Final: Cancer Genetics Flashcards Preview

Genetics > Final: Cancer Genetics > Flashcards

Flashcards in Final: Cancer Genetics Deck (37)
1

what is cancer

a genetic disease of cells in multicellular organisms

2

how does cancer begin

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

complicated process

3

progression of cancer

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

4

mutations in 3 specific kinds of genes promote cancer

genes that: regulate the cell cycle

terminate a cell's life

protect DNA against mutation

5

genes that regulate the cell cycle

stimulate or repress cell growth

6

genes that terminate a cells life

apoptosis genes

7

genes that protect DNA against mutation

genes for DNA lesion repair

8

3 other genetic causes of cancer

chromosome rearrangements

disruption of epigenetic programs

interference by viral genomes

9

3 possible cellular decisions at checkpoints

GO: proceed to next stage of cell growth

STOP: pause until further notice

DIE

10

gene names for possible cellular decisions

GO: proto-oncogenes

STOP: tumor suppressor genes

DIE: apoptosis genes

11

proto-oncogenes

stimulate cells to grow

if a mutation causes overactivity: oncogene, helps cause cancer

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

12

types of proto-oncogenes

membrane signal receptor proteins (growth factors)

cytoplasmic signal transduction proteins (growth factors)

transcription factors for growth genes

13

how genes cause cell growth

growth factor attaches to membrane signal receptor protein

alters a signal transduction protein

transcription factor in cell is turned on for growth

14

real examples of proto oncogenes

IGF1: protein growth hormone (insulin like growth factor)

RAS: signal transduction protein

15

RAS

a family of G-proteins

become oncogenes due to mutations that make them permanently turned on

60% of cancers show a mutation of RAS

16

4 ways a proto-oncogene becomes an oncogene

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

17

tumor suppressor genes

15 kinds

many stop cells from dividing

18

biological functions of tumor suppressor genes

repress genes needed for cell growth

halt cell cycle to repair DNA damage

promote or cause apoptosis

promote cell adhesion

19

p53 guardian of the genome

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

20

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

50-60%

21

retinoblastoma gene

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

22

apoptosis

several pathways controlled by mitochondria

23

dominant and recessive tumorigenic effects

proto-oncogenes: dominant (gain of function)

tumor suppressor genes: recessive (loss of function)

apoptosis: recessive (loss of function)

24

ECM and cancer

tissues are organized by ECM

it has regulatory functions in normal development and differentiating cells

25

contact inhibition

cells stop growing when they are touching other cells

monolayer forms then they stop growing

26

cancer and contact inhibition

cancer cells do not respond to contact inhibition

form multiple layers of cells

27

telomeres and cancer

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)

28

Hayflick limit

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

29

familial cancer

inherited tendency to cancer

30

xeroderma pigmentosa

can't go out in sun (UV) light

mutation in base dimer excision repair systems

31

hereditary nonpolyposis colorectal cancer

mutations in DNA mismatch repair system

tumor suppressor lesion repair gene

32

BRCA1 & BRCA2

genes involved in DNA regular, repair, and apoptosis

mutations increase risk for breast, ovarian, and prostate cancer

33

chronic myelogenous leukemia and the Philadelphia chromosome

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

34

ABL1 and BCR in CML

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

35

acute promyelocytic leukemia

reciprocal translocation of chromosomes 15 and 17

36

anti cancer molecules

block specific signal transduction proteins

Gleevec and Sutent inhibit tyrosine kinases

DCA (dichloroacetic acid) restores normal apoptosis to cancer cells

37

can't stop all cells from having a mutant gene, but we can stop...

genes from being expressed sometimes