Deck 16: The Genetics of Cancer

Question 1

Define cancer at the anatomical level.

Answer 1

Cancer is the uncontrolled proliferation of cells and the ability of cells to metastasize or migrate to other sites to form secondary growths.

Question 2

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

Answer 2

G1/S,G2/M,M

Question 3

Why do cancer researchers study molecular events associated with mitosis?

Answer 3

Although mitosis is a basic process related to genetic and general biological studies,it is also a significant event in the cell cycle.The cell cycle is regulated by a variety of gene products,which,when altered by mutation,may lead to cancer.

Question 4

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 5

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

Question 6

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

Question 7

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 8

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

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

Question 9

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

Question 10

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

Question 11

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

Question 12

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

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

Question 13

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?

Question 14

What functional differences exist between various cyclins?

Question 15

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

Question 16

What is the significance of CDK?

Question 17

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

Question 18

Define cancer at the genetic level.

Question 19

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

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

Question 20

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 21

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

Question 22

What two properties do various types of cancer cells share?

Question 23

Provide a simple definition of a carcinogen.

Question 24

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

Question 25

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

Question 26

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

Question 27

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

Question 28

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 29

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

Question 30

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

Question 31

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

Question 32

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

Question 33

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

Question 34

In what way might a virus contribute to cancer formation?

Question 35

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

Question 36

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 37

In what way can loss of heterozygosity lead to cancer?

Question 38

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

Question 39

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

Question 40

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

Question 41

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

Question 42

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

Question 43

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

Question 44

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

Question 45

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

Question 46

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

Question 47

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

Question 48

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