Deck 16: The Genetics of Cancer

Question 1

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?

Answer 1

Chromosomes 9 and 22 are involved in a translocation. This combination of chromosomal material is referred to as the Philadelphia chromosome.

Question 2

Name two classes of proteins that combine to directly control progression through the cell cycle.

Answer 2

protein kinases, cyclins

Question 3

What is the significance of CDK?

Answer 3

CDK symbolizes a class of protein kinases, which, when activated, selectively phosphorylate target proteins. Many of these phosphorylated proteins are involved in cell -cycle control.

Question 4

Which three stages or transitions in the cell cycle seem to serve as points of control (checkpoints)?

Question 5

Describe two classes of proteins known to be involved in the regulation of the cell cycle.

Question 6

Which of the following three general mechanisms appear to be involved in the conversion of proto -oncogenes to oncogenes?

A) suppression, tabulation, projection
B) point mutations, translocations, overexpression
C) familial, sporadic, phosphorylation
D) inversions, translocations, methylation
E) transdetermination, mutation, allosteric interactions

Question 7

A protein that functions as a cell -cycle regulator causes cell death (apoptosis) under high sunlight exposure. Which symbol given to this protein?

A) p53
B) phosphokinase
C) cyclin
D) p102
E) p34

Question 8

Which protein appears to regulate the entry of cells into an S phase? This protein is also known as the "guardian of the genome."

A) cyclin
B) p53
C) p34
D) p102
E) phosphokinase

Question 9

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

A) up regulator
B) pseudooncogene
C) tumor enhancer
D) oncogene
E) tumor suppressor

Question 10

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

A) one
B) two
C) four
D) six
E) insufficient information to answer this question

Question 11

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

Question 12

What functional differences exist between various cyclins?

Question 13

Driver mutations provide a growth advantage to a tumor cell. Which type of mutation is known to accumulate in cancer cells but has no direct contribution to the cancer phenotype?

A) carrier mutations
B) passenger mutations
C) alteration mutations
D) indirect mutations
E) induced mutations

Question 14

Why do cancer researchers study molecular events associated with mitosis?

Question 15

Mutant versions of genes that are normally involved in promoting the cell cycle are known as ________.

A) attenuators
B) proto -oncogenes
C) oncogenes
D) tumor suppressors
E) malignant genes

Question 16

Define cancer at the anatomical level.

Question 17

Describe the major cellular and molecular events that mark the entry of mitosis from G2.

Question 18

Chronic myelogenous leukemia appears to be associated with a chromosomal
rearrangement. How would a chromosomal rearrangement be responsible for this disease?

Question 19

Define cancer at the genetic level.

Question 20

Which protein combines with cyclins to exert local control of the cell cycle?

A) cyclin -dependent kinase
B) phosphatase
C) hexokinase
D) integrase
E) ATPase

Question 21

In what way can loss of heterozygosity lead to cancer?

Question 22

What is retinoblastoma, and what is its supposed genetic basis?

Question 23

Provide a simple definition of a carcinogen.

Question 24

Name three human cancers with a genetic predisposition. What appears to be the genetic cause of each?

Question 25

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?

Question 26

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

Question 27

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

Question 28

As more is learned about cancer, it has become clear that cancer, with few exceptions, has no genetic basis.

Question 29

Differentiate among the following types of genes: tumor -suppressor gene, proto -oncogene, and oncogene.

Question 30

List at least three environmental agents or factors that are known to cause cancer.

Question 31

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

Question 32

In what way might a virus contribute to cancer formation?

Question 33

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 _.
________,

Question 34

If someone has a predisposition to cancer, what genetic circumstance likely exists?

Question 35

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

Question 36

Much has been written about p53 in terms of cancer biology. What is p53, and what is its significance?

Question 37

Describe the molecular nature of mutation, as related to cancer, in a ras gene.

Question 38

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

Question 39

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

Question 40

What two properties do various types of cancer cells share?

Question 41

There are several checkpoints in the mitotic cell cycle. All occur in the S phase.

Question 42

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

Question 43

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

Question 44

A retrovirus uses reverse transcriptase to make a DNA copy of RNA.

Question 45

True or False: There are two types of retinoblastoma, familial and sporadic. In the familial form, a defective gene is generally inherited from one parent.

Question 46

When the normal retinoblastoma protein is dephosphorylated, it acts to suppress cell division by binding to and inactivating the E2F transcription factor.

Question 47

Any agent that causes damage to DNA is a potential carcinogen.

Question 48

When referring to tumor -suppressor genes and cancer, loss of heterozygosity is likely to suppress cancer formation.