Exam 16: The Genetics of Cancer

Describe the cellular and molecular function of the ras gene family and the consequences of mutations in ras.

Chronic myelogenous leukemia appears to be associated with a chromosomal rearrangement. Which chromosome(s) is(are) involved, and what is the name of the rearrangement?

Why do cancer researchers study molecular events associated with mitosis?

A tumor -suppressor gene normally functions to suppress cell division.

The genome of humans is remarkably stable, so much so that there are no cancers known to result from genomic instability.

The familial form of retinoblastoma is characterized by cancer appearing in both eyes relatively early in life. In contrast, the sporadic form is usually unilateral and appears later. What accounts for the difference?

Describe the general relationship that may exist between mutations and cancer.

Provide a simple definition of a carcinogen.

In sporadic cases of retinoblastoma, how many gene mutations are thought to be necessary in the same cell for a tumor to develop?

Describe three genetic mechanisms whereby proto -oncogenes can become overexpressed.

The gene p53 is called the "guardian of the genome" because it corrects mutations in the spindle apparatus before nondisjunction can occur.

In what way might a virus contribute to cancer formation?

The retinoblastoma protein (pRB), like p53, serves as a(n) ________ in regulating the cell cycle.

In what way can loss of heterozygosity lead to cancer?

What is the name of a normal gene that serves to promote cellular division?

(a) What is a tumor -suppressor gene? a() What are oncogenes? b() What is the normal (nonmutant) cellular version of an oncogene called?

What two properties do various types of cancer cells share?

The genetic difference between familial retinoblastoma and sporadic retinoblastoma appears to be based on those with the familial form starting out being whereas those with the sporadic form start out being _. ________,

Define cancer at the anatomical level.

List three general categories of genetic changes that lead to the formation of oncogenes.