Table of contents

1. Introduction to Genetics51m
2. Mendel's Laws of Inheritance3h 37m
3. Extensions to Mendelian Inheritance2h 41m
4. Genetic Mapping and Linkage2h 28m
5. Genetics of Bacteria and Viruses1h 21m
6. Chromosomal Variation1h 48m
7. DNA and Chromosome Structure56m
8. DNA Replication1h 10m
9. Mitosis and Meiosis1h 34m
10. Transcription1h 0m
11. Translation58m
12. Gene Regulation in Prokaryotes1h 19m
13. Gene Regulation in Eukaryotes44m
14. Genetic Control of Development44m
15. Genomes and Genomics1h 50m
16. Transposable Elements47m
17. Mutation, Repair, and Recombination1h 6m
18. Molecular Genetic Tools19m
- Genetic Cloning
  9m
- Methods for Analyzing DNA
  9m
19. Cancer Genetics29m
- Overview of Cancer
  21m
- Cancer Mutations
  7m
20. Quantitative Genetics1h 26m
21. Population Genetics50m
- Hardy Weinberg
  19m
- Allelic Frequency Changes
  31m
22. Evolutionary Genetics29m

19. Cancer Genetics

Cancer Mutations

Genetics

19. Cancer Genetics

Cancer Mutations

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2:41 minutes

Problem 29

Textbook Question

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?

Verified step by step guidance

Step 1: Understand that large chromosomal deletions can remove multiple genes simultaneously, including genes not previously identified as oncogenes or tumor suppressors, which may contribute to tumor development through loss of function.

Step 2: Consider the possibility that these deletions might affect regulatory regions or non-coding RNAs that control gene expression, leading to dysregulation of critical cellular pathways without direct mutations in known cancer genes.

Step 3: Explore the concept of haploinsufficiency, where losing one copy of a gene (due to deletion) reduces gene dosage enough to disrupt normal cellular function and promote tumorigenesis, even if the remaining allele is normal.

Step 4: Recognize that chromosomal deletions can cause genomic instability, increasing the likelihood of further genetic alterations that may not be immediately detectable but contribute to cancer progression.

Step 5: Investigate the role of structural variations and chromosomal rearrangements that accompany large deletions, which might create novel gene fusions or disrupt gene networks, providing alternative mechanisms for tumor development.

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Key Concepts

Here are the essential concepts you must grasp in order to answer the question correctly.

Chromosomal Deletions and Their Impact

Chromosomal deletions involve the loss of large DNA segments, which can remove multiple genes simultaneously. Such deletions may eliminate tumor suppressor genes or regulatory regions, disrupting normal cell growth control even if no single recurrent mutation is detected. This can lead to tumor development through combined gene dosage effects.

Non-Mutational Genetic Mechanisms in Cancer

Tumors can arise from genetic alterations beyond point mutations or epigenetic changes, such as structural variations like deletions, duplications, or translocations. These large-scale changes can alter gene expression or genome stability, contributing to cancer without involving classic oncogene activation or tumor suppressor gene mutation.

Role of Haploinsufficiency in Tumorigenesis

Haploinsufficiency occurs when a single functional copy of a gene is insufficient for normal function. Large chromosomal deletions may reduce gene dosage below a critical threshold, impairing tumor suppressor pathways and promoting cancer development, even in the absence of mutations or epigenetic silencing.

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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.

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

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

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

Provide an overview of the information contained in the graph.

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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.

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Multiple Choice

A mutation in a tumor suppressor gene causes what to happen?

True or False:Proto-oncogenes are mutated versions of oncogenes

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