Concepts of Genetics (12th Edition)
12th Edition
ISBN: 9780134604718
Author: William S. Klug, Michael R. Cummings, Charlotte A. Spencer, Michael A. Palladino, Darrell Killian
Publisher: PEARSON
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Chapter 22, Problem 17PDQ
In 2013 the actress Angelina Jolie elected to have prophylactic double-mastectomy surgery to prevent breast cancer based on a positive test for mutation of the BRCA1 gene. What are some potential positive and negative consequences of this high-profile example of acting on the results of a genetic test?
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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?
The diosgenin drug (DSG) has been tested on human cholangiocarcinoma cells (bile duct cancer cells). To this aim, the human cholangiocarcinoma cell lines HuCCT1, QBC939, SK-ChA-1, HuH28, RBE, and Mz-ChA-1 have been subjected to different conditions of treatment with DSG, then assessed for their viability using a MTS assay, and their cell cycle progression using flow cytometry (FCM).Note: The MTS assay is based on the reduction of the MTS tetrazolium compound by viable cells to generate a colored formazan dye that is soluble in cell culture media. This conversion is thoughtto be carried out by NAD(P)H-dependent dehydrogenase enzymes in metabolically active cells.The formazan dye is quantified by measuring its absorbance at 490-500 nm.
Question : To which kind of biological molecule does this DSG drug resemble? To which kind of properties do you expect for DSG?
Which of the examples of genetic testing below are prognostic tests? Which are diagnostic? (a) Individual sequencing (personal genomics) identifies a mutation associated with Alzheimer’s disease. (b) ASO testing determines that an individual is a carrier for the mutant b@globin allele (bS) found in sickle-cell anemia. (c) DNA sequencing of a breast tumor reveals mutations in the BRCA1 gene. (d) Genetic testing in a healthy teenager identifies an SNP correlated with autism. (e) An adult diagnosed with Asperger syndrome (AS) has a genetic test that reveals a SNP in the GABRB3 gene that is significantly more common in people with AS than the general population.
Chapter 22 Solutions
Concepts of Genetics (12th Edition)
Ch. 22 - In order to vaccinate people against diseases by...Ch. 22 - Prob. 2NSTCh. 22 - Prob. 1CSCh. 22 - Prob. 2CSCh. 22 - Prob. 3CSCh. 22 - HOW DO WE KNOW? In this chapter, we focused on a...Ch. 22 - Prob. 2PDQCh. 22 - Why are most recombinant human proteins produced...Ch. 22 - One of the major causes of sickness, death, and...Ch. 22 - Sequencing the human genome, the development of...
Ch. 22 - Prob. 6PDQCh. 22 - As genetic testing becomes widespread, medical...Ch. 22 - Prob. 8PDQCh. 22 - Prob. 9PDQCh. 22 - Does genetic analysis by ASO testing allow for...Ch. 22 - Maternal blood tests for three pregnant women...Ch. 22 - What is the main purpose of genome-wide...Ch. 22 - Describe how the team from the J. Craig Venter...Ch. 22 - Prob. 14PDQCh. 22 - Prob. 15PDQCh. 22 - Dominant mutations can be categorized according to...Ch. 22 - In 2013 the actress Angelina Jolie elected to have...Ch. 22 - Prob. 18PDQCh. 22 - Should the FDA regulate direct-to-consumer genetic...Ch. 22 - Prob. 20ESPCh. 22 - Following the tragic shooting of 20 children at a...Ch. 22 - Private companies are offering personal DNA...Ch. 22 - Prob. 23ESPCh. 22 - Prob. 24ESPCh. 22 - Prob. 25ESPCh. 22 - Craig Venter and others have constructed synthetic...
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- The p53 protein was discovered through its association with SV40 T antigen and assumed initially to be an oncoprotein. a. What is the current consensus as the function of p53 and what evidence caused this change in view? b. How does the effect of mutation in the p53 gene differ from the effect of mutation in the RB gene what is the molecular basis for this difference ?arrow_forwardDraw the Western Blot that would result from undertaking the same experiment in the presence of: i) An estrogen receptor agonist ii) An estrogen receptor antagonist iii) An estrogen receptor agonist in the presence of an excess amount of antagonist iv) Estrogen in the presence of an excess amount of antagonist v) An estrogen receptor inverse agonist.arrow_forwardThe 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?arrow_forward
- What percentage of cells in an organ or a tissue need toexpress a therapeutic gene to alleviate the effects of agenetic disorder?arrow_forwardA 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 cancerarrow_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
- 1) Create a graph as a better way to display the data in the table 2) Determine which mutations (5q, 18q, 17p, Ras) caused the progression to each stage of tumorigenesis.arrow_forwardThe MET oncogene is a growth factor receptor that is altered in many forms of cancer including lung and colon carcinomas as well as several forms of melanoma. One assay for characterizing the gene composition of tumor cells is Fluorescence in situ Hybridization (FISH) in which a fluorescently labeled DNA is used to show the presence of and level (i.e. number copies) of a gene inside cells. The experiment below is a FISH assay of two different tumor samples (Patient D and Patient E) using a MET gene probe labeled with a green fluorescent probe. The figure on the right presents the survival data from diagnosis of cancer patients with FISH data similar to Patient D or E. Based on this data, what has happened to the MET gene in Patient D population that has made their cancer more severe and reduced survival time (Limit 4-5 sentences). D Survival rate (%) 100 0 0 100 200 Time (days) 300 Earrow_forwardAlthough slow acting retroviruses lack oncogenes, retroviral infection can activate proto oncogenes leading to oncogenesis. a. Describe the mechanism of proto-oncogenes activation that can result from with infection with slow acting retroviruses. b. In what other ways can proto-oncogenes be converted to oncogenes?arrow_forward
- Genetic tests that detect mutations in the BRCA1 and BRCA2 tumor-suppressor genes 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?arrow_forwardIn the gene therapy trials for SCIDS, what DNA was added to the patients’ cells? Could this same procedure be used to treat a dominant disease – why or why not? What are some other options?arrow_forward1) What are the limitations of targeted versus whole-genome or whole-exome profiling of cancer mutations? 2) What can you infer about mutations that are common to almost all of the cells in a tumor? 3) Summarize the high-level differences between the VCF and MAF file formats. 4) How do germline and somatic mutations differ in terms of their effect on cancer risk and prognosis?arrow_forward
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