Section 23.1
What types of evidence indicate that cancer arises from genetic changes?
How is cancer different from most other types of genetic diseases?
Outline Knudsonās two-hit hypothesis of retinoblastoma and describe how it helps to explain unilateral and bilateral cases of retinoblastoma.
Briefly explain how cancer arises through clonal evolution.
Section 23.2
What is the difference between an oncogene and a tumor-suppressor gene? Give some examples of the functions of proto-oncogenes and tumor suppressers in normal cells.
What is haploinsufficiency? How might it affect cancer risk?
How do cyclins and CDKs differ? How do they interact in controlling the cell cycle?
Briefly outline the events that control the progression of cells through the G1/S checkpoint in the cell cycle.
Briefly outline the events that control the progression of cells through the G2/M checkpoint of the cell cycle.
What is a signal-transduction pathway? Why are mutations in components of signal-transduction pathways often associated with cancer?
How is the Ras protein activated and inactivated?
Why do mutations in genes that encode DNA-repair enzymes often produce a predisposition to cancer?
What role do telomeres and telomerase play in cancer progression?
Section 23.3
How is an epigenetic change different from a mutation?
How is DNA methylation related to cancer?
Section 23.4
Briefly outline some of the genetic changes commonly associated with the progression of colorectal cancer.
Section 23.5
Explain how chromosome deletions, inversions, and translocations may cause cancer.
Briefly outline how the Philadelphia chromosome leads to chronic myelogenous leukemia.
What is genomic instability? Give some ways in which genomic instability may arise.
Section 23.6
How do viruses contribute to cancer?
For more questions that test your comprehension of the key chapter concepts, go to for this chapter.