Human Anatomy & Physiology (11th Edition)
11th Edition
ISBN: 9780134580999
Author: Elaine N. Marieb, Katja N. Hoehn
Publisher: PEARSON
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- Sequencing the human genome, the development of microarray technology, and personal genomics promise to improve our understanding of normal and abnormal cell behavior. How are these approaches dramatically changing our understanding and treatment of complex diseases such as cancer?arrow_forward. The website CBioPortal (http://www.cbioportal.org)is an exceptionally useful program for visualizing thecancer genes and genomes of tumors from thousandsof patients with different kinds of cancer that havebeen analyzed by whole genome sequencing and insome cases, by RNA-Seq.Go the the CBioPortal site and click All underSelect Cancer Study and in Enter Gene Set typePTEN, then hit Submit. On the page that is returnedyou will see how the coding region of the PTEN geneis altered in tumors investigated in the various studies.Hitting the tab Mutations will let you see the detailsof these mutations relative to the PTEN protein, whilethe tab Expression lets you see how the gene’s expression (in terms of cDNA reads) is altered in individual tumor samples.a. Is PTEN an oncogene or a tumor suppressor gene?What kinds of evidence lead you to this conclusion?b. What kinds of cancer are most likely to involvealterations of PTEN?c. How would you identify patients whose tumorcells are particularly…arrow_forwardPls help ASAParrow_forward
- The vast majority of human cancers mutations in the p53 gene. What is the function of p53 normally in the cell? What happens when p53 is mutated? Is this a gain of function or loss of function mutation?arrow_forwardHuman 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.arrow_forwardEvery year, about a million Americans are diagnosed with cancer. This means that about 75 million Americans now living will eventually have cancer, And one in five will die of the disease. There are many kinds of cancers and many causes, such as smoking, overexposure to ultraviolet rays, a high fat and low fiber diet, and some workplace chemicals. Hundreds of millions of dollars are spent each year on searching for treatment, yet less money is spent on prevention. Should we devote more resources to treating cancer or to preventing it? Explain.arrow_forward
- Please answer question 8arrow_forwardWhich of the following mutations would not convert a proto-oncogene into an oncogene? A translocation that places the gene at a new locus where gene expression is increased. A mutation in the coding region that makes the protein resisitant to degradation. Gene duplication. A mutation in the coding region that makes the protein hyperactive. A deletion of an enhancer that lies 3’ to the coding region.arrow_forwardEpigenetic changes include all of the following EXCEPT: 1) changes in DNA sequence 2) DNA coiling 3) methylation 4) gene expressionarrow_forward
- You've discovered a new gene, G8R. Describe two experiments you could do to determine whether it is a proto-oncogene. Explain the experimental set-up as well a how you would interpret the results.arrow_forwardResearch cancer mutation. Provide the link to the research article that gives you your information. One good resource to use is PubMed. Then answer the following questions, in 3 paragraphs, 3-5 sentences each. 1. What kind of disease/cancer does this mutation cause? 2.What happens during transcription to cause this mutation? 3. Is this trait passed on to progeny? Can the progeny be a carrier or simply affected?arrow_forward
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