Deck 19: Cancer and Regulation of the Cell Cycle

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

A protein functions as a cell-cycle regulator that causes cell death (apoptosis)to a damaged cell.What is the symbol given to this protein?

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

Answer 2

D

Question 3

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) alteration mutations
B) passenger mutations
C) carrier mutations
D) indirect mutations
E) insignificant mutations

Answer 3

B

Question 4

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

Question 5

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

Question 6

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

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

Question 7

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

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

Question 8

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

Question 9

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

Question 10

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

Question 11

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) There is insufficient information to answer this question.

Question 12

Why do cancer researchers study molecular events associated with mitosis?

Question 13

Provide a definition of cancer at the genetic level.

Question 14

Which of the following general mechanisms appear to be involved in the formation of cancer cells?

A) genomic instability, DNA repair failure, chromatin modifications
B) inversions, operon formation, methylation
C) RNA failure, DNA phosphorylation, phosphorylation of adenyl cyclase
D) transdetermination, mutation, allosteric interactions
E) suppression, tabulation, projection

Question 15

What is the name of the protein that combines with cyclins to exert local control of the cell cycle?

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

Question 16

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

Question 17

What is the significance of CDK?

Question 18

What functional differences exist between various cyclins?

Question 19

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

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

Question 20

Provide a definition of cancer at the anatomical level.

Question 21

What are two properties that various types of cancer cells share?

Question 22

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

Question 23

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

Question 24

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

Question 25

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

Question 26

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.Why the difference?

Question 27

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

Question 28

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

Question 29

Provide a simple definition of a carcinogen.

Question 30

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

Question 31

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

Question 32

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 33

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

Question 34

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

Question 35

In what way might a virus contribute to cancer formation?

Question 36

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

Question 37

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

Question 38

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

Question 39

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

Question 40

In what way can loss of heterozygosity lead to cancer?

Question 41

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

Question 42

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

Question 43

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

Question 44

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

Question 45

There are two types of retinoblastoma,familial and sporadic.In the familial form,one generally inherits a defective gene from one parent.

Question 46

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

Question 47

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

Question 48

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