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MCB II Block 1 > Cancer II 3 > Flashcards

Cancer II 3 Flashcards

1
Q

PKb (Akt) phosphorylates

A

Bad - inhibits it

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2
Q

Draw out the Pi3K pathway

A

pg 102-103

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3
Q

PTEN is a (tumor suppressor or proto-oncogene)

A

tumor suppressor gene

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4
Q

what is the second most commonly lost tumor suppressor gene in cancer

A

PTEN

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5
Q

in protate cancer there is often loss of what

A

PTEN

p53

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6
Q

males with BRCA2 have increased risk for what

A

breast & prostate cancer

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7
Q

what is overactive in prostate cancer

A

PSA is increased

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8
Q

loss of function of BRCA genes in prostate cancer & increased expression of PSA, what specfically is the increased expression of PSA telling you

A

AR signaling pathway is overactive,

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9
Q

active PKB phosphorylates BAD and results in

A

increased cell survival

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10
Q

besides phosphorylating bad what does active Akt do

A

more acetyl CoA

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11
Q

cancer cells take up massive amounts of

A

glucose

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12
Q

how do cancer cells show up on PET scan

A

a lot of glucose in cancer cells

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13
Q

Warburg effect

A

somethign that happens in cancer cells
thorught to be early event in cancer progression
cells underoing lots of glycolysis but they aren’t using the oxygen even though they have enough. thought that in the initial stages, the cells do become hypoxic b/c they haven’t stimulated growth of own blood vessles yet
then they stimulate angiogenesis and oxygen and nutrients is restored, but they still undergo anaerobic glycolysis

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14
Q

lactic acid produced via whe warburg effect is thought to be

A

toxic to the surrounding cells

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15
Q

warburg effect & wound healing

A

it happens during initial stages of wound healing but then the cells revert again. so cells take up huge amount of glucose during wound healing to thelp them with the very rapid proliferation. also angiogenesis in wound healing

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16
Q

Patient was a 24-year-old woman with a nonmetastatic infiltrating ductal carcinoma of the breast.

Hx: Identical triplet sister developed breast cancer, previous year.
3rd identical triplet had bilateral prophylactic mastectomy at age 24.
Patient’s mother had cancer of uterine cervix at age of 22.
Both maternal grandparents had died of colon cancer in their sixties.

Patient underwent a mastectomy with gross resection of primary tumour
what is running in the family?
Does mother having cervical cancer have anything to do with the breast cancer?
grandparents with colorectal cancer have anything to do with the breast cancer?

A

BRCA mutation
No - cervical cancer major risk factor is HPV
No

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17
Q

mutation in BRCA1 gene - have they inherited one or two loss of function mutations

A

one

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18
Q

what has to happen for pt to inherit a BRCA1 mutation to have a tumor

A

second mutation/second hit

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19
Q

abnormal BRCA1 have high risk of

A

breast & ovarian cancer

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20
Q

when is herceptin given

A

overexpression in Her2 receptor for breast cancer

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21
Q

IKK is a

A

kinase

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22
Q

IKK inhibts

A

kapa B kinase

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23
Q

IkB when active what does it do

A

inhibtis NF-kB

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24
Q

when IKK is active

A

phorphorylates IkB

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25
Q

what is overactive in multiple myeloma

A

IKK pathway

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26
Q

NF-KB is

A

proto-oncogene

it increases expression of different genes involved in surival and proliferation of cell

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27
Q

NF-kB trascribes

A
  • so transcribes IAPs, BCL-XL & BCL-2
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28
Q

NF-kB increases what genes

A

invovled in survival

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29
Q

IkB inhibits

A

NF-kB

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30
Q

what does IKK do when active

A

phorphorylates IkB

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31
Q

velcade is a

A

drug, proteasome inhibitor

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32
Q

how does velcade work

A

there is overactivation of IKK signaling pathway in cancer.
phosphorylation of ikb and will get poly-ubiquinated b/c of that but the drug blocks the proteasome so it can’t et destroyed in the proteosome because the drug blocks the proteosome! so it’s still not releasting NF-kB

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33
Q

what need to happenf or tumor cells to keep replciating

A

reactivation of telomerase

angiogenesis

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34
Q

vasculogenesis

A

forming new vessels from scratch

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35
Q

angiogenesis

A

new blood vessels from existing bessels

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36
Q

in wound healing what occurs

A

angiogenesis

37
Q

when cells are hypoxic they secrete

A

vegF

38
Q

vegF does what

A

binds to nearby endothelial tissue and cause those endothelial cells to proliferate and migrate in toward the hypoxic tissue

39
Q

when does angiogenesis normally happen

A

Embryonic development

Menstrual cycle & pregnancy

Wound healing (macrophages release VEGF, FGF, PDGF)

Vascularisation of ischaemic tissue

40
Q

in response to ischemia stroke you wan to

A

increase angiogenesis

41
Q

what are some conditions with excessive angiogenesisi

A 
Psoriasis
Rheumatoid arthritis
Endometriosis & Menorrhagia
Atherosclerosis
Cancer
42
Q

what are some conditions with insufficient angiogenesis

A 
Stroke
Heart disease
Chronic wounds
Venous ulcers
Infertility
43
Q

angiogenesis normally very tightly

A

regulated

44
Q

in cancer what happens regarding angiogenesis

A

too many positive regulators of angiogenesis

45
Q

thrombospondin inhibits

A

angiogenesis

46
Q

angiostatin inhibits

A

angiogenesis

47
Q

VEGF stimultaes

A

angiogenesis

48
Q

thrombospondin

A

inhibits angiogenesis

49
Q

VEGF stands for

A

vascular endothelial growth factor

50
Q

when wound is repaired, amount of oxygen cells needs is restored and

A

angiogenesis will stop

51
Q

as tumor grows cells in middle become

A

hypoxic

52
Q

when cells become hypoxic they secrete

A

VEGF

53
Q

VEGF

A

diffuses in extracellular space and binds to nearby endothelial cells and activates VEGF receptors

54
Q

when VEGF binds to its receptors

A

activates RAS/MAP kinase pathway in the endothelial cells so they migrate towards the VEGF secretion, they proliferate and migrate into tumor

55
Q

VEGF is normal?

A

yes, it’s a normal response, in cancer it’s just on too much

56
Q

newly formed blood vessels are ?

it’s relationship to cancer

A

permeable - haven’t been stabilized properly so it’s really easy for cancer cells to get into vessels

57
Q

if there’s enough oxygen there is low amount of what TF

A

HIF

58
Q

HIF stands for

A

hypoxia inducible factor

59
Q

HIF

A

TF - transcribes VEGF

60
Q

what transcription factor transcribes VEGF

A

HIF

61
Q

if cells don’t have enough O2 they have accumulation of

A

HIF - starts to transcribe VEGF

62
Q

VE stands for

A

vascular endothelial cells

63
Q

what happens when cells are migrating?

A

in order for endothelial cells to migrate they have to secrete MMP to digest path through the surrounding tissue, decrease in cell- cell adhesion so they can move. eventually will have endothelial maturation and stabilization of them by the pericytes

64
Q

any migrating cell will have secretion of

A

MMP

65
Q

TIMP stands for?

A

tissue inhibitors of MMP

66
Q

TIMPS do waht

A

block MMP activity

67
Q

major activator of angiogenesis

A

VEGF

68
Q

hypoxia

A

cell doesn’t have enough oxygen

69
Q

hypoxia results in accumulation of

A

HIF

70
Q

HIF binds to

A

HRE

71
Q

HRE

A

region in promoter of genes responsive to hypoxia and results in promotion of VEGF

72
Q

HRE stands for

A

hypoxia response element

73
Q

HIF in presence of normoxia, proline hydroxylase does what to HIF

A

hydroxylates it

74
Q

normoxia

A

normal oxygen conditions

75
Q

HIF is always

A

produced in cells

76
Q

hydroxylated HIF recognized by

A

PVHL

77
Q

PVHL is part of

A

ubiquitn ligase complex

78
Q

PVHL

A

recognizes hydroxylated HIF and degrade it in protosome

79
Q

if cells become hypoxic PVHL cannot

A

hydroxylate HIF

80
Q

if there’s no HIF hyroxylated it wno’t

A

get polyubiquinated, will accumulate in cell

81
Q

VHL stands for

A

von Hippel-Lindau

82
Q

VHL MOI

A

AD

83
Q

VHL the pt inherits what

A

one LOF mutation in PVHL

84
Q

what happens if there is second hit in PVHL

A

if there is no PVHL, won’t get polyubiquinated, so increased VEGF expression even when there is enough oxygen.

85
Q

pts with VHL have what

A

hemangioblastoma -

86
Q

what is hemangioblastoma

A

tumor of blood vessel

87
Q

Haemangioma are what kind of tumor

A

benign

88
Q

Haemangioma within them there are too many

A

pro-angiogenic facotrs

not enough anti-angiogenic inhibitors

89
Q

when IkB is phosphorylated what does this do

A

targets IkB for polyubiquination and degradation in protosome - this frees NfkB

MCB II Block 1 (12 decks)

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