Genetics: Analysis and Principles
6th Edition
ISBN: 9781259616020
Author: Robert J. Brooker Professor Dr.
Publisher: McGraw-Hill Education
expand_more
expand_more
format_list_bulleted
Videos
Question
Chapter 25, Problem 23CONQ
Summary Introduction
To review:
Whether the alleles involved in genetic predisposition to cancer development are dominant or not. Also, show that the individuals who carry the dominant alleles do not get cancer during their lifetime.
Introduction:
Cancer is caused due to the mutations which occur in the genetic material of the cells. The mutated genes can be inherited or formed during the lifetime of the individuals. There is an increase in the chance of having cancer by the offspring if the parents are having oncogenic genes.
Expert Solution & Answer
Want to see the full answer?
Check out a sample textbook solution
Students have asked these similar questions
Describe two mechanisms by which genetic change causes cancer.
Describe the steps by which the TP53 gene responds to DNA damage and/or cellular stress to promote cell-cycle arrest and apoptosis. Given that TP53 is a recessive gene and is not located on the X chromosome, why would people who inherit just one mutant copy of a recessive tumor-suppressor gene be at higher risk of developing cancer than those without the recessive gene?
In 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.
Chapter 25 Solutions
Genetics: Analysis and Principles
Ch. 25.1 - Which of the following wouldnotbe consistent with...Ch. 25.1 - 2. Assuming complete penetrance, which type of...Ch. 25.1 - 3. Which of the following is not a common...Ch. 25.1 - Prob. 4COMQCh. 25.2 - Prob. 1COMQCh. 25.2 - Haplotype association studies are aimed at the...Ch. 25.3 - 1. Which of the following is not a method used in...Ch. 25.3 - 2. Which of the following prenatal genetic testing...Ch. 25.4 - Prob. 1COMQCh. 25.5 - 1. An oncogene is produced from a ________that has...
Ch. 25.5 - Which of the following is a type of genetic change...Ch. 25.5 - 3. Tumor-suppressor genes promote cancer...Ch. 25.5 - 4. Normal (nonmutant) tumor-suppressor genes often...Ch. 25.5 - Prob. 5COMQCh. 25.6 - Prob. 1COMQCh. 25 - 1. With regard to pedigree analysis, make a list...Ch. 25 - 2. Explain, at the molecular level, why human...Ch. 25 - 3. Many genetic disorders exhibit locus...Ch. 25 - Prob. 4CONQCh. 25 - Prob. 5CONQCh. 25 - Figure 25.1 illustrates albinism in two different...Ch. 25 - Prob. 7CONQCh. 25 - Prob. 8CONQCh. 25 - Ehler-Danlos syndrome is a rare disorder caused by...Ch. 25 - 10. Hurler syndrome is due to a mutation in a gene...Ch. 25 - Like Hurler syndrome, Fabry disease involves an...Ch. 25 - Achondroplasia is a rare form of dwarfism caused...Ch. 25 - Prob. 13CONQCh. 25 - 14. Marfan syndrome is due to a mutation in a...Ch. 25 - 15. Sandhoff disease is due to a mutation in a...Ch. 25 - Describe the two assumptions that underlie the...Ch. 25 - Prob. 17CONQCh. 25 - What is a prion? Explain how a prion relies on...Ch. 25 - 19. Some people have a genetic predisposition for...Ch. 25 - What is the difference between an oncogene and a...Ch. 25 - Prob. 21CONQCh. 25 - Prob. 22CONQCh. 25 - Prob. 23CONQCh. 25 - Prob. 24CONQCh. 25 - Prob. 25CONQCh. 25 - Prob. 26CONQCh. 25 - Prob. 27CONQCh. 25 - With regard to cancer cells, which of the...Ch. 25 - Prob. 29CONQCh. 25 - 1. Which of the following experimental...Ch. 25 - Prob. 2EQCh. 25 - 3. What is meant by the term genetic testing? How...Ch. 25 - Prob. 4EQCh. 25 - 5. Chapter 21 describes a method known as Western...Ch. 25 - 6. An experimental assay for the blood-clotting...Ch. 25 - 7. Discuss ways to distinguish whether a...Ch. 25 - 8. The codon change (Gly-12 to Val-12) in...Ch. 25 - Explain how DNA microarrays are used in molecular...Ch. 25 - Make a list of the benefits that may arise from...Ch. 25 - 2. Our government has finite funds to devote to...Ch. 25 - Prob. 3QSDC
Knowledge Booster
Learn more about
Need a deep-dive on the concept behind this application? Look no further. Learn more about this topic, biology and related others by exploring similar questions and additional content below.Similar questions
- Name 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_forwardWhat is the difference between saying that cancer is inherited and saying that the predisposition to cancer is inherited?arrow_forwardCancer is a major public health problem. Both inherited genes and environmental factors play a role in the development of cancer. Associations have also been documented between environmental pollutants and cancer. In general, cancers caused by occupational or environmental exposures are pathologically and clinically indistinguishable from other cancers. However, some cancers have a very high probability of being occupationally related, such as angiosarcoma of the liver due to vinyl chloride exposure, and mesothelioma from asbestos fiber exposure. Documentation of exposures that cause cancer relies heavily on epidemiological studies. Unfortunately, there are complicating factors, such as the long latency period before the cancers are actually diagnosed, well after many other workers had already been exposed. Therefore, what must the prevention of occupational and environmental cancers rely upon to predict effects on humans and establish limits for human exposure?arrow_forward
- Which of the following effectively describes the situation of someone with an inherited predisposition to cancer such as familial adenomatous polyposis or BRCA-associated familial breast cancer? Choose all that apply a) If they get malignant cancer, somatic mutations will not have been a factor b) Their cancer will most likely arise in their germ cells, not their somatic cells c) None of the answers effectively describes the situation d) Every cell of their body contains a gain-of-function allele of an oncogene e) Most cells in their body contain multiple cancer-causing mutations f) Every cell of their body contains a defective, loss-of-function allele of a tumor suppressor genearrow_forwardExplain how mutations in tumor-suppressor genes can be recessive at the level of the cell but cause dominantly inherited predispositions to cancer.arrow_forwardAcquired mutation in the p53 gene is the most common genetic alteration found in human cancer (> 50% of all cancers). A germline mutation in p53 is the causative lesion of Li- Fraumeni familial cancer syndrome. In many tumors, one p53 allele on chromosome 17p is deleted and the other is mutated. What type of protein is encoded by the p53 gene? (A) Caspase (B) DNA repair enzyme (C) Membrane cell adhesion molecule (D) Serine phosphatase (E) Telomerase (F) Transcription factor (G) Tyrosine kinasearrow_forward
- Distinguish between proto-oncogenes and tumor-suppressor genes. To become cancer promoting, do proto-oncogenes and tumor-suppressor genes undergo gain-of-function or loss-of-function mutations? Classify the following genes as proto-oncogenes or tumor-suppressor genes: p53, ras, BCL-2, JUN, MDM2, and p16.arrow_forwardRelatively few inherited forms of cancer involve the inheritance of mutant oncogenes. Instead, most inherited forms of cancer are defects in tumor-suppressor genes. Give two or more reasons why inherited forms of cancer seldom involve activated oncogenes.arrow_forwardD) The level of carbon dioxide increases with the level of available oxygen. 60) The TP53 gene provides instructions for making a protein called tumor protein p53. Known as the guardian of the genome, this protein acts as a tumor suppressor, which means that it regulates cell division by keeping cells from growing and dividing too fast or in an uncontrolled way. The p53 protein is located in the nucleus of cells throughout the body, where it attaches directly to DNA and plays a critical role in determining whether the DNA will be repaired or the damaged cell will self- destruct (undergo apoptosis). If the DNA can be repaired, p53 activates other genes to fix the damage. If the DNA cannot be repaired, this protein prevents the cell from dividing and signals it to undergo apoptosis. eg Suppose chromosomes in a skin cell are damaged by ultraviolet radiation. If the damaged genes do not affect p53, which choice correctly predict if the cell will become cancerous and why? No, the cell will…arrow_forward
- Describe the underlying causes of epigenetic changes associated with cancer.arrow_forwardBased on the figure below: If children with hereditary retinoblastoma often survive until adulthood and produce children, what is their risk of developing other types of tumors later in life? What is a risk for their children of developing retinoblastoma? Is there the tendency to develop retinoblastoma inherited as a dominant trait or as a recessive trait? Is there one mutant copy sufficient to predispose a person to develop the cancer or two copies are needed to develop retinoblastoma as a cancer?arrow_forwardIn 2010, the U.S. Department of Health and Human Services added alcoholic beverages to its list of known human carcinogens. Explain what types of cancer alcohol is related to; what steps should be taken to reduce the risk of developing alcohol-induced cancer; and what other factors, when combined with alcohol, increase the risk of developing cancer.arrow_forward
arrow_back_ios
SEE MORE QUESTIONS
arrow_forward_ios
Recommended textbooks for you
Human Anatomy & Physiology (11th Edition)BiologyISBN:9780134580999Author:Elaine N. Marieb, Katja N. HoehnPublisher:PEARSON
Biology 2eBiologyISBN:9781947172517Author:Matthew Douglas, Jung Choi, Mary Ann ClarkPublisher:OpenStax
Anatomy & PhysiologyBiologyISBN:9781259398629Author:McKinley, Michael P., O'loughlin, Valerie Dean, Bidle, Theresa StouterPublisher:Mcgraw Hill Education,
Molecular Biology of the Cell (Sixth Edition)BiologyISBN:9780815344322Author:Bruce Alberts, Alexander D. Johnson, Julian Lewis, David Morgan, Martin Raff, Keith Roberts, Peter WalterPublisher:W. W. Norton & Company
Laboratory Manual For Human Anatomy & PhysiologyBiologyISBN:9781260159363Author:Martin, Terry R., Prentice-craver, CynthiaPublisher:McGraw-Hill Publishing Co.
Inquiry Into Life (16th Edition)BiologyISBN:9781260231700Author:Sylvia S. Mader, Michael WindelspechtPublisher:McGraw Hill Education
Human Anatomy & Physiology (11th Edition)
Biology
ISBN:9780134580999
Author:Elaine N. Marieb, Katja N. Hoehn
Publisher:PEARSON
Biology 2e
Biology
ISBN:9781947172517
Author:Matthew Douglas, Jung Choi, Mary Ann Clark
Publisher:OpenStax
Anatomy & Physiology
Biology
ISBN:9781259398629
Author:McKinley, Michael P., O'loughlin, Valerie Dean, Bidle, Theresa Stouter
Publisher:Mcgraw Hill Education,
Molecular Biology of the Cell (Sixth Edition)
Biology
ISBN:9780815344322
Author:Bruce Alberts, Alexander D. Johnson, Julian Lewis, David Morgan, Martin Raff, Keith Roberts, Peter Walter
Publisher:W. W. Norton & Company
Laboratory Manual For Human Anatomy & Physiology
Biology
ISBN:9781260159363
Author:Martin, Terry R., Prentice-craver, Cynthia
Publisher:McGraw-Hill Publishing Co.
Inquiry Into Life (16th Edition)
Biology
ISBN:9781260231700
Author:Sylvia S. Mader, Michael Windelspecht
Publisher:McGraw Hill Education
What are Mutations and what are the different types of Mutations?; Author: Science ABC;https://www.youtube.com/watch?v=I16YlE8qTBU;License: Standard youtube license