Bio 121 Campbell Biology Truman College
17th Edition
ISBN: 9781323670637
Author: Urry, Cain
Publisher: PEARSON
expand_more
expand_more
format_list_bulleted
Videos
Question
Chapter 18, Problem 10TYU
Summary Introduction
Introduction: The mutations in genes that regulate cell growth either inhibiting or promoting, result in abnormal uncontrolled growth. The accumulation of these mutations leads to cancer. On the basis of regulation, the genes are categorized as proto-oncogenes and tumor-suppressor genes. Proto-oncogenes are normal growth promoting genes and their mutated forms causing tumor are oncogenes. Tumor-suppressor genes normally inhibit cell proliferation and tumor formation.
Expert Solution & Answer
Want to see the full answer?
Check out a sample textbook solution
Students have asked these similar questions
Proto-oncogenes can change into oncogenes that cause cancer.Which of the following best explains the presence of thesepotential time bombs in eukaryotic cells?(A) Proto-oncogenes first arose from viral infections.(B) Proto-oncogenes are mutant versions of normal genes.(C) Proto-oncogenes are genetic “junk.”(D) Proto-oncogenes normally help regulate cell division.
Suppose a gain-of-function mutation happens in an oncogene. Which of the
following changes is likely to result?
O a) tumor-promoting inflammation
O b) evading growth suppressors
Oc) sustaining proliferative signalling
O d) resisting cell death
/20. In class, we discussed diffferent types of genetic change that can cause a normal gene (proto-
oncogene) to become a cancer-causing gene (oncogene), Which of the following would not be a
cause?
A) translocation or transposition (movement of DNA within the same genome)
B) gene ampliffication (increased number of copies of a given gene)
C) epigenetic change
D) point mutation that changes the gene's product
E) loss of telomeres during DNA replication
ancer?
Chapter 18 Solutions
Bio 121 Campbell Biology Truman College
Ch. 18.1 - How does binding of the trp corepressor to the trp...Ch. 18.1 - Describe the binding of RNA Polymerase,...Ch. 18.1 - WHAT IF? A certain mutation in E. coli changes...Ch. 18.2 - In general, what are the effects of histone...Ch. 18.2 - MAKE CONNECTIONS Speculate about whether the same...Ch. 18.2 - Compare the roles of general and specific...Ch. 18.2 - Once mRNA encoding a particular protein reaches...Ch. 18.2 - WHAT IF? Suppose you compared the nucleotide...Ch. 18.3 - Compare miRNAs and siRNAs, including their...Ch. 18.3 - WH AT IF? Suppose the mRNA being degraded in...
Ch. 18.3 - MAKE CONNECTIONS Inactivation of one of the X...Ch. 18.4 - MAKE CONNECTIONS As you learned in Chapter 12,...Ch. 18.4 - MAKE CONNECTIONS Explain how the signaling...Ch. 18.4 - How do fruit fly maternal effect genes determine...Ch. 18.4 - Prob. 4CCCh. 18.5 - Prob. 1CCCh. 18.5 - Under what circumstances is cancer considered to...Ch. 18.5 - MAKE CONNECTIONS The p53 protein can activate...Ch. 18 - Compare and contrast the roles of a corepressor...Ch. 18 - Describe what must happen in a cell for a gene...Ch. 18 - Why are miRNAs called noncoding RNAs? Explsin how...Ch. 18 - Describe the two main processes that cause...Ch. 18 - Compare the usual functions of proteins encoded by...Ch. 18 - If a particular operon encodes enzymes for making...Ch. 18 - Muscle cells differ from nerve cells mainly...Ch. 18 - The functioning of enhancers is an example of (A)...Ch. 18 - Cell differentiation always involves (A)...Ch. 18 - Which of the following is an example of...Ch. 18 - What would occur if the repressor of an inducible...Ch. 18 - Absence of bicoid in mRNA from a Drosophila egg...Ch. 18 - Which of the following statements about the DNA in...Ch. 18 - Within a cell, the amount of protein made using a...Ch. 18 - Prob. 10TYUCh. 18 - draw it The diagram below shows five genes,...Ch. 18 - Prob. 12TYUCh. 18 - Prob. 13TYUCh. 18 - SCIENCE. TECHNOLOGY, AND SOCIETY Trace amounts of...Ch. 18 - WRITE ABOUT A THEME: INTERACTIONS In a Short essay...Ch. 18 - SYNTHESIZE YOUR KNOWLEDGE The flashlight fish has...
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
- Identify two genetic mechanisms whereby proto-oncogenes can become overexpressed. Select the two mechanisms. Identify two genetic mechanisms whereby proto-oncogenes can become overexpressed.Select the two mechanisms. 1) alterations in chromatin structure 2) a gain-of-function alteration 3)modification of proto-oncogenes products 4)mutations that result in an abnormal protein product 5)mutations within gene-regulatory regionsarrow_forwardWhich of the following is an example of a proto-oncogene? 1) cell cycle inhibitor 2) tumor suppressor 3) oncogene 4) repair enzyme 5) growth factor receptorarrow_forwardIn the pathway below, normal signalling driving cell division requires a mitogen (ligand), an RTK, Ras and proteins X and Y. Which of the following statements is true about the genes that encode the mitogen and Ras in healthy cells? mitogen active Ras protein CYTOSOL GTP active signaling protein Y active receptor active signaling protein X tyrosine kinase CELL DIVISONarrow_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_forwardWhich of the following statements about cancer is false? (a) oncogenes arise from mutations in proto-oncogenes (b) tumor suppressor genes normally interact with growthinhibiting factors to block cell division (c) more than 120cancer-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_forwardWhy is p53 considered a tumor suppressor protein? Question 12 options: a) Because p53 normally detects breaks in DNA. b) Because p53 normally causes progression from G1 to S phase to halt until damaged DNA is fully repaired. c) Because p53 normally repairs breaks in DNA. d) Because p53 normally stimulates transcription of Repair Polymerase. e) Because p53 normally reduces the mutation rate of DNA polymerase.arrow_forward
- Which of the following statements correctly describes p53? Which of the following statements correctly describes p53? A) It is a membrane receptor that binds to growth factors such as EGF. B) p53 binds to pre-replication complexes promoting the transition from G1 to S phase. C) p53 activates cyclin-CDK complexes. D) Activation of p53 leads to inhibition of the cyclin-CDK complexes. E) Cell division stops until p53 binds to DNA and repairs the damage.arrow_forward1. a)Proteins that stimulate/promote progression through the cell cycle are encoded by (oncogenes or tumor suppressor genes). Boldface one. b)Proteins that inhibit progression through the cell cycle are encoded by (oncogenes or tumor suppressor genes). Boldface one. c)What is the difference between a proto-oncogene and an oncogene? d)To cause cancer, proto-oncogenes require (1 or 2)allele(s) to be mutated and therefore are considered (dominant or recessive). The mutation results in a (loss or gain) of function. For each underlined pair, boldface one. e)To cause cancer, tumor suppressor genes require (1 or 2)allele(s) to be mutated and therefore are considered (dominant or recessive). The mutation results in a (loss or gain) of function. For each underlined pair, boldface one.arrow_forwardMany oncogenes result from mutations that cause excessive expression of a protein in cells where it is normally not expressed or is expressed at inappropriate times during development. This type of mutation can be described as ________. A) amorphic B) hypomorphic C)hypermorphic D) neomorphic E) dominant negativearrow_forward
- 3) Examine the graph showing the relative percentage normal and cancer cells spend in various stages of the cell cycle. Based on the information in the graphs, infer how cancer cells differ from typical, noncancerous cells. Select ALL that apply. A) Cancer cells do not replicate their DNA. B) Cancer cells replicate their DNA too quickly. C) Cancer cells do not go through interphase during their cell cycle. D) Cancer cells spend more time dividing compared to typical cells. E) Cancer cells do not always grow to the same size as typical cells. more than 1 answer. not gradedarrow_forwardMost human viruses associated with cancers activate: a.) nuclear factor-kB (NF-kb) b.) apoptosis c.) p53 d.) telemorasearrow_forwardFor each of the following situations, provide a plausible explanation for how it could lead to unrestricted cell division.(a) Colon cancer cells often contain mutations in the gene encoding the prostaglandin E2 receptor. PGE2 is a growth factor required for the division of cells in the gastrointestinal tract.(b) Kaposi sarcoma, a common tumor in people with untreated AIDS, is caused by a virus carrying a gene for a protein similar to the chemokine receptors CXCR1 and CXCR2. Chemokines are cell-specific growth factors.(c) Adenovirus, a tumor virus, carries a gene for the protein E1A, which binds to the retinoblastoma protein, pRb. (d) An important feature of many oncogenes and tumor suppressor genes is their celltype specificity. For example, mutations in the PGE2 receptor are not typically found in lung tumors. Explain this observation. (Note that PGE2 acts through a GPCR in the plasma membrane.)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