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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
what are raf mek erk
intracellular kinase
26
genes in Ras/MAPK pathway are proto-oncogene or tumor suppressor?
proto-oncogene
27
draw out ras/mapk pathway
pg 208-209
28
there can be mutation in different genes that lead to the ___ syndrome and different mutations in the same gene that can lead to ____ syndrome
same | different
29
overexpression of receptors, even normal levels of signaling what will be result
overactivation of pathways
30
activating mutations: tyrosine kinase domain is
constantly on - receptor doesn't require signaling to activate it
31
HER family of receptors are found mutated
in a bunch of cancers
32
HER stand for
human epidermal growth factor receptor
33
HER1, 3, 4 have
ligand binding domain
34
HER2 is unusal b/c
no ligand binding domain | growth factor receptor that is always open and ready to heterodimerize with another
35
what is receptor overexpressed in 1/3 of breast cancer cases
HER2 (or EGFR2)
36
breast cancers where what are expressed have worst diagnosis
HER2
37
EGFR is also known as
Erb or Her receptors
38
even with low levels of EGF there will be
excessive stimulation of the pathways
39
monoclonal antibody that blocks HER2 signaling, what drug?
Trastuzumab (Herceptin)
40
if pts cancer positive for HER2 how will you treat
trastuzumab (Herceptin)
41
mAb stands for
monoclonal antibody
42
Trastuzumab (Herceptin) is what
monoclonal antibody that targets HER2 and blocks HER2 signaling
43
any drug that ends in mab is a
monoclonal antibody
44
if there are HER2 splice varients, what does that mean in regards to treatment
Trastuzumab (Herceptin) will not be affective, poor prognosis. new drugs are in trial targeting the splice varients
45
when Trastuzumab (Herceptin) binds to HER2 receptors causes
endocytosis
46
how do we switch off RTK pathway
when molecule binds it activates the pathway but gets endocytosed quickly, they get monoubiquitin tag and get degraded in lysosome.
47
if HER2 receptor is overactivated how does that affect EGF and ras pathway
pg 2018
48
EGFR is associated specifically with what that helps cancer
cell invasion and metasesis
49
How often is EGFR1 overexpressed in cancers
all the time! it's very common for EGFR1 to be overexpressed in tumor/cancer
50
Cetuximab how does it work
binds to HER1 receptor (EGFR1)
51
Gefitinib (Iressa) & Erlotinib (Tarceva)
block receptor | block tyrosine kinase activity of EGFR1 receptor
52
if drug ends in inib what does it mean
small molecule tyrosine kinase inhibitor
53
activating mutation in EGFR1 receptor (it's constitutively active), would you give them Cetuximab
no - it doesn't need the growth factor to bind to it to be active
54
activating mutation in EGFR1 receptor, what drug could you give them
``` gefitinib (iressa) or erlotinib (tarceva) ```
55
Ras is very commonly mutated in
many cancers | esp. colorectal cancers
56
loss of function in NF1 leads to
activation of ras
57
Neurofibromatosis has complete
penetrance
58
MOI of NF1
AD
59
symtpoms of NF1
nerofibromas cafe au lait spots lisch nodules
60
drugs to nhibit ras
Farnesyl transferase inhibitors
61
Ras is a small
g protein
62
Ras is there to exchange
exchange GDP for GTP
63
in order for ras to be activated it is covalently attached to
small lipid group (otherwise it would just be floating in the cytoplasm)
64
drugs in clinical trials to block ras do what
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
is ras an intermediate
yes
66
Fos and Myc transcribe
cyclin D
67
transcription of what transcription factors are enchanced upon growth factor receptor activation
fos and myc
68
how are microarrays used for cancer, describe in detail
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
normal to green wherever there is red there is wherever there is green there is
normal to green wherever there is red there is overexpression wherever there is green - loss of function
70
philadelphia chrom has translocation b/w
9 & 22
71
what is result of philadelphia chrom.
activation of intracellular kinase (BCR-ABL) | this activates the Grb-2 Ras/map kinase pathway
72
Gleevec
blocks kinase in cancer cells (like philadelphia chromosome)
73
hormone cancers example
breast and prostate
74
overactivate of hormone stimulating pathways are examples of
breast and prostate cancer
75
steroid hormone, describe properties and how it works
lipid soluble | can bind to receptor in cytoplasm or nucleus and activate the steroid hormone receptor
76
steroid hormone receptor, what kind of protein
TF
77
target gene of steroid hormone receptor?
cyclin D
78
estrogen receptor is a
TF
79
one target of estrogen receptor is
cyclin d
80
tamoxifen
binds to estrogen receptor but doesn't activate - competitive inhibition
81
what drug is used in breast cancer to stop cyclin d from being activated
tamoxifen
82
PSA blood test with digital rectal exam for
prostate cancer
83
where is most cancer found in prostate
peripheral and transitional zone
84
stage 1 prostate carcinoma
cancer still located in prostate,
85
stage 2 prostate carcinoma
local invasion, tumor spread throughout tissue in prostate
86
stage III prostate carcioma
invasion to surrounding structures
87
stage IV prostate carcinoma
metastisis
88
what does staging tell regarding cancer
how much it has spread
89
AR (androgen receptor) is what kind of receptor
steroid hormone - therefore also a transcription factor
90
describe how AR (androgen receptor) works
AR receptor when active transcribe gene targets, includes cyclin D& oncomeres (microRNA that target tumor suppressor gene),
91
describe how AR (androgen receptor) works
AR receptor when active transcribe gene targets, includes cyclin D& oncomir (microRNA that target tumor suppressor gene),
92
AR (androgen receptor) binds to
hormone response element
93
hormone response element is in promoter for
cyclin D and PSA
94
if there is overexpression of PSA it tells you
the cell is also overexpressing cyclin D - means there is probably tumor growing
95
PSA is specifically a marker of the
androgen receptor
96
draw out Androgen receptor activation pathway and PSA
pg 240
97
colorectal cancer that invovles cyclin D
beta catenin (look this up)
98
oncomir
microRNA associated w/ cancer
99
early stage of prostate cancer smptoms
``` frequent urination nocturia haematuria dysuria impotence ```
100
advanced prostate cancer symptoms
will add'l have bone pain | spinal cord compression
101
what is androgen ablation
Androgen receptor antagonists (flutamide, bicalutamide) = main therapeutic intervention for the treatment of hormone-sensitive prostate cancer
102
what is flutamide
androgen receptor antagonist
103
how does flutamide work
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
one treatment of cancer is to block androgen receptor, what will cancer eventually do
.eventually cancers become androgen indepdent and will progress and metastasise.
105
one treatment of cancer is to block androgen receptor, what will cancer eventually do
.eventually cancers become androgen indepdent and will progress and metastasize

MCB II Block 1 (12 decks)

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