CAMPBELL BIOLOGY IN FOCUS-W/MASTR.BIO.
3rd Edition
ISBN: 9780134875040
Author: Urry
Publisher: PEARSON
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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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. MAKE CONNECTIONS The p53 protein can activategenes involved in apoptosis. Review Concept 11.5, anddiscuss how mutations in genes coding for proteins thatfunction in apoptosis could contribute to cancer.
In your own words:
Describe the molecular mechanisms involved in P53’s role as a tumor repressor protein.
Identify 2 proteins important for cell cycle regulation and explain why they play a critical role in cancer
Chapter 12 Solutions
CAMPBELL BIOLOGY IN FOCUS-W/MASTR.BIO.
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_forwardMatch each of the changes that can contribute to cancer with its correct description. Loss of function of regulators that send old or damaged cells into apoptosis Hyperactivation of signalling pathways that tell the cell to grow and divide 1. Sustaining proliferative signalling Loss of function of structural proteins that anchor cells to surrounding tissue and/or activation of cell migration 2. Evading growth suppressors 3. Activating invasion and metastasis Loss of function of 4. Enabling replicative immortality regulators that stop inappropriate growth and cell division 5. Inducing angiogenesis 6. Resisting cell death Loss of function of regulators that force aging cells to exit the cell cycle and enter GO or replicative senescence 00arrow_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
- Describe the molecular mechanisms involved in P53’s role as a tumor repressor proteinarrow_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_forwardWhat 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_forward
- WRITE ABOUT A THEME: ORGANIZATION The properties oflife emerge at the biological level of the cell. The highly regulated process of apoptosis is not simply the destruction of acell; it is also an emergent property. Write a short essay (about100–150 words) that briefly explains the role of apoptosis inthe development and proper functioning of an animal, and describe how this form of programmed cell death is a process thatemerges from the orderly integration of signaling pathways.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_forwardHi, 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_forward
- Describe 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_forwardDescribe what happens to the G1 cell cycle check point of a skin cell that is stimulated to divide by neighboring cells following an injury. Describe the pathway from the growth factor signal to the cell cycle checkpoint regulation of gene expression resulting in cell duplication. Briefly explaining the mechanismarrow_forwardWhat role do aurora kinase play in the cell cycle and how would using these kinases as target for cancer treated work?arrow_forward
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