Campbell Biology In Focus
2nd Edition
ISBN: 9780134203072
Author: Lisa A. Urry, Michael L. Cain, Steven A. Wasserman, Peter V. Minorsky, Jane B. Reece
Publisher: PEARSON
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Textbook Question
Chapter 12.4, Problem 3CC
MAKE CONNECTIONS The gene that is activated on the Philadelphia chromosome codes for an intracellular kinase. Review the discussion of cell cycle control and cancer in Concept 9.3, and explain how the activation of this gene could contribute to the development of cancer
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Chapter 12 Solutions
Campbell Biology In Focus
Ch. 12.1 - Which one of Mendels laws relates to the...Ch. 12.1 - MAKE CONNECTIONS Review the description of meiosis...Ch. 12.1 - WHAT IF? Propose a possible reason that the first...Ch. 12.2 - A white-eyed female Drosophila is mated with a...Ch. 12.2 - Neither Tim nor Rhoda has Duchenne muscular...Ch. 12.2 - MAKE CONNECTIONS Consider what you learned about...Ch. 12.3 - When two genes are located on the same chromosome,...Ch. 12.3 - For each type of offspring of the testcross in...Ch. 12.3 - WHAT IF? Genes A, B, and C are located on the same...Ch. 12.4 - About 5% of individuals with Down syndrome have a...
Ch. 12.4 - WHAT IF? The ABO blood type locus has been mapped...Ch. 12.4 - MAKE CONNECTIONS The gene that is activated on the...Ch. 12.4 - Women born with an extra X chromosome (XXX) are...Ch. 12 - A man with hemophilia (a recessive, sex-linked...Ch. 12 - Pseudohypertrophic muscular dystrophy is an...Ch. 12 - A space probe discovers a planet inhabited by...Ch. 12 - Using the information from problem 3, scientists...Ch. 12 - A man with red-green color blindness (a recessive,...Ch. 12 - You design Drosophila crosses to provide...Ch. 12 - A wild-type fruit fly (heterozygous for gray body...Ch. 12 - Assume that genes A and B are 50 map units apart...Ch. 12 - Prob. 9TYUCh. 12 - SCIENTIFIC INQUIRY DRAW IT Assume you are mapping...Ch. 12 - FOCUS ON EVOLUTION Crossing over is thought to be...Ch. 12 - FOCUS ON INFORMATION The continuity of life is...Ch. 12 - SYNTHESIZE YOUR KNOWLEDGE Butterflies have an X-Y...
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- Another model, the random model, proposes that any cell in a malignant tumor has the potential to form a new tumor. Does the cancer stem cell hypothesis contradict this idea?arrow_forwardfor question 1, choose wheater each choice is either tumor suppressor or proto oncogene\ for question 2, which behaviors are or are not responsible for the behavior of the strain of yeastarrow_forwardDescribe the effects of the over-expression of mdm2 on cell proliferation and apoptosis on cell signaling pathways and metabolism or cell cycle control. Briefly explain the normal role of each component in the context of the pathway and why its loss or modification would have the expected effect.arrow_forward
- What is the most likely outcome is we lose the tumor suppressor proteins, cyclin- dependent kinase inhibitors. Select one: o a. Cyclin-cylin dependent kinases will phosphorylate retinoblastoma protein and cell- cycle will not proceed. o b. Cyclin-cylin dependent kinase complex will not phosphorylate retinoblastoma protein and cell-cycle will not proceed. o c. Cyclin-cylin dependent kinase complex will not phosphorylate retinoblastoma protein and cell-cycle will proceed. o d. Cyclin-cylin dependent kinases will phosphorylate retinoblastoma protein and cell- cycle will proceed.arrow_forwardPredict the effects of the following mutations on the ability of a cell to undergo apoptosis:a. Mutation in Bad such that it cannot be phosphorylated by protein kinase B (PKB)b. Overexpression of Bcl-2c. Mutation in Bax such that it cannot form homodimersOne common characteristic of cancer cells is a loss of function in the apoptotic pathway. Which of the mutations listed above might you expect to find in some cancer cells?arrow_forwardDiscuss the complete cell cycle in a human cell, mitosis and meiosis, and the regulatory components (i.e. the proteins associated with cellular checkpoints) of the cell cycle. Tumor growth results when the cell cycle checkpoints are ignored. Give an example of how tumor growth could result from either a loss-of-function or a gain-of-function mutation.arrow_forward
- Hi, can you explain this concept: cell cycle progression can be halted at several points by the tumor suppressor gene product p53, activated in response to checkpoints sensing DNA and possibly also chromosome damage; loss of p53 would remove this brake to cycling. How these events can lead to cancer progression?arrow_forwardWhat role do aurora kinase play in the cell cycle and how would using these kinases as target for cancer treated work?arrow_forwardDescribe the general process of cell signalling pathways: what events take place for a signal to cause cellular changes? Provide examples and how perturbation of these events can result in “cancer pathways”. In addition, describe in detail a typical cancer pathway and its strategy to activate gene expression. What is the origin of many cancer pathways, i.e., during which stage of an organism’s live process(es) are they physiologically activated? Why is this important for cancer development?arrow_forward
- please helparrow_forwardModify the diagram above to illustrate specific protein(s) that would participate in regulating this pathway if DNA damage was detected in these cells. What effect would this have on the progression of the cell cycle? If there is more than one possible outcome be sure to outline each one.arrow_forwardThe Human papillomavirus (HPV) has been linked to an increased risk of cervical cancer. The HPV E6 and E7 proteins govern the cell via altering cellular proteins. The E6 protein interacts with the tumor suppressor protein p53 and directs its ubiquitin-mediated destruction. Can you elaborate about the P63 gene: its function and if it can be altered/mutated by HPV? If it does, what is the relationship between P53 and P63? Thank you!arrow_forward
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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