Human Heredity: Principles and Issues (MindTap Course List)
11th Edition
ISBN: 9781305251052
Author: Michael Cummings
Publisher: Cengage Learning
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Chapter 12, Problem 18QP
You are in charge of a new gene therapy clinic. Two cases have been referred to you for review and possible therapy.
Case 1. A mutation in the promoter of a proto-oncogene causes the gene to make too much of its normal product, a receptor protein that promotes cell division. The uncontrolled cell division has caused cancer.
Case 2. A mutation in an exon of a tumor-suppressor gene makes this gene nonfunctional. The product of this gene normally suppresses cell division. The mutant gene cannot suppress cell division, and this has led to cancer. What treatment options can you suggest for each case?
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Question 5
Select the correct statements
0
An oncogene is a cancer producing gene
A proto-oncogene is only found in cancer cells
Tumor suppressor genes are genes whose normal products inhibit cell division
A proto-oncogene is a normal cellular gene that has the potential to become an oncogene
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You are evaluating a patient with Nonpolyposis colorectal cancer and his biopsy pathology report reveals a defect in some TSGs involved in DNA mismatch repair, which of these genes is least likely to be implicated in this patients cancer?
Group of answer choices
SMAD4
MSH2
MLH1
PMS1
Can you match the type of mutations that can occur from the selected below?
a. either proto-oncogene or tumor suppressor gene
b. proto-oncogene
c. tumor suppressor gen
1. Frameshift mutation
2. Missense mutation
3. Nonsense mutation
Chapter 12 Solutions
Human Heredity: Principles and Issues (MindTap Course List)
Ch. 12.10 - If improved diagnostic tests are developed from...Ch. 12.10 - If you had cancer, would you donate tissue samples...Ch. 12.10 - Prob. 1GRCh. 12.10 - Another model, the random model, proposes that any...Ch. 12 - Mike was referred for genetic counseling because...Ch. 12 - Mike was referred for genetic counseling because...Ch. 12 - Mike was referred for genetic counseling because...Ch. 12 - Theodor Boveri predicted that malignancies would...Ch. 12 - Distinguish between a familial and a sporadic...Ch. 12 - Benign tumors: a. are noncancerous growths that do...
Ch. 12 - Prob. 4QPCh. 12 - Prob. 5QPCh. 12 - Prob. 6QPCh. 12 - Prob. 7QPCh. 12 - Prob. 8QPCh. 12 - What is the difference between a proto-oncogene...Ch. 12 - Distinguish between dominant inheritance and...Ch. 12 - Describe the likelihood of developing bilateral...Ch. 12 - Prob. 12QPCh. 12 - The search for the BRCA1 breast cancer gene...Ch. 12 - What are the roles of cellular proto-oncogenes,...Ch. 12 - Which of the following mutations will result in...Ch. 12 - Prob. 16QPCh. 12 - The following family has a history of inherited...Ch. 12 - You are in charge of a new gene therapy clinic....Ch. 12 - Prob. 19QPCh. 12 - Can you postulate a reason or reasons why children...Ch. 12 - Prob. 21QPCh. 12 - In Section 12-1, Julie is concerned that she may...Ch. 12 - Prob. 23QPCh. 12 - What are some factors that epidemiologists have...Ch. 12 - Smoking cigarettes has been shown to be associated...Ch. 12 - Prob. 26QPCh. 12 - Studies have shown that there are significant...
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- are changes to the order of nucleotides in a segment of DNA that codes for a protein. Proto-oncogenes Tumor suppressor genes Gene mutations Negative regulatorsarrow_forwardWhich of the following statements about cancer is false? (a) oncogenes arise from mutations in proto-oncogenes (b) tumor suppressor genes normally interact with growth-inhibiting factors to block cell division (c) more than 120 cancer-driving genes have been discovered (d) oncogenes were first discovered in mouse models for cancer (e) the development of cancer is usually a multistep process involving both oncogenes and mutated tumor suppressor genesarrow_forwardMatch the gene name with the gene description. rb BRCA-1 tumor suppressor А. p53 B. proto-oncogene В. Ras EGF Receptorarrow_forward
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- The diagram shows the relative activity of a proto-oncogene and a tumor supressor gene in a normal cell, as well as the activity in four other cells. Normal cell A в D tumor suppressor gene proto-oncogene Which of these cells would be expected to be cancer cells? cell B cell D cell C cell Aarrow_forwardThe chapter points out that about one of every five women and one of every four men in the United States will die from cancer. Why arerates of death from cancer different in men and women? Provide some possible explanations. 3. A couple has one child with bilateral retinoblastoma. The mother is free from cancer, but the father has unilateral retinoblastoma and he has a brother who has bilateral retinoblastoma. a. If the couple has another child, what is the probability that this next child will have retinoblastoma? b. If the next child has retinoblastoma, is it likely to be bilateral or unilateral? c. Explain why the father’s case of retinoblastoma is unilateral, whereas his son’s and brother’s cases are bilateralarrow_forwardDiscussion: (1 or 2 paragraphs with your own opinion like how Circulating Tumor DNA as Biomarkers for Cancer Detection technology can be early detector of cancer)arrow_forward
- Looking at this statement, develop an argument and critically evaluate/discuss it, then discuss difficulties with PARP inhibitor therapy and developments/progression in the future, the statement is "New synthetic lethal strategies targeting DNA damage response in solid tumours have been developed as a result of the success of PARP inhibitor therapy in ovarian cancer.arrow_forwardWhy is it harder to develop a drug that targets a tumor suppressor gene compared to an oncogene (limit 3-4 sentences)?arrow_forwardTumor 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, P367Earrow_forward
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