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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
RAS
signal transducing oncoprotein GTP binding protein (G proteins)
26
KRAS mutation
carcinoma in colon and pancreas
27
HRAS mutation
bladder tumor
28
NRAS mutation
hematopoietic tumor
29
RAS activation
active when binds GTP inactive when binds GDP activated RAS stimulates MAP cascade
30
GAP
influences GTPase activity of RAS
31
mutations in RAS
constitutive activated - bound to GTP
32
downstream to RAS
RAS/RAF/MAP kinase pathway
33
BRAF
mutation downstream in the RAS pathway | -development of benign nevi
34
development of melanoma
mutation in RAS/RAF/MAP kinase pathway
35
chronic myeloid leukemia
ABL translocation from 9 to 22 -associates with BCR constitutively active ABL-BCR tyrosine kinase
36
polycythemia vera and myeloproliferative disorders
mutations in JAK2 kinase
37
MYC
oncogene | -activate genes that are involved in proliferation
38
burkit lymphoma
B-cell tumor overexpression of MYC protein -translocation from chromsome 8 to 14
39
neuroblastoma
amplification of N-MYC
40
CDKs
regulate progression of cell through cell cycle -activated by cyclin phosphorylate target proteins
41
cyclin D
overexpressed in cancers of breast, esophagus, liver, and lymphomas
42
CDK4
overexpressed in melanomas, sacromas, and glioblastomas
43
CDKI
inhibitors of CDKs | -exert negative control over cell cycle
44
p16
CDKI | mutated in pancreatic carcinomas, glioblastomas, leukemias, etc.
45
S phase
point of no return in cell cycle
46
G1-S checkpoint
checks for DNA damage
47
G2-M checkpoint
monitors completion of DNA replication and checks whether cell can safely initiate mitosis -important for cells exposed to ionizing radiation
48
G1-S cell cycle arrest
regulated by p53 - induction of p21
49
tumor suppressor gene
apply brakes to cell proliferation push into apoptosis or cause cell to differentiate
50
retinoblastoma
RB tumor suppressor gene familial and sporadic requires two hits
51
two-hit hypothesis
two mutations (one on each allele) required for to produce retinoblastoma
52
familial retinoblastoma
inherit one mutated copy | -spontaneous mutation is second hit
53
sporadic retinoblastoma
- spontaneous mutation of both alleles - hit 1 and 2 - more rare
54
LOH
loss of heterozygosity
55
von-hippel lindau
tumor suppressor gene that causes familial clear cell renal carcinomas
56
RB protein
active when hypophosphorylated inactive when hyperphosphorylated (during G1-S transition) reinforces G1 - gap between mitosis and DNA replication
57
gap 1
between mitosis (M) and DNA replication (S)
58
gap 2
between DNA replication (S) an mitosis (M)
59
pass G1 checkpoint
obligated to complete mitosis
60
initiation of DNA replication
E-CDK2 and cyclin E cyclin E - dependent on E2F transcription factors
61
activity of RB
``` when active (hypophosphorylated) -binds to E2F - so no cyclin E ``` - methods of action: - binds and sequesters E2F - recruit chromatin remodeling histomes
62
inactivation of RB
mitogenic signaling to CDK4/6 - cyclin D complex - phosphorylate RB - make it inactive E2F free to transcribe cyclin E
63
E2F
transcription factor for cyclin E allows DNA replication to occur
64
absent RB
eg. retinoblastoma no brakes on cell cycle
65
cyclin D
inactivates RB - hyperphosphoryation
66
li-framueni syndrome
inherited defect in p53 -predisposition to get a second hit and develop cancer increased risk before age 50
67
function of p53
transcription factor -sense cellular stress activates cell cycle arrest induces permanent cell cycle arrest trigger programmed cell death
68
temporary cell cycle arrest
quiescence
69
permanent cell cycle arrest
senescence
70
action of p53
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
miRNAs
bind to 3-untranslated region of mRNA -to prevent translation mir34 - activated by p53
72
DNA damage pathway
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
ataxia telangiectasia
mutation with ATM (senses DNA damage)
74
p21
inhibits cyclin-CDK complexes and phosphorylation of RB | -prevents cell from entering G1
75
GADD45
DNA repair stimulated by p53
76
BAX
apoptosis stimulated by p53
77
irradiation and chemotherapy
target cells by DNA damage and apoptosis requires p53 function lung and colorectal cancers - often have mutations - don't respond to these therapies
78
familial adenomatous polyposis
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
function of APC
down-regulate beta-catenin | -WNT signaling absence - degrades beta catenin
80
WNT sigaling
blocks APC activity allows beta-catenin to translocate to nucleus
81
beta-catenin activity
upregulates cellular proliferation (through TCF) -downregulated by APC mutations can lead to cancer
82
E-cadherins
bind beta-catenin -and inactivate it (contact inhibited) -loss of this contact - leads to carcinoma
83
TGF-beta
inhibitor of proliferation pancreatic cancer and colon cancer
84
cowden syndrome
mutated PTEN frequent benign growths
85
NF1
one mutant allele leads to benign neurofibromas and optic nerve gliomas produces neurofibromin
86
neurofibromin
regulates signal transduction of RAS | -facilitates active/inactive form transition
87
wilms tumor
pediatric kidney cancer | -WT1
88
nevoid basal cell carcinoma syndrome
PTCH mutation | -tumor suppressor gene

PBD I Exam 2 (18 decks)

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