Skip to main content
Biology LibreTexts

13.E: Cancer Genetics (Exercises)

  • Page ID
  • These are homework exercises to accompany Nickle and Barrette-Ng's "Online Open Genetics" TextMap. Genetics is the scientific study of heredity and the variation of inherited characteristics. It includes the study of genes, themselves, how they function, interact, and produce the visible and measurable characteristics we see in individuals and populations of species as they change from one generation to the next, over time, and in different environments.

    Study Questions:

    13.1 Why do oncogenes tend to be dominant, but mutations in tumor suppressors tend to be recessive?

    13.2 What tumor suppressing functions are controlled by p53? How can a single gene affect so many different biological pathways?

    13.3 Are all carcinogens mutagens? Are all mutagens carcinogens? Explain why or why not.

    13.4 Imagine that a laboratory reports that feeding a chocolate to laboratory rats increases the incidence of cancer. What other details would you want to know before you stopped eating chocolate?

    13.5 Do all women with HPV get cancer? Why or why not? Do all women with mutations in BRCA1 get cancer? Why or why not?

    Chapter 13 – Answers

    13.1 Oncogenes usually arise from gain-of-function mutations, which tend to be haplosufficient. Mutations in tumor supressors are usually loss-of-function mutations, which tend to be haploinsufficient.

    13.2 p53 activates DNA repair, apoptosis, and inhibitors of cell division. Different genes involved in each of these pathways have enhancer elements to which p53 binds; therefore they call all be activated by p53.

    13.3 Some substances can promote cancer without causing a mutation, for example by inducing the cell cycle or accelerating it so that there is less time to repair DNA damage. All mutagens are potentially carcinogens, although some potential mutagens may not cause significant damage to cells in the body due to detoxification or other reasons that limit their efficacy.

    13.4 Was the dose fed to the rats relevant? Were similar effects seen in other organisms? Do epidemiological studies support these conclusions?

    13.5 Cancer results from an accumulation of mutations that activate cell division and disable tumor suppression. HPV infection or BRCA1 mutation, alone do not satisfy all of these requirements. Also, not all strains of HPV are equally carcinogenic, and the body’s defense may be able to suppress the activity of the virus.