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MOD - Neoplasm > Neoplasia - oncogenes and tumor suppressor genes > Flashcards

Neoplasia - oncogenes and tumor suppressor genes Flashcards

1
Q

“governor” of the cell cycle

A

RB:
Tumor Suppressor Gene
inhibitor of cell cycle progression

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2
Q

RB function

A

inhibitor of G1/S transition

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3
Q

RB protein

A

Retinoblastoma protein

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4
Q

RB familial syndromes

A

Familial B/L retinoblastoma syndrome (retinoblastoma, osteosarcoma, etc)

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5
Q

RB sporadic cancers

A
  • U/L Retinoblastoma

- Osteosarcoma carcinomas of breast, colon, lung

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6
Q

Tumor Suppressor genes

A

Loss of function (can’t stop growth)

Need BOTH ALLELES KO

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7
Q

Oncogenes

A

Gain of function (abnormal growth)

Need ONE ALLELE to be KO

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8
Q

proto-oncogene

A

Normal genes that regulate cell cycle and proliferation

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9
Q

E7 viral oncoprotein

A 
HPV
Inactivates Rb (>>Rb cannot bind to E2F >> progress thru G1/S>>uncontrolled growth)
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10
Q

“guardian of the genome”

A

TP53:
Tumor Suppressor Gene
enables genomic stability - regulates cell cycle progression, DNA repair, cell senescence, apoptosis

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11
Q

TP53 protein

A

p53 protein

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12
Q

TP53 function

A

Responses to DNA damage or hypoxia:

  • senescence
  • cell cycle arrest at G1 for DNA repair *
  • apoptosis
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13
Q

TP53 familial syndrome

A

Li-Fraumeni syndrome (diverse cancers)

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14
Q

TP53 sporadic cancers

A

most human cancers - most frequently mutated gene in cancer

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15
Q

APC gene

A

tumor suppressor gene
inhibitor of mitogenic signaling pathways
THINK - colonic neoplasia

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16
Q

APC protein

A

adenomatous polyposis coli protein

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17
Q

APC function

A

degrades B-catenin to inhibit WNT signaling (decrease proliferation)

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18
Q

APC familial syndrome

A

familial colonic polyps and carcinomas

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19
Q

APC sporadic cancers

A

carcinomas of stomach, colon, pancreas, melanoma
THINK - Colon Cancer: APC KO (increased polyp risk)&raquo_space; K-RAS KO (formation of polyp)&raquo_space; p53,SMADs/increased COX KO (carcinoma)

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20
Q

VHL gene

A

tumor suppressor gene

inhibits “pro-growth” programs of metabolism

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21
Q

VHL protein

A

Von Hippel Lindau (VHL) protein

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22
Q

VHL function

A

inhibitor/degredation of hypoxia-induced transcription factors (i.e. HIF1-alpha)&raquo_space; for response to hypoxia&raquo_space; increase VEGF and PDGF

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23
Q

VHL familial syndromes

A

Von Hippel Lindau Syndrome (cerebellar hemangioblastoma, retinal angioma, renal cell carcinoma, pheochromocytoma)

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24
Q

Cerebellar hemangioblastoma

A

VHL familial

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25
Q

Retinal angioma

A

VHL familial

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26
Q

Renal Cell Carcinoma

A

VHL sporadic and familial

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27
Q

VHL sporadic cancer

A

Renal Cell Carnicoma

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28
Q

Two-hit hypothesis

A

RB - both copies of gene must be KO
Familial - one already KO, other KO is somatic
Sporadic - both KOs are somatic

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29
Q

pheochromocytoma

A

VHL

30
Q

Chromosome 3

A

VHL

31
Q

Angiogenesis stimulator, blood vessels

A

VHL

32
Q

Governor of cell cycle

A

RB

33
Q

Guardian of the Genome

A

p53

34
Q

hypophosphorylated RB

How is it inactivated?

A 
hypOp = active.
hypERp = inactivated; can be done by HPV E7 binding to active RB
35
Q

chromosome 17

A

TP53

36
Q

E6 viral oncoprotein

A

HPV,

Inactivates p53

37
Q

E6 cancers

A

cervical carcinoma

squamous cell carcinomas of head and neck

38
Q

hypophosphorylated p53

A

hpOph = active

39
Q

p53 and DNA damage cell cycle arrest mechanism

A

Normal: DNA damage sensed by ATM/ATR kinase-containing complexes&raquo_space; kinases phosph p53&raquo_space; p53 liberated from MDM2 (inhibitor)&raquo_space;
p53 causes p21 transcription&raquo_space; p21 inhibits CDK4&raquo_space; CDK4 maintains RB hypOph&raquo_space; blocks cell cycle

40
Q

LiFraumeni-Syndrome

A

inherit one defective copy of TP53

41
Q

5q21

A

APC

42
Q

colonic tumors

A

70% to 80% of sporadic are APC

43
Q

WNT and B-catenin

A

APC, colon cancer

44
Q

increased levels of angiogenic GF and alterations in cellular metabolism

A

VHL loss of function mutation

45
Q

NF1 protein

A

Neurofibromin-1

46
Q

NF1 function

A

Tumor suppressor gene - inhibits mitogenic signaling pathway - inhibits RAS/MAPK signaling

47
Q

NF1 familial syndrome

A

NF type1 (neurofibromas&raquo_space;COT» malignant peripheral nerve sheath tumors)

48
Q

NF1 sporadic cancers (2)

A

neuroblastoma, juvenile myeloid leukemia

49
Q

NF2 protein

A

Merlin

50
Q

NF2 function

A

Tumor suppressor gene - inhibits mitogenic signaling pathway - cytoskeletal stability, Hippo pathway signaling

51
Q

NF2 familial syndromes

A

NF type2 (benign B/L acoustic schwannoma and meningioma)

52
Q

NF2 sporadic cancers

A

schwannoma, meningioma

53
Q

No merlin

A

NF2 - cannto est stable cell-to-cell junctions and do not arrest cycle

54
Q

BRCA1, BRCA2 genes

A

tumor suppressor genes

DNA repair factors

55
Q

BRCA1, BRCA2 proteins

A

Breast Cancer-1

Breast Cancer-2

56
Q

BRCA1, BRCA2 Function

A

repair of ds-DNA

57
Q

BRCA1, BRCA2 familial syndromes

A
  • Familial breast (M/F) and ovarian carcinoma

- Chronic lymphocytic leukemia (BRCA2)

58
Q

TGF-B function

A

Tumor suppressor gene
Loss-of-function
Inhibits proliferation

59
Q

Colon cancer, endometrial, stomach cancer

A

TGF-B type II receptor

60
Q

MYC

A

mutation = oncogene

Transcription factor, gain of function

61
Q

MYC function

A
  • Activated by RAS/MAPK
  • proto-oncogene: activates expression of cell growth genes (D cyclins, rRNA, Warburg); telomerase; reprogram somatic cells into pluripotent stem cells
62
Q

c-MYC, t(8;14)

A

Burkitt Lymphoma (ch8)

63
Q

Burkitt Lymphoma

A

EBV
t(8;14)
MYC oncogene (c-myc)

64
Q

n-MYC

A

neuroblastoma

65
Q

L-MYC

A

lung carcinoma

66
Q

Philadelphia Chromosome

A

CML

67
Q

Initiating fusion gene of CML

A

BCR-ABL

68
Q

deletion

A 
RB gene (ch13) = retinoblastoma
VHL (ch3) = (-) tumor suppresison
69
Q

BCR-ABL chromosomes

A

BCR = ch22

ABL=ch9

70
Q

BCR function and ABL function

A

BCR function - drives self association of BCR-ABL

ABL function - RTK activity

71
Q

Cancer associate with BCR-ABL

A

Chronic Myelogenous Leukemia (CML)

MOD - Neoplasm (5 decks)

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