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Flashcards in neoplasia cancer 1 Deck (67):
1

proliferation in defiance of normal regulation

cancer

2

carcinogen

causes cancer

3

mutagen

chemical that cuases cancer

4

where does cancer begin?

in a single cell clone

5

normal gene

proto-oncogene

6

mutated gene intiating ccer

oncogen

7

what triggers the process of cell-cycle

cell cycle control sysem

8

stages of cell cycle

s g2 m g1

9

where does cell cycle start

end of G to process to S phase

10

gap in the action

no DNA being synthesized and mitosis is not occuring

11

when is gap stages

between g2 and g1

12

what occurs during S phase

Dna and Histone synthesis

13

cell division

mitosis

14

what regulates cell cycle stages

cyclins and cyclin-dependent kinases

15

what do cyclins do?

bind to and acivate cycline-dependent kinases

16

what happens to specific cyclins after phase

rapidly destroyed while cyclins for next phase are synthesized

17

longest phase

g1

18

what occurs in g1 phase?

protein synthesis and cells grow in size

19

checkpoint towards end of g1

determines if DNa after mitosis and everything else is ok to process

20

when do tumor supressors work?

late g1

21

Key regulation in cell cycle

specific cyclin in early g1 to turn on cell cycle and late g1 to turn on s-phase

22

how to convert a normal cell to a cancer cell?

more than one mutation is required

23

breats and colorectal multi-hit ex

9-11 mutatations per cancer cell

24

organization of dna in nuclei in eurkaryotes

identical

25

what wraps dna in eucaryotes?

nucleosomes

26

nucleososomes have?

2 histones3, 2h4 2h2a 2h2b

27

how to regualte gene expression?

tightly wrapping DNA around nucelosomes

28

how to increase expression?

make RNA then protein

29

what does Ez do?

add 3 mh3 to h3k27

30

role of Ez

silencing some genes

31

news flash of Ez

increased in breast and prostate cancer

32

cancer that is due to mutations in an enzyme that methylates h3k4

leukemia

33

how are epigenetic changes passed?

from daughter cell to duaghter cell

34

what does cancer always involve?

mutations
multi hit
cell cycle
epigenetics
decreased tumor suppresor
increased activity of mutant protooncogenes

35

how is rtk activitated?

growth factor binds -->rtk dimerizes-->Activated RTK phosphorylates itself

36

what happens after phosp or rtk?

1. grb2.sem-5 binds to tyr on rtk via sh2 doman
2. binds to Sos & RAS via two SH3 domains
3. activates grf to exhnage ras bound gdp for GTP which makes RAS bind to RAF
3. RAF phosphorylates MEK-
4. MEK phosphorylates MAPK
5. mapk goes to nucleus phosphorylates FOS, Jun, MYo = turn on for growth

37

Ras GTPase activity occurs why?

from a GAP (gtpase activiating protein) that regulates growth activity of the pathway by inctiviated RAS

38

mutations leads to a loss of?

Ras GTPase activiate-->Ras is always on

39

mutations in myc or fos or jun can lead to ?

cancer

40

which transcriptions factor is common in many types of cancer?

Myc

41

how is P13 kinases activated?

by activated RTK by binding to one of those phosphotyrosines on an activiated RTK

42

what does Akt do?

promote growth and survival while inhbiting apopt.

43

what does akt stimulate

mTOR that stimlates protein sysnthesis in growing or surviving cells

44

what is capable of stopping P13 system

PTEN- regulator at first step
(tumor surpressor)

45

which cyclin starts the cell cycle G1?

D-cdk

46

which cyclin ends G1 phase?

C-Cdk

47

how is the cell cycle rapidly turned on?

myc -->D-Cyclin-->phosphorylates Rb--->Rb comes of E2F-->E2F is active

48

what governs cell division to make more cells?

cell cycle

49

mitogen

component in growth factor pathaways that promote growth

50

how do mitogens regulate cell division?

by their effects during the G1-phase of the cell cycle

51

what can cause unique retinal cancer

inheritred mutation of Rb protein that prevents it from binding to E2F proteins

52

what is increase expression of RB capable of?

regulate/stop cell division that is too rapid

53

1st way p53 works/

stimulates p21-->p21 binds to c-cdk g1/s and during s to prevent further progession

54

p53 response to dna damage

phosphorylated and prevents degradation. Blocks entry into M-phase and futher progresison of cell cycle

55

strongest way p53 works

stimulates programmed cell death

56

why would p53 levels increase

resonse to large increases in RAS and MYC that turn on cell

57

what can lead to a loss of function

mutaions in tumor repressors like P53

58

what prevents the formation of D-cyclin complex

P16

59

what is persistent change in gene expression without a change in DNA sequence?

Epigenetics

60

what happens if p16 is methylated?

turns of the expression of p16-->cancer

61

what happens if developmental genes are no longer silenced

develop cancer

62

metastisis

breaking away from other cells in tumor to penetrate blood vessel or lymph vessel

63

metastiastic cells are resistant

to apoptosis and thrive independetly

64

what cuases angiognesis

hypoxia-->release of VEGF-->stimulate new growth of blood vessels

65

what drugs inhibits activit of vEGF

avastin

66

poster child for cancer drugd

gleevac

67

cancer is ___specific. Not_____specific

gene, orgran