Many of the mutations in cancer samples are not necessarily driver mutations, but rather passenger mutations that are along for the ride. Just because the tumors with a strong environmental component possess a higher frequency of mutations does not mean more oncogenes or more failure of tumor suppressors is occurring. Hematologic childhood cancers have a lower frequency of mutations than tumors with a strong environmental component such as lung cancers and melanoma; WHY?

Many of the mutations in cancer samples are not necessarily driver mutations, but rather passenger mutations that are along for the ride. Just because the tumors with a strong environmental component possess a higher frequency of mutations does not mean more oncogenes or more failure of tumor suppressors is occurring. Hematologic childhood cancers have a lower frequency of mutations than tumors with a strong environmental component such as lung cancers and melanoma; WHY?

Human Heredity: Principles and Issues (MindTap Course List)

11th Edition

ISBN:9781305251052

Author:Michael Cummings

Publisher:Michael Cummings

Chapter12: Genes And Cancer

Section: Chapter Questions

Problem 6QP

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Similar questions

Which 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 genes
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?
DNA sequencing has provided data to indicate that cancer cells may contain tens of thousands of somatic mutations, only some of which confer a growth advantage to a cancer cell. How do scientists describe and categorize these recently discovered populations of mutations in cancer cells?
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?
Which of the following mutations is MOST likely to cause cancer? A) a mutation that causes a cyclin gene to be expressed at all times during the cell cycle B) a mutation that causes an oncogene to be turned off so that no protein is made C) a mutation that causes a Cdk gene to be turned off so that no protein is made D) a mutation that causes a tumor suppressor gene to be over-expressed
Mutations in three broad classes of genes have been implicated in the onset of cancer. Can you explain how?
In what category of cancer-related genes is it possible to find inherited variants that are associated with cancer? Why? Group of answer choices 1. Tumor suppressor genes, because genes in this category are very important in the process of developing cancer. 2. Proto-oncogenes, because individuals who carry only one cancer-causing allele will have a wildtype phenotype. 3. Proto-oncogenes, because there are very few genes in this category, so mutations in them are rare. 4. Tumor suppressor genes, because individuals who carry only one cancer-causing allele will have a wildtype phenotype.
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.
Can we treat cancer by restoring tumor suppressor function such as mutated p53 or pRb? If so, how can this be?
Mutations in proto-oncogenes that turn them into oncogenes tend to be dominant, while cancer-causing mutations in tumor suppressor genes tend to be recessive. Please explain why.
Tumor suppressor genes and oncogenes are implicated in carcinogenesis. However, one can predict whether a gene potentially encodes for a protein that influences carcinogenesis by examining their mutational profile. You sequence the genome of 4 cancers and identify 3 genes of interest. Which of the following genes has the best potential to an oncogene? Tumor 1 Tumor 2 Tumor 3 Tumor 4 Gene A S24F, N465T R33T T345S, G366R P367E, P368Y Gene B S34R, F360I S34R V254I S34E, T67Y Gene C S24F, I322E C255I, E344D S34E, P367E
Compare and contrast oncogenes and tumor suppressors. Contrast oncogenes and proto-oncogenes. Describe the types of mutations that convert proto-oncogenes into oncogenes. Summarize some functions of common oncogenes in cell survival and uncontrolled growth. Contrast tumor suppressors to oncogenes. Describe the types of mutations in tumor suppressors that are found in common cancers. Summarize the functions of common tumor suppressors in cell survival and cell growth.