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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
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

Patho (9 decks)

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