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MCB II Block 1 > Cancer 6 > Flashcards

Cancer 6 Flashcards

1
Q

when chrom. fuse together, when they go through mitosis again every time you go through mitosis what will happen to chromatins

A

breakage

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2
Q

loss of p53 then what will happen when telomere gets too short

A

will continue proliferating

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3
Q

massive chrom. damage can result in

A

cell death, if telomerase is inactive then chrom. stabilized and have a cancer cell

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4
Q

draw what happens if a tellomeric repeat at end of one chrom is deleted

A

pg 196

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5
Q

why do sister chromatids break during mitosis if they have been fused

A

they are joined together if telomerase is lost, when the sister chromatids are separated (they were fused b/c of loss of telomerase) they have to break apart to be seaparted, its going to break randomly

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6
Q

what are the six fundamental properties altered in cancer

A 
sustained angiogenesiss
self-sufficiency in growth signals
insensitivity to antigrowth signals
evasion of apoptosis
limitless replicative potential
tissue invasion and metastasis
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7
Q

antigrowth signal lost in cancer example (think colorectal)

A

TGFbeta 2 receptor lost in (HNPCC)

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8
Q

endocrine signaling

A

secretory cell travels in blood stream and affects different sites
many are hormones

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9
Q

paracrine signaling

A

secretory cell secreting some growth factor binding to adjac. cells
molecules which act at sites in close proximity, important in development, e.g. short range growth factors, nerve to nerve, nerve to muscle

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10
Q

cancer cells influence behavior of surrounding

A

stromal cells

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11
Q

autocrine signaling

A

signaling itself

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12
Q

how does cancer do autocrine signaling

A

its signaling itself

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13
Q

draw examples of endocrine paracrine and autocrine signaling

A

pg 203

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14
Q

normal epithelial cells have to be attached via

A

integrine signaling via basal lamina

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15
Q

how can cancer cells not attach to basal lamina

A

lost integrine receptor signaling

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16
Q

TRK stand for

A

receptor tyrosing kianse

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17
Q

most growth factor receptors are

A

RTKs

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18
Q

RTK, describe how they work and what happens after ligand binds

A

two receptor bind to ligand which allows for dimerization
when ligand binds to receptor, causes conformational change which allows it to heterodiemrze with another open receptor, dimerization results in cross autophosphorylation
activated receptor activates different signaling pathways

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19
Q

PI3 kinase activation

A

activation of growth receptor
heterodimerize, activation of kinase activity
phosphorylate and activate PI-3 kinase
PI 3 kinase phorphorylates PIP2 →PIP3
PIP3 activates PKB (Akt), phorphorylates and inactivates Bad
Bad normally heterodimer with Bcl-2 (sequesters is)
when PKB phorphorylates Bad it no longer binds to Bcl-2 and Bcl-2 is active and Bcl-2 blocks apoptosis pathway which leads to cell survival b/c it blocks cell death

PTEN moves PIP3 to PIP2 so apoptosis occurs

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20
Q

PKB is also known as

A

Akt

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21
Q

draw PIP2 pathway

A

pg 207

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22
Q

What is PTEN

A

phosphatase

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23
Q

What is function of PTEN

A

removes phosphate group, moves PIP3 to PIP2 and allows apoptosis to proceed

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24
Q

describe Ras/MAPK pathway

A

activate growth facotr receptors, dimerize, activation, binding of bridging protein: GRB2 (SH2 and SH3 domains), recruits SOs (ras-Gef) which activates Ras, which activates Raf then Mek then Erk/MAPK, this reults in activation of TFs (Fos, Jun, Myc)
if activation of Myc restuls in cell proliferation

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25
Q

what are raf mek erk

A

intracellular kinase

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26
Q

genes in Ras/MAPK pathway are proto-oncogene or tumor suppressor?

A

proto-oncogene

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27
Q

draw out ras/mapk pathway

A

pg 208-209

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28
Q

there can be mutation in different genes that lead to the ___ syndrome
and different mutations in the same gene that can lead to ____ syndrome

A

same

different

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29
Q

overexpression of receptors, even normal levels of signaling what will be result

A

overactivation of pathways

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30
Q

activating mutations: tyrosine kinase domain is

A

constantly on - receptor doesn’t require signaling to activate it

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31
Q

HER family of receptors are found mutated

A

in a bunch of cancers

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32
Q

HER stand for

A

human epidermal growth factor receptor

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33
Q

HER1, 3, 4 have

A

ligand binding domain

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34
Q

HER2 is unusal b/c

A

no ligand binding domain

growth factor receptor that is always open and ready to heterodimerize with another

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35
Q

what is receptor overexpressed in 1/3 of breast cancer cases

A

HER2 (or EGFR2)

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36
Q

breast cancers where what are expressed have worst diagnosis

A

HER2

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37
Q

EGFR is also known as

A

Erb or Her receptors

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38
Q

even with low levels of EGF there will be

A

excessive stimulation of the pathways

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39
Q

monoclonal antibody that blocks HER2 signaling, what drug?

A

Trastuzumab (Herceptin)

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40
Q

if pts cancer positive for HER2 how will you treat

A

trastuzumab (Herceptin)

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41
Q

mAb stands for

A

monoclonal antibody

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42
Q

Trastuzumab (Herceptin) is what

A

monoclonal antibody that targets HER2 and blocks HER2 signaling

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43
Q

any drug that ends in mab is a

A

monoclonal antibody

44
Q

if there are HER2 splice varients, what does that mean in regards to treatment

A

Trastuzumab (Herceptin) will not be affective, poor prognosis. new drugs are in trial targeting the splice varients

45
Q

when Trastuzumab (Herceptin) binds to HER2 receptors causes

A

endocytosis

46
Q

how do we switch off RTK pathway

A

when molecule binds it activates the pathway but gets endocytosed quickly, they get monoubiquitin tag and get degraded in lysosome.

47
Q

if HER2 receptor is overactivated how does that affect EGF and ras pathway

A

pg 2018

48
Q

EGFR is associated specifically with what that helps cancer

A

cell invasion and metasesis

49
Q

How often is EGFR1 overexpressed in cancers

A

all the time! it’s very common for EGFR1 to be overexpressed in tumor/cancer

50
Q

Cetuximab how does it work

A

binds to HER1 receptor (EGFR1)

51
Q

Gefitinib (Iressa) & Erlotinib (Tarceva)

A

block receptor

block tyrosine kinase activity of EGFR1 receptor

52
Q

if drug ends in inib what does it mean

A

small molecule tyrosine kinase inhibitor

53
Q

activating mutation in EGFR1 receptor (it’s constitutively active), would you give them Cetuximab

A

no - it doesn’t need the growth factor to bind to it to be active

54
Q

activating mutation in EGFR1 receptor, what drug could you give them

A 
gefitinib (iressa)
or erlotinib (tarceva)
55
Q

Ras is very commonly mutated in

A

many cancers

esp. colorectal cancers

56
Q

loss of function in NF1 leads to

A

activation of ras

57
Q

Neurofibromatosis has complete

A

penetrance

58
Q

MOI of NF1

A

AD

59
Q

symtpoms of NF1

A

nerofibromas
cafe au lait spots
lisch nodules

60
Q

drugs to nhibit ras

A

Farnesyl transferase inhibitors

61
Q

Ras is a small

A

g protein

62
Q

Ras is there to exchange

A

exchange GDP for GTP

63
Q

in order for ras to be activated it is covalently attached to

A

small lipid group (otherwise it would just be floating in the cytoplasm)

64
Q

drugs in clinical trials to block ras do what

A

they block the covalently attachment of ras to the small lipid group, so ras won’t be at plasma membrane and won’t be able to be activated

65
Q

is ras an intermediate

A

yes

66
Q

Fos and Myc transcribe

A

cyclin D

67
Q

transcription of what transcription factors are enchanced upon growth factor receptor activation

A

fos and myc

68
Q

how are microarrays used for cancer, describe in detail

A

you spot different gene sequences on a chip and extract mRNA from tumor cells and normal cells, convert to cDNA label with fleurochrome and hybridize, then can see if there is too much or not enough expression of mRNA
tumor to red
normal to green
wherever there is red there is overexpression
wherever there is green - loss of function

69
Q

normal to green
wherever there is red there is
wherever there is green there is

A

normal to green
wherever there is red there is overexpression
wherever there is green - loss of function

70
Q

philadelphia chrom has translocation b/w

A

9 & 22

71
Q

what is result of philadelphia chrom.

A

activation of intracellular kinase (BCR-ABL)

this activates the Grb-2 Ras/map kinase pathway

72
Q

Gleevec

A

blocks kinase in cancer cells (like philadelphia chromosome)

73
Q

hormone cancers example

A

breast and prostate

74
Q

overactivate of hormone stimulating pathways are examples of

A

breast and prostate cancer

75
Q

steroid hormone, describe properties and how it works

A

lipid soluble

can bind to receptor in cytoplasm or nucleus and activate the steroid hormone receptor

76
Q

steroid hormone receptor, what kind of protein

A

TF

77
Q

target gene of steroid hormone receptor?

A

cyclin D

78
Q

estrogen receptor is a

A

TF

79
Q

one target of estrogen receptor is

A

cyclin d

80
Q

tamoxifen

A

binds to estrogen receptor but doesn’t activate - competitive inhibition

81
Q

what drug is used in breast cancer to stop cyclin d from being activated

A

tamoxifen

82
Q

PSA blood test with digital rectal exam for

A

prostate cancer

83
Q

where is most cancer found in prostate

A

peripheral and transitional zone

84
Q

stage 1 prostate carcinoma

A

cancer still located in prostate,

85
Q

stage 2 prostate carcinoma

A

local invasion, tumor spread throughout tissue in prostate

86
Q

stage III prostate carcioma

A

invasion to surrounding structures

87
Q

stage IV prostate carcinoma

A

metastisis

88
Q

what does staging tell regarding cancer

A

how much it has spread

89
Q

AR (androgen receptor) is what kind of receptor

A

steroid hormone - therefore also a transcription factor

90
Q

describe how AR (androgen receptor) works

A

AR receptor when active transcribe gene targets, includes cyclin D& oncomeres (microRNA that target tumor suppressor gene),

91
Q

describe how AR (androgen receptor) works

A

AR receptor when active transcribe gene targets, includes cyclin D& oncomir (microRNA that target tumor suppressor gene),

92
Q

AR (androgen receptor) binds to

A

hormone response element

93
Q

hormone response element is in promoter for

A

cyclin D and PSA

94
Q

if there is overexpression of PSA it tells you

A

the cell is also overexpressing cyclin D - means there is probably tumor growing

95
Q

PSA is specifically a marker of the

A

androgen receptor

96
Q

draw out Androgen receptor activation pathway and PSA

A

pg 240

97
Q

colorectal cancer that invovles cyclin D

A

beta catenin (look this up)

98
Q

oncomir

A

microRNA associated w/ cancer

99
Q

early stage of prostate cancer smptoms

A 
frequent urination
nocturia
haematuria
dysuria
impotence
100
Q

advanced prostate cancer symptoms

A

will add’l have bone pain

spinal cord compression

101
Q

what is androgen ablation

A

Androgen receptor antagonists (flutamide, bicalutamide) = main therapeutic intervention for the treatment of hormone-sensitive prostate cancer

102
Q

what is flutamide

A

androgen receptor antagonist

103
Q

how does flutamide work

A

fluatmide which is androgen receptor antagonist. flutamid binds and inactivates receptor. just like tamoxifin the flutamide is not killing the cancer cells, it blocks the signaling pathway.

104
Q

one treatment of cancer is to block androgen receptor, what will cancer eventually do

A

.eventually cancers become androgen indepdent and will progress and metastasise.

105
Q

one treatment of cancer is to block androgen receptor, what will cancer eventually do

A

.eventually cancers become androgen indepdent and will progress and metastasize

MCB II Block 1 (12 decks)

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