Essentials of Genetics (9th Edition) - Standalone book
9th Edition
ISBN: 9780134047799
Author: William S. Klug, Michael R. Cummings, Charlotte A. Spencer, Michael A. Palladino
Publisher: PEARSON
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Textbook Question
Chapter CHST4, Problem 6RQ
Give two examples of how genomic studies have altered our understanding of cancers.
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Give two examples of how genomic studies have altered our understanding of cancers.
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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?
Chapter CHST4 Solutions
Essentials of Genetics (9th Edition) - Standalone book
Ch. CHST4 - What is pharmacogenomics, and how does it differ...Ch. CHST4 - Describe how the drug Herceptin works. What types...Ch. CHST4 - Prob. 3RQCh. CHST4 - Prob. 4RQCh. CHST4 - What types of genetic tests are currently...Ch. CHST4 - Give two examples of how genomic studies have...Ch. CHST4 - Why is it necessary to examine gene-expression...Ch. CHST4 - Prob. 8RQCh. CHST4 - In this chapter, we present three case studies...Ch. CHST4 - What are the biggest challenges that must be...
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- There are three broad categories of cancer-related genes: proto-oncogenes, tumor suppressor genes, and DNA stability/repair genes. Define each of these categories and indicate which one you think the RB1 gene belongs to and why.arrow_forwardWhat are predisposition genes? why are the responsible for cause of cancer ?arrow_forwardWhat is/are the role/s of molecular techniques in understanding cancer? Cite some references from the web.arrow_forward
- How can researchers pinpoint the particular driver mutations most responsible for the cancer phenotype?arrow_forwardBriefly describe the structural variability of cancer genomes.arrow_forwardWith regard to human cancer cells, which of the following statements is true? A. Cancer cells within one tumor usually do not share common mutations B. Cancer cells generally have lost the ability to divide C. Oncogenes are non-human genes not related to normal genes in the human genome D. Mutations in DNA repair genes result in an increased chance of getting cancer.arrow_forward
- List the types of changes in the human genome thatcan help lead to cancer.arrow_forwardDescribe the differences between point mutations, chromosomal translocations, and gene amplification in the process of cancer.arrow_forwardExplain the molecular mechanisms of cancers caused by a P53 gene mutation.arrow_forward
- Cancer-causing mutations in genes can have different effects on the protein products expressed. a) What type of mutation would be dominant in the development of cancer? Why? b) What type of mutation would be expressed as a recessive trait in the development of cancer? Why? c) Based upon your answers to parts (a) and (b), how would you treat these situations using a gene therapy approach?arrow_forwardGenetic tests that detect mutations in the BRCA1 and BRCA2 tumor-suppressor genes are widely available. These tests reveal a number of mutations in these genes—mutations that have been linked to familial breast cancer. Assume that a young woman in a suspected breast cancer family takes the BRCA1 and BRCA2 genetic tests and receives negative results. That is, she does not test positive for the mutant alleles of BRCA1 or BRCA2. Can she consider herself free of risk for breast cancer?arrow_forwardWhich 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_forward
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