Biology
12th Edition
ISBN: 9780134813448
Author: Audesirk, Teresa, Gerald, Byers, Bruce E.
Publisher: Pearson,
expand_more
expand_more
format_list_bulleted
Videos
Question
Chapter 43.6, Problem 2TC
Summary Introduction
To determine:
The effect of inactivating
Introduction:
The proto-oncogenes, such as
Expert Solution & Answer
Want to see the full answer?
Check out a sample textbook solution
Students have asked these similar questions
Imatinib is an anti-cancer drug that inhibits the function of CD117, a receptor protein coded for by the KIT gene. Mutations in the KIT gene are implicated in gastrointestinal cancers. Aimee, who has a gastrointestinal tumor asked her doctor if she could try Imatinib, but her doctor first required that she get a biopsy of her tumor.
Hair loss is a well-known side effect of chemotherapy; why does this side effect occur?
(1) Chemotherapy targets cells undergoing division. Hair stem cells are constantly replenishing (growing) just like cancer cells. They are then also targeted by chemotherapy, causing hair loss.
(2) Chemotherapy targets all cells, whether dividing or not dividing, and hair cells are collateral in the fight against cancer
(3) Chemotherapy targets proteins in our cells and hair cells have an abundance of proteins
Human cells are highly resistant to transformation. Experiments have shown that 5 regulatory circuits (pathways) have to be altered before human cells can grow as tumor cells in immunocompromised mice.
State each of these circuits. Explain how the alteration of the protein of that particular circuit leads to uncontrolled growth.
the mitogenic signaling pathway controlled by Ras.
the cell cycle checkpoint controlled by pRb.
the alarm pathway controlled by p53.
the telomere maintenance pathway controlled by hTERT.
the signaling pathways are controlled by protein phosphatase 2A, which modulates the activity of the mTOR, Myc, β-catenin, and PKB/ Akt signaling proteins.
The p53 pathway is important for regulating the cell cycle. In a normal cell, there is a protein called mdm2 that can bind to p53 and deactivate it. A diseased individual has amutation in the gene that codes for mdm2, resulting in an mdm2 protein that is less able to bind to p53. Will this mutation increase, decrease, or cause no change in the rate of cell death? Explain.
Chapter 43 Solutions
Biology
Ch. 43.1 - define development and describe how cell division...Ch. 43.2 - Prob. 1CYLCh. 43.3 - describe early development in amphibians,...Ch. 43.3 - Prob. 2CYLCh. 43.4 - Prob. 1TCCh. 43.4 - Prob. 2TCCh. 43.4 - Does the development of a human limb, and the rest...Ch. 43.4 - Prob. 1CYLCh. 43.4 - Prob. 2CYLCh. 43.5 - Prob. 1TC
Ch. 43.5 - Prob. 1CSCCh. 43.5 - Prob. 2TCCh. 43.5 - Prob. 3TCCh. 43.5 - Prob. 1HYEWCh. 43.5 - describe human embryonic development from...Ch. 43.5 - describe the structure and function of the...Ch. 43.5 - Prob. 3CYLCh. 43.6 - Prob. 1TCCh. 43.6 - Prob. 1CYLCh. 43.6 - Prob. 2CYLCh. 43.6 - Prob. 3CYLCh. 43.6 - Prob. 2TCCh. 43 - Prob. 1MCCh. 43 - Animals with Indirect development a. develop...Ch. 43 - Prob. 3MCCh. 43 - Prob. 4MCCh. 43 - Prob. 5MCCh. 43 - Prob. 6MCCh. 43 - Prob. 7MCCh. 43 - Prob. 8MCCh. 43 - Prob. 1FIBCh. 43 - Prob. 2FIBCh. 43 - Prob. 3FIBCh. 43 - Prob. 4FIBCh. 43 - Distinguish between direct and indirect...Ch. 43 - Describe the structure and function of the four...Ch. 43 - What is gastrulation? Describe gastrulation in...Ch. 43 - Prob. 4RQCh. 43 - Prob. 5RQCh. 43 - In humans, where does fertilization occur, and...Ch. 43 - Prob. 7RQCh. 43 - Prob. 8RQCh. 43 - How do changes in the breast prepare a mother to...Ch. 43 - Prob. 10RQCh. 43 - Prob. 1ACCh. 43 - Prob. 2AC
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
- For 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_forwardOne important role of Fas and Fas ligand is to mediate the elimination of tumor cells by killer lymphocytes. In a study of 35 primary lung and colon tumors, half the tumors were found to have amplified and overexpressed a gene for a secreted protein that binds to Fas ligand. How do you suppose that overexpression of this protein might contribute to the survival of these tumor cells? Explain your reasoning.arrow_forwardwhich of hthe following would result in a persisting proliferation response to growth factor receptor activation after the ligand is no longer binding to its rceptor kinase? 1. Both a mutation that blocks the GTPas activity of Ras and a mutation that blocks the exchange of GDP with GTP would cause the response to persist. 2. a mutation that blocks the GTPas activity of Ras 3. neither a mutation that blocks the GTPas activity of Ras nor a mutation that blocks the exchange of GDP with GTP would cause the response to persist 4. a mutatiaon that blocks the exchange of GDP with GTParrow_forward
- The SIRT3 protein has been reported to increase the growth of certain types of cancer cells. Researchers studying the metabolism and development of stomach cancer cells investigated the potential role of the SIRT3 protein in these cells. In the first investigation, the researchers quantified the relative amount of SIRT3 in normal stomach cells and in each of four different lines of stomach cancer cells (Figure 1). Using data from a group of 100 patients with stomach cancer, the researchers also analyzed the relative amount of SIRT3 protein detected in samples of the cancer cells and in normal cells immediately adjacent to the cancer cells (Figure 2). Figure 1. SIRT3 protein levels in normal stomach cells (NS) and stomach cancer cell lines from four different patients (SC-1, SC-2, SC-3, SC-4), shown relative to the level in normal stomach cells (NS). Error bars represent ±SEx¯. Figure 2. The number of patients, from 100 tested, whose stomach cancer cells or normal stomach cells…arrow_forwardYou are studying growth factor GFA, which you know stimulates the proliferation of goblet cells in theintestine.Goblet cells are responsible for producing and secreting mucin, a mixture of glycosaminoglycans thatprotects the intestinal wall.Some patients suffering from inflammatory bowel disease (IBD) appear to have fewer goblet cells, thereforeless mucin and less protection from toxins and various other pro-inflammatory factors.These patients also have mutations in the gene encoding the GFA receptor (GFAR) in goblet cells,GFAR is a receptor tyrosine kinase (RTK) that autophosphorylates in response to GFA binding, thusbecoming active.QUESTION:explain what changes in GFAR could be caused by these IBD-associatedmutations and why.arrow_forwardMutations that inactivate p53 have a recessive phenotype, whereas mutations affecting Ras are dominant. Explain the difference.arrow_forward
- why EGFR play a role in CRC and other cancer?arrow_forwardDescribe the effects of the mutation causing the p21 promoter to no longer bind p53 on cell signaling pathways and metabolism or cell cycle control.arrow_forwardOverexpression of the Myc protein is a common feature of many types of cancer cells, contributing to their excessive cell growth and proliferation. By contrast, when Myc is overexpressed in most normal cells, the result is not excessive proliferation, but cell-cycle arrest or apoptosis.Which one of the following statements provides the most likely explanation for why overexpression of Myc can have such different outcomes in normal cells and in cancer cells? A. Normal cells contain checks and balances that prevent Myc-induced proliferation. B. In normal cells, Myc protein acts as a mediator in cell-cycle arrest and apoptosis. C. The target protein for Myc-induced proliferation is missing from most normal cells. D. In normal cells, when Myc is overexpressed, the excess Myc protein precipitates.arrow_forward
- You are working in a cell biology lab that investigates non-small cell lung cancer cells, which of these cellular features will be suggestive of senescence in the cells observed? Choose all that apply: Group of answer choices Large flattened morphology Reduced incorporation of 5-bromodeoxyuridine (in DNA replication) Increased p53 expression Decreased expression of p15INK4Barrow_forwardWhy do cancer cells undergo EMT and MET? What are the cellular changes (expression or suppression of molecules) associated with EMT and MET? What does each change facilitate?arrow_forwardIf you were to design an experiment to get p53 back into cancer cells, how would you go about that work? How would you direct p53 into the nucleus of cancer cells without directing it to the nucleus of healthy cells? As an overabundance of p53 in healthy cells would cause problems. Could someone in depth answer these questions for me and explain them cellularly.arrow_forward
arrow_back_ios
SEE MORE QUESTIONS
arrow_forward_ios
Recommended textbooks for you
Biology: The Dynamic Science (MindTap Course List)BiologyISBN:9781305389892Author:Peter J. Russell, Paul E. Hertz, Beverly McMillanPublisher:Cengage Learning
Biology: The Dynamic Science (MindTap Course List)
Biology
ISBN:9781305389892
Author:Peter J. Russell, Paul E. Hertz, Beverly McMillan
Publisher:Cengage Learning
Cell Differentiation | Genetics | Biology | FuseSchool; Author: FuseSchool - Global Education;https://www.youtube.com/watch?v=gwAz_BtVuLA;License: Standard YouTube License, CC-BY