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PBD I Exam 2 > Neoplasia III > Flashcards

Neoplasia III Flashcards

1
Q

androgen receptor gene

A

AR

-used to determine tumor clonality

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2
Q

clonality in lymphocytes

A

look at Ig and T cell receptor rearrangements

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3
Q

haploinsufficiency

A

loss of gene function due to loss of single allele

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4
Q

tumor suppressor genes

A

must lose both alleles

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5
Q

proto-oncogenes

A

only need to lose one allele

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6
Q

X-linked markers

A

females are mosaics of X inactivation

  • can assess the clonality of cancer based on this
  • examine the X-linked genes
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7
Q

fundamental changes resulting in malignant phenotype

A

self-sufficient growth signaling - no external stimuli

insensitive to growth inhibitor signals - TGF-beta and CDKIs

evasion of apoptosis - inactivate p53

limiteless potential

sustained angiogenesis

ability to evade and metastasize

defects in repair of DNA

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8
Q

oncogenes

A

from mutations in proto-oncogenes

ability to promote cell growth in absence of growth signals

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9
Q

oncoproteins

A

products of oncogene

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10
Q

proto-oncogene

A

in normal cell
-growth factors, or their receptors, signal transducers, transcription factors, cell cycle components

-mutations gives rise to oncogenes

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11
Q

steps in cell proliferation

A

1 binding growth factor
2 activation of GF receptor - signal transduction across membrane
3 transmission of signal across cytosol
4 nuclear regulatory factors initiate transcription
5 entry into cell cycle

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12
Q

self-sufficiency in growth

A

oncogenes - oncproteins

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13
Q

growth factor signaling

A

often paracrine

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14
Q

cancer cell growth factors

A

can become autocrine

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15
Q

glioblastoma growth factor

A

express both PDGF and PDGF receptor

-autocrine signaling

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16
Q

growth factor receptors

A

tyrosine kinases

-usually transiently activated

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17
Q

oncigenic grwoth factor receptors

A

constitutive dimerization and activation

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18
Q

neuroendocrine growth factor receptor

A

RET receptor
-in parafollicular C cells of thyroid, adrenal medulla, parathyroid cell precursors

mutations - MEN types 2a and 2b

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19
Q

MEN 2a

A

mutation in RET extracellular domain

  • constitutive dimerization
  • medullary thyroid carcinomas and adrenal and PT tumors
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20
Q

MEN 2b

A

mutation in RET cytoplasmic domain

  • alter specificity of tyrosine kinase
  • thyroid and adrenal tumors
  • no parathyroid involvement
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21
Q

FLT3

A

FMS-like tyrosine kinase 3 receptor

  • mutation can lead to constitutive signaling
  • detected in myeloid leukemias
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22
Q

gastrointestinal stromal tumors

A

constitutively activating mutation in c-KIT or PDGFR

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23
Q

ERBB1

A

receptor for EGF

  • overexpressed in squamous cell carcinoma of lung
  • also tumors of head and neck
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24
Q

ERBB2

A

receptor for EGF

-overexpressed in breast cancer and adenocarcinoma of ovary, lung, stomach, and salivary gland

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25
Q

RAS

A

signal transducing oncoprotein

GTP binding protein (G proteins)

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26
Q

KRAS mutation

A

carcinoma in colon and pancreas

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27
Q

HRAS mutation

A

bladder tumor

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28
Q

NRAS mutation

A

hematopoietic tumor

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29
Q

RAS activation

A

active when binds GTP
inactive when binds GDP

activated RAS stimulates MAP cascade

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30
Q

GAP

A

influences GTPase activity of RAS

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31
Q

mutations in RAS

A

constitutive activated - bound to GTP

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32
Q

downstream to RAS

A

RAS/RAF/MAP kinase pathway

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33
Q

BRAF

A

mutation downstream in the RAS pathway

-development of benign nevi

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34
Q

development of melanoma

A

mutation in RAS/RAF/MAP kinase pathway

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35
Q

chronic myeloid leukemia

A

ABL translocation from 9 to 22
-associates with BCR

constitutively active ABL-BCR tyrosine kinase

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36
Q

polycythemia vera and myeloproliferative disorders

A

mutations in JAK2 kinase

37
Q

MYC

A

oncogene

-activate genes that are involved in proliferation

38
Q

burkit lymphoma

A

B-cell tumor

overexpression of MYC protein

-translocation from chromsome 8 to 14

39
Q

neuroblastoma

A

amplification of N-MYC

40
Q

CDKs

A

regulate progression of cell through cell cycle
-activated by cyclin

phosphorylate target proteins

41
Q

cyclin D

A

overexpressed in cancers of breast, esophagus, liver, and lymphomas

42
Q

CDK4

A

overexpressed in melanomas, sacromas, and glioblastomas

43
Q

CDKI

A

inhibitors of CDKs

-exert negative control over cell cycle

44
Q

p16

A

CDKI

mutated in pancreatic carcinomas, glioblastomas, leukemias, etc.

45
Q

S phase

A

point of no return in cell cycle

46
Q

G1-S checkpoint

A

checks for DNA damage

47
Q

G2-M checkpoint

A

monitors completion of DNA replication and checks whether cell can safely initiate mitosis

-important for cells exposed to ionizing radiation

48
Q

G1-S cell cycle arrest

A

regulated by p53 - induction of p21

49
Q

tumor suppressor gene

A

apply brakes to cell proliferation

push into apoptosis
or cause cell to differentiate

50
Q

retinoblastoma

A

RB tumor suppressor gene
familial and sporadic

requires two hits

51
Q

two-hit hypothesis

A

two mutations (one on each allele) required for to produce retinoblastoma

52
Q

familial retinoblastoma

A

inherit one mutated copy

-spontaneous mutation is second hit

53
Q

sporadic retinoblastoma

A
  • spontaneous mutation of both alleles
  • hit 1 and 2
  • more rare
54
Q

LOH

A

loss of heterozygosity

55
Q

von-hippel lindau

A

tumor suppressor gene that causes familial clear cell renal carcinomas

56
Q

RB protein

A

active when hypophosphorylated
inactive when hyperphosphorylated (during G1-S transition)

reinforces G1 - gap between mitosis and DNA replication

57
Q

gap 1

A

between mitosis (M) and DNA replication (S)

58
Q

gap 2

A

between DNA replication (S) an mitosis (M)

59
Q

pass G1 checkpoint

A

obligated to complete mitosis

60
Q

initiation of DNA replication

A

E-CDK2 and cyclin E

cyclin E - dependent on E2F transcription factors

61
Q

activity of RB

A 
when active (hypophosphorylated)
-binds to E2F - so no cyclin E
  • methods of action:
  • binds and sequesters E2F
  • recruit chromatin remodeling histomes
62
Q

inactivation of RB

A

mitogenic signaling to CDK4/6 - cyclin D complex

  • phosphorylate RB
  • make it inactive

E2F free to transcribe cyclin E

63
Q

E2F

A

transcription factor for cyclin E

allows DNA replication to occur

64
Q

absent RB

A

eg. retinoblastoma

no brakes on cell cycle

65
Q

cyclin D

A

inactivates RB - hyperphosphoryation

66
Q

li-framueni syndrome

A

inherited defect in p53
-predisposition to get a second hit and develop cancer

increased risk before age 50

67
Q

function of p53

A

transcription factor
-sense cellular stress

activates cell cycle arrest
induces permanent cell cycle arrest
trigger programmed cell death

68
Q

temporary cell cycle arrest

A

quiescence

69
Q

permanent cell cycle arrest

A

senescence

70
Q

action of p53

A

bound to MDM2 normally and this decreases its half life

  • with DNA stress or damage - released from MDM2
  • increases its half life

transcribes genes that result in cell cycle arrest and apoptosis

71
Q

miRNAs

A

bind to 3-untranslated region of mRNA
-to prevent translation

mir34 - activated by p53

72
Q

DNA damage pathway

A

ATM and ATR (sensors)

downstream - phosphorylate p53 and DNA repair proteins
-pause in cell cycle (p21)

-p53 also increases GADD45 (repair)

apoptosis stimulated by BAX and PUMA transcription

73
Q

ataxia telangiectasia

A

mutation with ATM (senses DNA damage)

74
Q

p21

A

inhibits cyclin-CDK complexes and phosphorylation of RB

-prevents cell from entering G1

75
Q

GADD45

A

DNA repair

stimulated by p53

76
Q

BAX

A

apoptosis

stimulated by p53

77
Q

irradiation and chemotherapy

A

target cells by DNA damage and apoptosis

requires p53 function

lung and colorectal cancers - often have mutations - don’t respond to these therapies

78
Q

familial adenomatous polyposis

A

mutations in APC

  • one mutant allele can lead to thousands of adenomatous polyps
  • can undergo malignant transformation

both copes must be mutated for tumor to arise

79
Q

function of APC

A

down-regulate beta-catenin

-WNT signaling absence - degrades beta catenin

80
Q

WNT sigaling

A

blocks APC activity

allows beta-catenin to translocate to nucleus

81
Q

beta-catenin activity

A

upregulates cellular proliferation (through TCF)
-downregulated by APC

mutations can lead to cancer

82
Q

E-cadherins

A

bind beta-catenin
-and inactivate it (contact inhibited)

-loss of this contact - leads to carcinoma

83
Q

TGF-beta

A

inhibitor of proliferation

pancreatic cancer and colon cancer

84
Q

cowden syndrome

A

mutated PTEN

frequent benign growths

85
Q

NF1

A

one mutant allele leads to benign neurofibromas and optic nerve gliomas

produces neurofibromin

86
Q

neurofibromin

A

regulates signal transduction of RAS

-facilitates active/inactive form transition

87
Q

wilms tumor

A

pediatric kidney cancer

-WT1

88
Q

nevoid basal cell carcinoma syndrome

A

PTCH mutation

-tumor suppressor gene

PBD I Exam 2 (18 decks)

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