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Mini II > Pre-Cancer: Molecular Basis of Cancer > Flashcards

Pre-Cancer: Molecular Basis of Cancer Flashcards

1
Q

what is the pre-cancerous condition of the stomach that leads to gastric adenocarcinoma?

A

Atrophic Gastritis of pernicious anemia

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2
Q

what pre-cancerous condition leads to melanoma in the skin?

A

dysplastic nevus

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3
Q

Barrett esophagus leads to?

A

Adenocarcinoma of esophagus

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4
Q

H. pylori infection can lead to?

A 
Adenocarcinoma of stomach
MALT lymphoma (MALToma)
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5
Q

Chronic ulcerative colitis can lead to?

A

Adenocarcinoma of colon

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6
Q

Hep B, Hep C, cirrhosis can all lead to?

A

Hepatocellular carcinoma

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7
Q

Atypical ductal hyperplasia can lead to?

A

Adenocarcinoma of boob

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8
Q

Lichen sclerosis can lead to?

A

Squamous cell carcinoma of Vulva

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9
Q

Chronic cystitis can lead to?

A

Urothelial carcinoma of urinary bladder

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10
Q

RB1- predisposition for?

A

Retinoblastoma

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11
Q

p53- predisposition for?

A

Li-Fraumeni syndrome (multiple tumors)

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12
Q

APC- predisposition for?

A

Familial adenomatous polyposis

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13
Q

NF1, NF2- predisposition for?

A 
Neurofibromatosis 1
Neurofibromatosis 2 (bilateral Schwannoma of acoustic nerve)
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14
Q

BRCA1, BRCA2- predisposition for?

A

Breast cancer, Ovarian cancer

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15
Q

MEN1, RET- predisposition for?

A

Multiple endocrine neoplasia 1 and 2

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16
Q

p16INK4A (CDKN2A)- predisposition for?

A

Melanoma

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17
Q

MSH2, MLH1, MSH6- predisposition for?

A

Hereditary non-polyposis colon cancer

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18
Q

Retinoblastoma

what is the two hit theory?
What is the MOA behind Retinoblastoma?
What are the clinical signs?
Predisposition for ___ in adolescents?

A

Loss of RB tumor suppressor gene on chromo 13. It is a malignancy of eye in children

“two-hit theory”
- one gene inactivated in germ cells, the other after birth.

  • White pupillary reflex & visual loss
  • Predisposition for Osteosarcoma in adolescence
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19
Q

Familial Adenomatous Polyposis (FAP). Leads to development of what?

A

Inactivation of APC tumor suppressor gene

Development of Colorectal carcinoma from malignant transformation of polyps by age 30

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20
Q

Multiple Endocrine Neoplasia

A

MEN II –> mutation of rET protooncogene

familial occurence is combination:

  1. medullary thyroid carcinoma
  2. bilateral pheochromocytoma
  3. hyperparathyroidism due to hyperplasia or tumor
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21
Q

Herditary Non-polyposis Colorectal Cancer (HNPCC)

A
  • familial clustering of cancers at several sites
  • colon cancers at young age (often R sided)
  • DNA mismatch repair (MSH2 and MLH1 and MSH6)

“Cluster of genes, cluster of cancer”

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22
Q

Xeroderma pigmentosum

A

Mutated Nucleotide Excision Repair (NER) enzymes.

Defect in DNA repair of UV damaged skin

Predisposition to multiple skin cancers- Basal cell carcinoma, squamous cell carcinoma, malignant melanoma

excessive photosensitivity and 2000x increase in skin cancers

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23
Q

Ataxia-telangiectasia

A

Mutated ATM gene which usually repairs DNA damaged by ionizing radiation

Predisposition to lymphoma, leukemia, breast cancer

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24
Q

Bloom’s syndrome

A

Mutated BLM gene. DNA helicase family

Predisposition to lymphoma, leukemia

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25
Q

Fanconi’s anemia

A

Mutated FAC gene

Predisposition to lymphoma, leukemia and bone marrow aplasia

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26
Q

Breast/ovarian cancer

A

Inactivated BRCA1, BRCA2 genes

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27
Q

Familial melanoma

A

Mutated p16INK4A gene

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28
Q

Overexpression of PDGFB gene or TGF-alpha

A

Astrocytoma

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29
Q

Overexpression of HST1 gene

A

Osteosarcoma

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30
Q

Amplification of FGF3 gene

A

Stomach
Bladder
Breast
Melanoma

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31
Q

Overexpression of HGF

A

Hepatocellular carcinoma

Thyroid cancer

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32
Q

amplification of ERBB2 (HER) causes ____ cancer

A

Breast carcinoma

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33
Q

Point mutation of RET causes ________ cancers

A

Multiple endocrine neoplasia 2A and B
and
Familial medullary thyroid carcinomas

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34
Q

Translocation on ABL gene

A

CHRONIC myelogenous leukemia

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35
Q

Point mutation at ABL gene

A

ACUTE lymphoblastic leukemia

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36
Q

Point mutation at BRAF gene

A

Melanoma

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37
Q

What causes burkitt lymphoma?

A

translocaiton on MYC

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38
Q

What causes neuroblastoma?

A

Amplification of N-MYC

39
Q

Point mutation in ____ gene is found in 15-20% of all cancers

A

RAS

40
Q

t(9;22)

A

Chronic myeloid leukemia (CML)

ABL, BCR genes- forms Philadelphia chromosome

41
Q

t(8;14)

A

Burkitt lymphoma

Overexpression of c-MYC, IGH

(overexpression of proto-oncogene M). You get “starry sky”.

42
Q

t(14;18)

A

Follicular lymphoma

Overexpression of BCL2 (anti-apoptosis). results in immortality of B-lymphocytes

43
Q

t(15;17)

A

Acute myeloid leukemia

PML and RARA genes

44
Q

t(11;14)

A

Mantle cell lymphoma
Cyclin D1 and IGH genes

generalized non-tender lymphadenopathy in elderly male patient

45
Q

t(11;22)

A

Ewing Sarcoma

FLI1 and EWSR1 genes
“X-ray tibia, onion-skin pattern, round-dark blue nuclei”

46
Q

Presence of _____ in >90% of tumors

A

Telomerase

47
Q

what skin condition leads to squamous cell carcinoma of skin?

A

actinic (solar) keratosis

48
Q

what precancerous condition in the oral cavity leads to oral squamous cell carcinoma?

A

oral leukoplakia

49
Q

what cancer is associated with the bronchial mucosa?

A

squamous cell carcinoma of lung. The precursor lesion is squamous metaplasia –> dysplasia

50
Q

tubular/villous adenoma can lead to what cancer

A

adenocarcinoma of colon

51
Q

endometrial hyperplasia can lead to?

A

adenocarcinoma of endometrium

52
Q

a serous borderline tumor of ovary can lead to what?

A

serous papillary cystadenocarcinoma of ovary

53
Q

inherited AR syndromes of defective DNA repair (4)

A

xeroderma pigmentosa
ataxia telangiectasia
bloom syndrome
fanconi anemia

54
Q

familial cancers (2)

A

breast and ovarian

55
Q

what are the 5 categories of oncogenes?

A
  1. GF (ex: PDGF, FGF)
  2. GF receptors (ex: EGF receptor)
  3. Signal transducers (ex: RAS, B-catenin)
  4. Cell cycle regulators (Cyclin D, CDK4, Cyclin E)
  5. transcription factor (i.e. C-MYC or N-MYC)
56
Q

Point mutaiton of K-RAS causes ____

A

colon, lung and pancreatic cancers

57
Q

point mutation of H-RAS causes ____

A

bladder and kidney tumors

58
Q

Point mutaiton of N-RAS causes ____

A

melanomas, hematologic malignancies

59
Q

List 4 growth factors?

A

PDGF-beta
FGF
TGF-alpha
HGF

60
Q

List 4 GF receptors?

A

ERBB2/HER
RET
PDGFRB
KIT

61
Q

List 3 signal transducers?

A

RAS (K, H, and N)
ABL (non-receptor tyrosine kinase)
BRAF (RAS)

62
Q

List 2 transcriptional activators?

A

MYC

n-MYC

63
Q

List 2 cell cycle regulators?

A

CCNDA1

CDK4

64
Q

what proto-oncogene causes mantle cell lymphoma?

A

CCND1

65
Q

what proto-oncogene causes melanoma?

A

CDK4

66
Q

point mutation in BRAF leads to ?

A

melanoma

67
Q

point mutation in RET leads to?

A

MEN 2a and B familial medullary thyroid carcinoma

68
Q

point mutation in KRAS leads to? (kristen rat sarcoma viral oncogene homolog)

A

pancreas and colon cancer

69
Q

RAS proto-oncogene MOA

A

When RAS is bound to GDP it is “OFF”

GF binds, GDP gets removed –> RAS-GTP = “active” and can send message to nucleus.

“GAP” GTPase associated protein helps shut down active form of RAS by converting back to inactivated RAS-GDP (cuts away phosphate).

in a mutant RAS, phosphate cannot be removed from active RAS by GAP.

70
Q

APC

function? associated cancer?

A

prevents nuclear transcription. Tumore supressor gene.

familial polyposis coli (inherited mutation)
and
sporadic colon cancer (somatic mutation)

71
Q

BRAC1 and BRCA2

function? associated cancer?

A

regulated DNA repair

breast and ovarian cancer

72
Q

RB

function? associated cancer?

A

inhibits G1 to S

retinoblastoma and osteogenic sarcoma

73
Q

NF-1

function? associated cancer?

A

encodes neurobromin 1 = GTPase that acts as negative regulator of RAS

neurofibromatosis type I

74
Q

NF-2

function? associated cancer?

A

cytoskeleton protein involved in contact inhibition

Neurofibromatosis type II- bilateral Schawannoma of acoustic nerve (hearing disturbances)

75
Q

P53

function? associated cancer?

A

inhibits G1 to S, repairs DNA, activates BAX (initiates apoptosis)

50% of all cancers
Li-Fraumeni
Oncogenesis in HPV

76
Q

VHL

function? associated cancer?

A

ubiquitin-ligase complex and hypoxia inducible factor 1a (HIF1a)

Von Hippel Lindau disease, hereditary renal cell carcinoma, pheochromocytoma and renal cysts

77
Q

PTEN

function? associated cancer?

A

regulates nuclear transcription

cowden syndrome, CARCINOMA OF ENDOMETRIUM, breast and thyroid

78
Q

WT1

function? associated cancer?

A

Transcriptional activator of genes invovled in normal development of genitorurinary tissue

Wilms’ tumor

79
Q

what is the main gene involved in neuroblastoma?

A

N-MYC

80
Q

What is Trastumuzab (Herceptin) associated with?

A

it is monoclonoal Ab against Her-2/Neu for Breast cancer

81
Q

What is the MOA of APC?

A

normal function: down-regulates Beta-Catenin and prevents its accumulation.

when APC is lost: B- catenin increases and it travels to nucleus where ther eis continuas WNT signaling causing FAP non-familial colorectal Cancer and sporadic adenoma

82
Q

What is E-Cadherin?

A

it is a cell adhesion molecule that keeps eepithelial cells attached to each other.

for tumor to spread locally and metastasize it must detach.

associated with AD familial gastric carcinoma and sporadic carcinomas.

83
Q

What is CDKN2A? (cycklin dependent kinase inhibitor 2A?

A

encodes 2 tumor suppressor genes (P16INK4a and ARF)

associated with AD famililal melanoma

84
Q

what is RB?

A

tumor suppressor that inhibits movement from G1 to S phase

85
Q

What is RB associated with?

A

retinoblastoma, osteogenic sarcoma, soft tissue carcinoma

86
Q

What is the MOA of RB?

A

RB “holds” E2F = “hypophosphorylated state” and cell replication is preventated (i.e. cell can’t move from G1 to S).

RB gets phosphorylated by cyclin D/CDK4 which then releases E2F.

If RB gets mutated, E2F is free and cells can easily go from G1 to S and cause tumor.

87
Q

What is Knudson’s 2 hit hypothesis

A

Both alleles of RB locus must be inactivaed.

40% of retinoblastoma are familial
1st hit = all somatic cells of body (one defective copy is inherited from affected parent and other copy is normal)
2nd hit =retinal cells (somatic mutation –> loss of normal RB gene –> retinoblastoma)

60% cases sporadic
cells homozygouse for mutant RB –> cancer
Recessive –> heterozygous cells are normal

88
Q

P53 MOA

A

inhibits G1 to S, repairs DNA and activates BAX.

89
Q

how many copies of the P53 must be knocked out for tumor formation?

A

both

90
Q

Li-Fraumeni syndrome

A

increased risk of carcinomas/sarcomas– inherited p53 mutation

91
Q

what causes oncogenesis in HPV?

A

viral proteins E6 and E7

bind to inhibit RB and p53

92
Q

MOA of BCL-2?

A

stabilizes mitochondrial membrane so cytochome C can’t be released. If it is inhibited, cytochrome C can leak out of mitochondria and activate apoptosis.

Translocation 14:18 overexpresses BCL-2 which prevents apoptosis of B cells and prevents apoptosis of B cells (B cell lymphoma) follicular lymphoma.

93
Q

Telomerase

A

limitless replicative potential. Normal somatic cells have 60 to 70 doublings.

telomerase is in over 90% tumors

Mini II (17 decks)

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