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Patho > neoplasia cancer 1 > Flashcards

neoplasia cancer 1 Flashcards

1
Q

proliferation in defiance of normal regulation

A

cancer

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2
Q

carcinogen

A

causes cancer

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3
Q

mutagen

A

chemical that cuases cancer

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4
Q

where does cancer begin?

A

in a single cell clone

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5
Q

normal gene

A

proto-oncogene

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6
Q

mutated gene intiating ccer

A

oncogen

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7
Q

what triggers the process of cell-cycle

A

cell cycle control sysem

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8
Q

stages of cell cycle

A

s g2 m g1

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9
Q

where does cell cycle start

A

end of G to process to S phase

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10
Q

gap in the action

A

no DNA being synthesized and mitosis is not occuring

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11
Q

when is gap stages

A

between g2 and g1

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12
Q

what occurs during S phase

A

Dna and Histone synthesis

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13
Q

cell division

A

mitosis

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14
Q

what regulates cell cycle stages

A

cyclins and cyclin-dependent kinases

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15
Q

what do cyclins do?

A

bind to and acivate cycline-dependent kinases

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16
Q

what happens to specific cyclins after phase

A

rapidly destroyed while cyclins for next phase are synthesized

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17
Q

longest phase

A

g1

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18
Q

what occurs in g1 phase?

A

protein synthesis and cells grow in size

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19
Q

checkpoint towards end of g1

A

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

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20
Q

when do tumor supressors work?

A

late g1

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21
Q

Key regulation in cell cycle

A

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

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22
Q

how to convert a normal cell to a cancer cell?

A

more than one mutation is required

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23
Q

breats and colorectal multi-hit ex

A

9-11 mutatations per cancer cell

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24
Q

organization of dna in nuclei in eurkaryotes

A

identical

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25
Q

what wraps dna in eucaryotes?

A

nucleosomes

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26
Q

nucleososomes have?

A

2 histones3, 2h4 2h2a 2h2b

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27
Q

how to regualte gene expression?

A

tightly wrapping DNA around nucelosomes

28
Q

how to increase expression?

A

make RNA then protein

29
Q

what does Ez do?

A

add 3 mh3 to h3k27

30
Q

role of Ez

A

silencing some genes

31
Q

news flash of Ez

A

increased in breast and prostate cancer

32
Q

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

A

leukemia

33
Q

how are epigenetic changes passed?

A

from daughter cell to duaghter cell

34
Q

what does cancer always involve?

A 
mutations
multi hit
cell cycle
epigenetics
decreased tumor suppresor
increased activity of mutant protooncogenes
35
Q

how is rtk activitated?

A

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

36
Q

what happens after phosp or rtk?

A
  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
  4. RAF phosphorylates MEK-
  5. MEK phosphorylates MAPK
  6. mapk goes to nucleus phosphorylates FOS, Jun, MYo = turn on for growth
37
Q

Ras GTPase activity occurs why?

A

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

38
Q

mutations leads to a loss of?

A

Ras GTPase activiate–>Ras is always on

39
Q

mutations in myc or fos or jun can lead to ?

A

cancer

40
Q

which transcriptions factor is common in many types of cancer?

A

Myc

41
Q

how is P13 kinases activated?

A

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

42
Q

what does Akt do?

A

promote growth and survival while inhbiting apopt.

43
Q

what does akt stimulate

A

mTOR that stimlates protein sysnthesis in growing or surviving cells

44
Q

what is capable of stopping P13 system

A

PTEN- regulator at first step

tumor surpressor

45
Q

which cyclin starts the cell cycle G1?

A

D-cdk

46
Q

which cyclin ends G1 phase?

A

C-Cdk

47
Q

how is the cell cycle rapidly turned on?

A

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

48
Q

what governs cell division to make more cells?

A

cell cycle

49
Q

mitogen

A

component in growth factor pathaways that promote growth

50
Q

how do mitogens regulate cell division?

A

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

51
Q

what can cause unique retinal cancer

A

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

52
Q

what is increase expression of RB capable of?

A

regulate/stop cell division that is too rapid

53
Q

1st way p53 works/

A

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

54
Q

p53 response to dna damage

A

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

55
Q

strongest way p53 works

A

stimulates programmed cell death

56
Q

why would p53 levels increase

A

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

57
Q

what can lead to a loss of function

A

mutaions in tumor repressors like P53

58
Q

what prevents the formation of D-cyclin complex

A

P16

59
Q

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

A

Epigenetics

60
Q

what happens if p16 is methylated?

A

turns of the expression of p16–>cancer

61
Q

what happens if developmental genes are no longer silenced

A

develop cancer

62
Q

metastisis

A

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

63
Q

metastiastic cells are resistant

A

to apoptosis and thrive independetly

64
Q

what cuases angiognesis

A

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

65
Q

what drugs inhibits activit of vEGF

A

avastin

66
Q

poster child for cancer drugd

A

gleevac

67
Q

cancer is ___specific. Not_____specific

A

gene, orgran

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