Final: Cancer Genetics

Question 1

what is cancer

Answer 1

a genetic disease of cells in multicellular organisms

Question 2

how does cancer begin

Answer 2

with genes that are supposed to regulate cell growth and division in organs of the body

complicated process

Question 3

progression of cancer

Answer 3

starts with a single cell that acquires multiple mutations

each mutation along the way starts a new clone of cells

mutations must be of particular types in particular genes

Question 4

mutations in 3 specific kinds of genes promote cancer

Answer 4

genes that: regulate the cell cycle

terminate a cell’s life

protect DNA against mutation

Question 5

genes that regulate the cell cycle

Answer 5

stimulate or repress cell growth

Question 6

genes that terminate a cells life

Answer 6

apoptosis genes

Question 7

genes that protect DNA against mutation

Answer 7

genes for DNA lesion repair

Question 8

3 other genetic causes of cancer

Answer 8

chromosome rearrangements

disruption of epigenetic programs

interference by viral genomes

Question 9

3 possible cellular decisions at checkpoints

Answer 9

GO: proceed to next stage of cell growth

STOP: pause until further notice

DIE

Question 10

gene names for possible cellular decisions

Answer 10

GO: proto-oncogenes

STOP: tumor suppressor genes

DIE: apoptosis genes

Question 11

proto-oncogenes

Answer 11

stimulate cells to grow

if a mutation causes overactivity: oncogene, helps cause cancer

if a mutation inactivates a proto-oncogene: cannot cause cancer

Question 12

types of proto-oncogenes

Answer 12

membrane signal receptor proteins (growth factors)

cytoplasmic signal transduction proteins (growth factors)

transcription factors for growth genes

Question 13

how genes cause cell growth

Answer 13

growth factor attaches to membrane signal receptor protein

alters a signal transduction protein

transcription factor in cell is turned on for growth

Question 14

real examples of proto oncogenes

Answer 14

IGF1: protein growth hormone (insulin like growth factor)

RAS: signal transduction protein

Question 15

RAS

Answer 15

a family of G-proteins

become oncogenes due to mutations that make them permanently turned on

60% of cancers show a mutation of RAS

Question 16

4 ways a proto-oncogene becomes an oncogene

Answer 16

translocation or transposition: reconnects a gene to wrong promotor so it’s turned on too much

gene amplification: makes duplicate copies of a gene so too much product is made

point mutation in CRM control element: turns up gene expression too high

point mutation in protein coding region: new version of protein with too strong an effect

Question 17

tumor suppressor genes

Answer 17

15 kinds

many stop cells from dividing

Question 18

biological functions of tumor suppressor genes

Answer 18

repress genes needed for cell growth

halt cell cycle to repair DNA damage

promote or cause apoptosis

promote cell adhesion

Question 19

p53 guardian of the genome

Answer 19

DNA-binding protein with 4 subunits

multifunctional transcription factor that turns on genes that shut down the cell cycle

stops cells at G1/S, intimate DNA repair, cause apoptosis

Question 20

p53 found non-functional in __ to __% of tumors

Answer 20

50-60%

Question 21

retinoblastoma gene

Answer 21

when both RB alleles are knocked out in a single retina cell you get retinoblastoma

Question 22

apoptosis

Answer 22

several pathways controlled by mitochondria

Question 23

dominant and recessive tumorigenic effects

Answer 23

proto-oncogenes: dominant (gain of function)

tumor suppressor genes: recessive (loss of function)

apoptosis: recessive (loss of function)

Question 24

ECM and cancer

Answer 24

tissues are organized by ECM

it has regulatory functions in normal development and differentiating cells

Question 25

contact inhibition

Answer 25

cells stop growing when they are touching other cells

monolayer forms then they stop growing

Question 26

cancer and contact inhibition

Answer 26

cancer cells do not respond to contact inhibition

form multiple layers of cells

Question 27

telomeres and cancer

Answer 27

embryonic stem cells can regenerate their own telomeres

cancer cells have their own telomerase and can divide an unlimited number of time (no Hayflick limit)

Question 28

Hayflick limit

Answer 28

number of generations a cell can go through before telomeres are too short

Question 29

familial cancer

Answer 29

inherited tendency to cancer

Question 30

xeroderma pigmentosa

Answer 30

can’t go out in sun (UV) light

mutation in base dimer excision repair systems

Question 31

hereditary nonpolyposis colorectal cancer

Answer 31

mutations in DNA mismatch repair system

tumor suppressor lesion repair gene

Question 32

BRCA1 & BRCA2

Answer 32

genes involved in DNA regular, repair, and apoptosis

mutations increase risk for breast, ovarian, and prostate cancer

Question 33

chronic myelogenous leukemia and the Philadelphia chromosome

Answer 33

P chromosome result of reciprocal translocation btw chromosomes 9 and 22 (must happen at specific breakpoints)

causes CML 4,500 cases and 2,400 deaths

Question 34

ABL1 and BCR in CML

Answer 34

ABL1: growth regulation on chromosome 9

BCR: signal transduction on chromosome 22

fusion of these genes causes expression of growth (ABL1) whenever BCR is used

causes white blood cells grow uncontrollably

Question 35

acute promyelocytic leukemia

Answer 35

reciprocal translocation of chromosomes 15 and 17

Question 36

anti cancer molecules

Answer 36

block specific signal transduction proteins

Gleevec and Sutent inhibit tyrosine kinases

DCA (dichloroacetic acid) restores normal apoptosis to cancer cells

Question 37

can’t stop all cells from having a mutant gene, but we can stop…

Answer 37

genes from being expressed sometimes