34R V254I S34E, T67Y Gene C S24F, I322E C255I, E344D S34E, P367EA patient comes into your clinic exhibiting generic cancer symptoms. In order to help form a diagnosis, you ask about patient history and they tell you that they worked for years in an agricultural job, primarily in handling food for large bovine animals and then later working with insect pesticide treatment of grain fields. You decide to test for elevated levels of the environmental agent(s) in their body and focus your cancer diagnosis on based on the established associations of epigentic effects and cancer. O nickel and cadmium; stomach and skin cancer O benzene; breast, prostate and thyroid cancer O polycyclic aromatic hydrocarbons and benzene; lung, breast, stomach and skin cancer O arsenic and endocrine disruptors; skin, bladder, liver and kidney cancer