Essentials of Genetics (9th Edition) - Standalone book
9th Edition
ISBN: 9780134047799
Author: William S. Klug, Michael R. Cummings, Charlotte A. Spencer, Michael A. Palladino
Publisher: PEARSON
expand_more
expand_more
format_list_bulleted
Question
Chapter 16, Problem 27PDQ
Summary Introduction
To review:
An experiment to determine the role of RB1 (retinoblastoma 1) mutation in osteosarcoma.
Introduction:
RB1 gene is a tumor suppressive gene that regulates cell division and cell proliferation. It codes RB protein that inhibits a transcription factor required for cell division and regulates uncontrolled cell growth. Mutation in one RB1 gene enhances risk of developing various cancers, while a mutation in both copies of the RB1 gene is required to develop cancer.
Expert Solution & Answer
Want to see the full answer?
Check out a sample textbook solutionStudents have asked these similar questions
Retinoblastoma is an extremely rare cancer of the retina in the eye. The disease mainly affects children up to the age of 5 years because it can only occur while the nerve precursor cells are still dividing. In its nonhereditary form, a tumor usually occurs in only one eye; in its hereditary form, multiple tumors develop in both eyes.To explore the basis for these differences, a cDNA clone of the Rb gene was used to probe the structure of the gene in cells from normal individuals and from individuals with nonhereditary or hereditary retinoblastoma. As shown in the figure Part A, normal individuals have four restriction fragments (A, B, C, and D) that hybridize to the Rb cDNA probe, indicating that each restriction fragment encodes at least one Rb exon. Samples from fibroblasts and tumor cells of affected persons show some differences in the patterns of hybridization, with some bands missing entirely and some bands present at half intensity. The order of the restriction fragments in the…
Several research studies are under way that involve the use of genetherapies to inhibit the growth of cancer cells. Oncogenes are mutant genes that are overexpressed and cause cancer. New gene therapies are aimed at silencing oncogenes by producing antisense RNA that recognizes the mRNAtranscribed from oncogenes. Based on your understanding of antisense RNA , explain how this strategy would prevent the growth of cancer cells.
A couple with a child affected with DBA undergoes in vitro fertilization (IVF) and genetic testing of the resulting embryos to ensure that the embryos will not have DBA. However, they also want the embryos screened to ensure that the one implanted can serve as a suitable donor for their existing child. Their plan is to have stem cells from the umbilical cord of the new baby transplanted to their existing child with DBA, thereby curing the condition. What are the ethical pros and cons of this situation?
Chapter 16 Solutions
Essentials of Genetics (9th Edition) - Standalone book
Ch. 16 -
CASE STUDY | I thought it was safe
A middle-aged...Ch. 16 -
CASE STUDY | I thought it was safe
A middle-aged...Ch. 16 -
CASE STUDY | I thought it was safe
A middle-aged...Ch. 16 - HOW DO WE KNOW? In this chapter, we focused on...Ch. 16 -
2. Review the Chapter Concepts list on page 307....Ch. 16 - What is the relationship between signal...Ch. 16 - Where are the major regulatory points in the cell...Ch. 16 -
5. Describe kinases and cyclins. How do they...Ch. 16 - (a) How does pRB function to keep cells at the G1...Ch. 16 - What is the difference between saying that cancer...
Ch. 16 -
8. What is apoptosis, and under what...Ch. 16 - Define tumor-suppressor genes. Why is a mutation...Ch. 16 - A genetic variant of the retinoblastoma protein,...Ch. 16 -
11. Part of the Ras protein is associated with...Ch. 16 - If a cell suffers damage to its DNA while in S...Ch. 16 - Prob. 13PDQCh. 16 - Prob. 14PDQCh. 16 - Prob. 15PDQCh. 16 - Prob. 16PDQCh. 16 - Prob. 17PDQCh. 16 - How do normal cells protect themselves from...Ch. 16 - Prob. 19PDQCh. 16 - Explain how environmental agents such as chemicals...Ch. 16 - Radiotherapy (treatment with ionizing radiation)...Ch. 16 - Genetic tests that detect mutations in the BRCA1...Ch. 16 - Prob. 23PDQCh. 16 - Prob. 24PDQCh. 16 - Prob. 25PDQCh. 16 - Prob. 26PDQCh. 16 - Prob. 27PDQCh. 16 - Prob. 28PDQ
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
- The p53 gene is a tumor-suppressor gene while Ras is a proto-oncogene. Mutation in either one can result in the transformation of a normal cell into a cancer cell. Explain the difference between the functions of the two proteins and how their mutation can lead to cancer development.arrow_forwardLoss of p53 function occurs in the majority of human tumors. 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.arrow_forwardResearchers have identified some tumors that have no recurrent mutations or deletions in known oncogenes or tumor-suppressor genes and no detectable epigenetic alterations. However, these tumors often have large chromosomal deletions. What are some possible explanations that could account for the genetic causes behind these tumors?arrow_forward
- Cellular levels of tumor suppressor protein p53 is maintained by a ubiquitin ligase protein, called Mdm2. Over expression of Mdm2 destabilizes p53. Another protein p19ARF inhibits the activity of Mdm2, thus stabilizing p53. Loss of p19ARF function converts normal cells into cancer cells With the above information, which of the following statements are true? Mdm2 is a tumor suppressor gene but p19ARF is an oncogene Both Mdm2 & P19ARF are oncogenes Both Mdm2 & P19ARF are tumor suppressor genes O Mdm2 is an oncogene but p19ARF is a tumor suppressor genearrow_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_forwardOn the image, you can see the results of a DNA microarray used for cancer prognosis, where tissue samples from healthy and cancerous tissues were analyzed. cDNA from healthy cells and cancer cells were labeled with green and red fluorescence, respectively, mixed equally, and hybridized with the chip. It is known that gene A is more highly expressed in breast cancer type I, while genes B and C have lower expression in type II, which is highly aggressive. Based on the gene expression levels shown in the image, the cancer sample does not correspond to either type I or type II breast cancer, why is that?arrow_forward
- Cancer often results from a multistage process involving an initiating event (mediated by a viral infection or a carcinogenic chemical), followed by exposure to tumor promoters. Tumor promoters, a group of molecules that stimulate cell proliferation, cannot induce tumor formation by themselves. The phorbol esters, found in croton oil (obtained from the seeds of the croton plant, Croton tiglium), are potent tumor promoters. (Other examples of tumor promoters include asbestos and several components of tobacco smoke.) In one of the tumor-promoting actions of the phorbol esters, these molecules mimic the actions of DAG. In contrast to DAG, the phorbol esters are not easily disposed of. Explain the possible biochemical consequences of phorbol esters in an “initiated” cell. What enzyme is activated by both DAG and phorbol esters?arrow_forwardAnother cancer cell line that you are working on came from a patient in your medical clinic. You recognize that this is a new type of breast cancer that has never been described before. a. How could you use sequence analysis to determine if this patient inherited the mutation from one of her parents or if it spontaneously occurred in her cells? (Unfortunately her parents have passed away.) b. How could you use sequence analysis to determine if this gene is a tumor suppressor or an oncogene? (For partial credit briefly define tumor suppressor and oncogene.)arrow_forwardAn experiment is carried out as depicted in Figure 1. Two drugs, staurosporine and camptothecin, are used to treat normal and cancer cells. Staurosporine is an inhibitor of protein kinases and can induce apoptosis by an undetermined mechanism. Camptothecin is known to inhibit the DNA topoisomerase type I. Discuss and conclude the effects of the drugs on the two different types of cells in this experiment. Normal cells Cancer cells 1. Add staurosporine 1. Add staurosporine Cells are arrested at restriction point Cells are arrested at restriction point 2. Add camptothecin 2. Add camptothecin Figure 1 Cells are arrested at restriction point Cells are killed when they pass through S phase 3. Remove both drugs Cell cycle resumes Dead cellsarrow_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_forwardWith age, somatic cells are thought to accumulate genomic "scars"as a result of the inaccurate repair of double-strand breaks by non homologous end-joining (NHEJ). Estimates based on the frequency of breaks in primary human fibroblasts suggest that by age 70 each human somatic cell may carry some 2000 NHEJ-induced mutations due to inaccurate repair. If these mutations were distributed randomly around the genome, how many genes would you expect to be affected? Would you expect cell function to be compromised? Why or why not? (Assume that 2% of the genome - 1.5% coding and 0.5% regulatory - is crucial information.)arrow_forwardOur understanding of the molecular biology of cancer formation has been greatly enhanced by studying oncogenic viruses. Answer the following questions regarding oncogenic retroviruses? Explain how a gain of function mutation in the Ras protein caused by a retrovirus might lead to cancer formation.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:PEARSONBiology 2eBiologyISBN:9781947172517Author:Matthew Douglas, Jung Choi, Mary Ann ClarkPublisher:OpenStaxAnatomy & 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 & CompanyLaboratory 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