ESSENTIALS OF GENETICS ALC & MOD MSTG/ET VP
1st Edition
ISBN: 9780134452890
Author: KLUG
Publisher: Pearson Education
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Chapter CHST1, Problem 3DQ
How can the role of epigenetics in cancer be reconciled with the idea that cancer is caused by the accumulation of mutations in tumor-suppressor genes and proto-oncogenes?
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How can the role of epigenetics in cancer be reconciled with the idea that cancer is caused by the accumulation of genetic mutations in tumor-suppressor genes and proto-oncogenes?
Why does a single mutation in a proto-oncogene, turning it into an oncogene potentially lead to a cancerous phenotype, while it takes two mutations in tumor suppressor genes to lead to a cancerous phenotype?
What is the difference in an oncogene and tumor suppressor gene and how can each potentially lead to cancer?
Chapter CHST1 Solutions
ESSENTIALS OF GENETICS ALC & MOD MSTG/ET VP
Ch. CHST1 - What are the major mechanisms of epigenetic genome...Ch. CHST1 -
2. What parts of the genome are reversibly...Ch. CHST1 - What are the roles of proteins in histone...Ch. CHST1 - Describe how reversible chemical changes to...Ch. CHST1 -
5. What is the histone code?
Ch. CHST1 - Prob. 6RQCh. CHST1 - Why are changes in nucleosome spacing important in...Ch. CHST1 -
8. How do microRNAs regulate epigenetic...Ch. CHST1 - What is the role of imprinting in human genetic...Ch. CHST1 - Imprinting disorders do not involve changes in DNA...
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- What is the difference between a proto-oncogene and a tumor-suppressor gene?arrow_forwardExplain the difference between a proto-oncogene and a tumor suppressor gene.arrow_forwardWhich of the following mutations will result in cancer? a. homozygous recessive mutation in a tumor-suppressor gene coding for a nonfunctional protein b. dominant mutation in a tumor-suppressor gene in which the normal protein product is overexpressed c. homozygous recessive mutation in which there is a deletion in the coding region of a proto-oncogene, leaving it nonfunctional d. dominant mutation in a proto-oncogene in which the normal protein product is overexpressedarrow_forward
- 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_forwardWhich of the following statements about cancer is false? (a) oncogenes arise from mutations in proto-oncogenes (b) tumor suppressor genes normally interact with growth-inhibiting factors to block cell division (c) more than 120 cancer-driving genes have been discovered (d) oncogenes were first discovered in mouse models for cancer (e) the development of cancer is usually a multistep process involving both oncogenes and mutated tumor suppressor genesarrow_forwardDistinguish between proto-oncogenes and tumor-suppressor genes. To become cancer promoting, do proto-oncogenes and tumor-suppressor genes undergo gain-of-function or loss-of-function mutations? Classify the following genes as proto-oncogenes or tumor-suppressor genes: p53, ras, BCL-2, JUN, MDM2, and p16.arrow_forward
- How can a mutation in a tumor-suppressor gene contribute to the development of cancer?arrow_forwardExplain how p53 functions as a tumor suppressor gene. How can mutations in p53 lead to cancer, and how might gene therapy or other drug interventions inhibit the growth of a tumor?arrow_forwardWhy don’t all loss-of-function mutations that are recessive at the cellular level behave as dominants at the organismal level? Is this property restricted to tumor-suppressor gene mutations?arrow_forward
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