Biology of Neoplasms

Question 1

3 classes of genes involved in cancer

Answer 1

growth promotors

growth suppressors

caretakers- ensures stability of genome, repair genes

Question 2

DNA alterations seen in cancer

Answer 2

point mutations

deletion/insertion

repeat alterations

amplification- multiple copies of a gene

translocation- chimeric gene

Question 3

epigenetic changes

Answer 3

can be heritable or acquired, but do not change the DNA sequence

usually result in gene silencing

ex. DNA methylation, RNA silencers

Question 4

phenotypic hallmarks of cancer

Answer 4

dysregulation of cell proliferation by constituative growth stimulatory pathways

insensitivity to growth inhibition

evasion of apoptosis

limitless replicative potential

angiogenesis

invasion and metastasis

Question 5

oncogenes

Answer 5

required for or promote cell proliferation

Question 6

tumor suppressor genes

Answer 6

inhibit proliferation

Question 7

caretaker genes

Answer 7

repair genes

Question 8

landscaper genes

Answer 8

products required for malignant phenotype- involved in angiogenesis, cell-cell and cell matrix adhesion, and proteolytic enzymes required for invasion

Question 9

protooncogene examples

Answer 9

growth factors, growth factor receptors, signal tranducers, steroid hormone receptors, transcription factors, cell cycle proteins

Question 10

common growth factor oncogene

Answer 10

v-sis- platelet derived growth factor

Question 11

common growth factor receptor oncogene

Answer 11

EGF-R family

Question 12

cell cycle proteins

Answer 12

cyclins and cyclin dependent kinases

Question 13

signal tranduction muscles

Answer 13

non receptor protein tyrosine kinases

serine/threonine kinases

GTP binding proteins- mutation of ras gene is most common abnormality of dominant oncogenes in human tumors

Question 14

activation of protooncogenes

Answer 14

gain of function mutations- dominant, only one needed

qualitative- change in the shape of the gene

quantitative- change in the numbre expressed

Question 15

EGFR in lung cancer

Answer 15

mutations in the tyrosine kinase domain of EGFR- constituitively activated

most common in exons 19 and 21

drugs bind to ATP binding site and provide competitive inhibition to receptor activation

Question 16

are tumor suppressor genes dominant or recessive?

Answer 16

recessive- need to lose both copies to develop cancer

Question 17

two hit hypothesis

Answer 17

1 inactivated gene is inherited, 1 gene is inactivated during life- susceptibility

Question 18

loss of heterozygosity

Answer 18

when one gene product is lost, you will only see one PCR band

nondisjunction

mitotic replication

gene conversion

deletion

point mutations

Question 19

what process are tumor suppressor genes usually found

Answer 19

cell cycle checkpoints

Question 20

retinoblastoma

Answer 20

regulatory point between G1 and S regulated by cyclin D/CDK

inhibits passage into S phase, and deletion results in excessive growth

Question 21

p16

Answer 21

cyclin dependent kinase inhibitor- shuts down cell cycle

Question 22

p53

Answer 22

transcription responsible for cell cycle arrest, and loss results in mutation frequency increases

activated by DNA damage

activates p21 which blocks cell cycle. DNA will be repaired if possible, otherwise causes apoptosis

most common mutation seen in cancer

mutations can be dominant- unusual for tumor suppressors

Question 23

human papilloma virus

Answer 23

binds to p53 (e6) and Rb (e7) and inactivate them, causing cancer

Question 24

BRCA are what type of genes

Answer 24

caretaker- repair genes

Question 25

microsatellites

Answer 25

short tandem repeats- prone to slippage during DNA replication and thus errors