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Ch. 24 - Cancer Genetics

Chapter 23, Problem 29

Researchers have identified some tumors that have no recurrent mutations or deletions in known oncogenes or tumor-suppressor genes and no detectable epigenetic alterations. However, these tumors often have large chromosomal deletions. What are some possible explanations that could account for the genetic causes behind these tumors?

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Hello everyone here's our next question. Which of the following does not contribute to tumor development. So let's look over our answer choices, remembering we're looking for the one that is not a part of tumor development. Choice A says activation of tumor suppressor gene. Um Well if you have a tumor suppressor gene and you've activated it um that's obviously going to help suppress the growth of tumors. So would not contribute to tumor development. So this is going to be our answer here. Since this suppresses tumor growth. That tumor suppressor gene regulates cell growth and maintains healthy growth and spread of cells. So we're going to highlight choice A as our answer here. But let's just look through other choices to be thorough. Choice B says gene duplications and gene duplications definitely do contribute to tumor development. Specifically the amplification of the ah M. d. m. two gene can prevent The binding of the p. tumor suppressor. And as we saw above and we talked about tumor suppressors, that's something that prevents the tumor suppressor from acting definitely contributes to development. So Choice B. Is not our answer here. Then. Choice C. Says an increase in gene copy numbers and that can also contribute to tumors. Um Specifically example of that is a high number so high number of E. R. B. B. two gene copies um is associated with breast cancer. So this is another factor that can contribute to development. And so not our answer. And then finally, choice D mutations and genes necessary for DNA repair again, if your cells cannot repair DNA damage that damage DNA quite often is a factor and tumor development. That's why things like UV light are carcinogens because they cause DNA damage. So Choice D also not our answer. So again, which of the following does not contribute to tumor development. Choice, a activation of tumor suppressor gene. See you in the next video.
Related Practice
Textbook Question

The table in this problem summarizes some of the data that have been collected on mutations in the BRCA1 tumor-suppressor gene in families with a high incidence of both early-onset breast cancer and ovarian cancer.

Predisposing Mutations in BRCA1
Kindred    Codon    Nucleotide     Coding Effect     Frequency in
                               Change                                    Control
                                                                                Chromosomes    
 1901          24           -11 bp          Frameshift           0/180
                                                       or splice
 2082        1313         C→T           Gln→Stop            0/170
 1910        1756         Extra C        Frameshift           0/162
 2099        1775         T→G            Met→Arg            0/120
 2035         NA*          ?                  Loss of                NA*
                                                       transcript                                      _
Source: (1994). Science 266:66–71. © AAAS.

Note the coding effect of the mutation found in kindred group 2082. This results from a single base-pair substitution. Draw the normal double-stranded DNA sequence for this codon (with the 5' and 3' ends labeled), and show the sequence of events that generated this mutation, assuming that it resulted from an uncorrected mismatch event during DNA replication.

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Textbook Question

The table in this problem summarizes some of the data that have been collected on mutations in the BRCA1 tumor-suppressor gene in families with a high incidence of both early-onset breast cancer and ovarian cancer.

Predisposing Mutations in BRCA1
Kindred    Codon    Nucleotide     Coding Effect     Frequency in
                               Change                                    Control
                                                                                Chromosomes    
 1901          24           -11 bp          Frameshift           0/180
                                                       or splice
 2082        1313         C→T           Gln→Stop            0/170
 1910        1756         Extra C        Frameshift           0/162
 2099        1775         T→G            Met→Arg            0/120
 2035         NA*          ?                  Loss of                NA*
                                                       transcript                                      _
Source: (1994). Science 266:66–71. © AAAS.

Examine the types of mutations that are listed in the table, and determine if the BRCA1 gene is likely to be a tumor-suppressor gene or an oncogene.

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Textbook Question

The table in this problem summarizes some of the data that have been collected on mutations in the BRCA1 tumor-suppressor gene in families with a high incidence of both early-onset breast cancer and ovarian cancer.

Predisposing Mutations in BRCA1
Kindred    Codon    Nucleotide     Coding Effect     Frequency in
                               Change                                    Control
                                                                                Chromosomes    
 1901          24           -11 bp          Frameshift           0/180
                                                       or splice
 2082        1313         C→T           Gln→Stop            0/170
 1910        1756         Extra C        Frameshift           0/162
 2099        1775         T→G            Met→Arg            0/120
 2035         NA*          ?                  Loss of                NA*
                                                       transcript                                      _
Source: (1994). Science 266:66–71. © AAAS.

Although the mutations listed in the table are clearly deleterious and cause breast cancer in women at very young ages, each of the kindred groups had at least one woman who carried the mutation but lived until age 80 without developing cancer. Name at least two different mechanisms (or variables) that could underlie variation in the expression of a mutant phenotype, and propose an explanation for the incomplete penetrance of this mutation. How do these mechanisms or variables relate to this explanation?

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Textbook Question

Skin cancer carries a lifetime risk nearly equal to that of all other cancers combined. Following is a graph [modified from K. H. Kraemer (1997). Proc. Natl. Acad. Sci. (USA) 94:11–14] depicting the age of onset of skin cancers in patients with or without XP, where the cumulative percentage of skin cancer is plotted against age. The non-XP curve is based on 29,757 cancers surveyed by the National Cancer Institute, and the curve representing those with XP is based on 63 skin cancers from the Xeroderma Pigmentosum Registry.

Provide an overview of the information contained in the graph. 

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Textbook Question

Skin cancer carries a lifetime risk nearly equal to that of all other cancers combined. Following is a graph [modified from K. H. Kraemer (1997). Proc. Natl. Acad. Sci. (USA) 94:11–14] depicting the age of onset of skin cancers in patients with or without XP, where the cumulative percentage of skin cancer is plotted against age. The non-XP curve is based on 29,757 cancers surveyed by the National Cancer Institute, and the curve representing those with XP is based on 63 skin cancers from the Xeroderma Pigmentosum Registry.

Explain why individuals with XP show such an early age of onset. 

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Textbook Question

Although cancer is not a contagious disease in humans or other vertebrates, there have been rare cases in which cancers have spread from one organism to another. Describe three cases of these contagious cancers and what conditions might have led to their appearance. For an introduction to this topic, see http://www.cancer.org/cancer/cancerbasics/is-cancer-contagious.

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