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a.
To determine:
Whether the gene that codes for EGFR is a tumor-suppressor gene or a proto-oncogene.
Introduction:
Tumor-Suppressor genes are normal genes that are responsible for inhibiting cell proliferation. A proto-oncogene is a normal gene that has the potential to convert in an oncogene due to any mutation.
b.
To determine:
Whether a patient with a GBM expressing EGFRvIII should be treated with a higher or lower dose of X-rays than with patients having GBMs with normal EGFR proteins.
Introduction:
It is given that the cells that express EGFRvIII are difficult to induce to undergo programmed cell death. There are other methods used to kill the cells containing this mutant protein like radiology, chemotherapy, and so on.
c.
To determine:
The method by which the mutant EGFR protein might be responsible for causing cancer.
Introduction:
It is given that EGFR is a transmembrane protein. The N-terminal of this protein has an extracellular part that binds epidermal growth factor and the C-terminal kinase part that is normally activated when EGF binds to EGFR.
d.
To determine:
Whether the drug blocking the kinase activity of EGFR would be a potential treatment for GBMs expressing EGFRvIII or it would make the tumors grow faster.
Introduction:
It is given that IressaTM is a drug that blocks the kinase activity of EGFR. The kinase is an enzyme that phosphorylates other proteins.
e.
To determine:
Whether patients with high amounts of ERCC1 mRNAs should be treated with higher or lower doses of cisplatin than patients with normal amounts of ERCC1 mRNAs.
Introduction:
It is given that cisplatin is a platinum compound that is associated with DNA damage and causes cell death. The ERCC1 gene codes for a DNA repair protein.
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Chapter 19 Solutions
Genetics: From Genes to Genomes, 5th edition
- A region on chromosome 6 has been linked to schizophrenia, but researchers have not found a specific gene associated with this disease. What steps would be necessary to locate the gene?arrow_forwardAlthough it is well known that X-rays cause mutations, they are routinely used to diagnose medical problems, including potential tumors, broken bones, and dental cavities. Why is this done? What precautions need to be taken?arrow_forwardWhat is the definition of Driver Mutations & Passenger Mutations? Also describe why each are informative in characterizing tumors.arrow_forward
- To further understand PSEN2 mutations the age of onset of Alzheimer's Disease and AB 42/40 ration is investigated for different mutations in PSEN2. Table 3 - Age at onset of FAD and measured Aß 42/40 ratios for each patient. PSEN2 Mutation Age at onset (Years) AB 42/40 ratio PSEN2 WT Select one: True False N/A 1 1229F M223L F237P M233V F237L N410Y 33 7.3+ 0.7 46 35 3.81 32 4.5 0.2 0.4 14.7 52 31 2.2 ± 1.2 1.8 20.76 + Question 18) Very early onset PSEN2 mutations have a more severe impact on the AB 42/40 ratios than mutations that cause onset at a later age?arrow_forwardDefine a Point mutation and give an example. What is sickle cell anemia and what causes it. What is nondisjunction? How does nondisjunction cause disorders? NUMER YOUR ANSWERSarrow_forwardGene mutations can be classified in two major ways:(1) hereditary or germline mutations that are inherited from a parent and are present throughout a person’s life in virtually every cell in the body.(2) acquired or somatic mutations that occur at some time during a person’s life and are present only in certain cells, not in every cell in the body.If there is no family history of a particular disease but a child has the disease then it may have arisen due to a(n) ________ mutation early during development. A) acquired B) inherited C) silent D) transitionarrow_forward
- The C-myc gene is a proto-oncogene which is highly expressed in breast tissue and appears to cause proliferation of breast tissue and its elevated expression is associated with breast cancer. Based just on the ChIP data from the previous questions (also shown below), which of the three drugs (estrogen, tamoxifen and raloxifene) would you recommend for treating breast cancer? Justify your response and explain the potential side effects of each drug.arrow_forwardName two ways in which loss of p53 function contributes to a malignant phenotype. Explain how benzo(a) pyrene can cause loss of p53 function. Hint: Loss of p53 function occurs in the majority of human tumors.arrow_forwardNeurofibromatosis type 1 (NF1) is an inherited is an inheritent dominant disorder. The phenotype usually involves the production of many skin neurofibromas. Answer the following questions about the disorder: a) Are the NF1 neurofibromatosis-causing mutations that are inherited by affected children from affected parents likely to be loss-of-function or gain-of-function mutations? b) Neurofibromin, the protein product of NF1, is associated with the Ras protein. Ras is involved in the transduction of extracellular signals from growth factors. The active form of Ras is complexed with GTP; the inactive form is complexed with GDP. Would the wild-type neurofibromin protein favor the formation of Ras-GTP or Ras-GDP? c) Which of the following events in a normal cell from an individual inheriting a neurofibromatosis-causing allele could cause the descendents of that cell to turn into a neurofibroma? i. A second point mutation in…arrow_forward
- Which of the following statements are true about the rate of mutation in tumor cells (select all that apply)? A. Mutation rate of tumor cells is reduced compared to normal cells of the same tissue type B. Mutation rate of tumor cells is unchanged compared to normal cells of the same tissue type C. Mutation rate in tumor cells is higher compared to normal cells of the same tissue type D. Affected by genome instability within the tumor cellsarrow_forwardIn 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.arrow_forwardWhile a stem cell transplant from an unaffected donor is currently the only cure for DBA, genome-editing technologies may one day enable the correction of a mutation in a patient’s own bone marrow stem cells. However, what specific information would be needed, beyond a symptom-based diagnosis of DBA, in order to accomplish this?arrow_forward
- Human Heredity: Principles and Issues (MindTap Co...BiologyISBN:9781305251052Author:Michael CummingsPublisher:Cengage Learning
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