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Neoplasia Flashcards

1
Q

somatic mutation hypothesis of cancer

A

cell growth, differentiation, and survival are under genetic control and malignant transformation is due to mutations in specific classes of genes

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2
Q

3 classes of genes involved in cancer

A

growth promoters
growth suppressors
caretakers

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3
Q

Growth Promoters

A

mutations ACTIVATE encoded protein

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4
Q

growth suppressors

A

mutations INACTIVATE encoded protein

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5
Q

caretakers

A

doesnt inhibit or activate, but promotes stability of genome (proteins involved in DNA repair)– when inactivated, likelihood of mutation events in either oncogenes or tumor suppressor genes increases

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6
Q

6 phenotypic hallmarks of cancer

A

1) dysregulation of cell proliferation (too proliferative)
2) insensitivity to growth inhibitory signals
3) evasion of apoptosis
4) limitless replicative potential
5) angiogenesis
6) invasion and metastasis

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7
Q

gene products involved in apoptosis or cell senescence

A
  • pro or anti-apoptotic proteins

- immortalization genes (telomerase)

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8
Q

landscaper genes

A

proteins involved in regulating angiogenesis

proteins involved in cell-cell and cell-matrix adhesion

proteolytic enzymes req for invasion

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9
Q

proto-oncogene

A

gene that encodes a protein that mediates or stimulates cell proliferation

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10
Q

oncogene

A

inappropriately activated proto-oncogene, either by mutation or changed expression

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11
Q

6 types of proteins encoded by oncogenes

A
  • growth factors
  • growth factor receptors
  • signal transduction molecules
  • steroid hormone receptors
  • transcription factors
  • cell cycle proteins
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12
Q

ex of growth factor

A

v-sis which encodes PDGF in an autocrine stimulation loop

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13
Q

ex of growth factor receptor

A

transmembrane receptor tyrosine kinase
EGF-R in lung
HER-2-neu in other parts

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14
Q

ex cell cycle proteins

A

cyclins and CDKs

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15
Q

ras

A

GTP binding protein involved in signal transduction from RTKs

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16
Q

ki ras

A

lung, ovarian, pancreatic cancer

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17
Q

N-ras

A

leukemias

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18
Q

3 ex signal transduction molecules

A
  • non-receptor protein tyrosine kinases: src
  • cytoplasmic serine/threonine kinases: raf
  • GTP-binding proteins: ras
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19
Q

dominant mutations

A

gain of function

  • Qualitative: changes in structure of gene resulting in uncontrolled function
  • Quantitative: up-regulation of expression of structurally normal protein
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20
Q

ras pathway

A

growth factor receptor (tyrosine kinase)

  • ->adaptor proteins
  • ->ras GDP-GTP exchange
  • ->raf
  • ->MEK
  • -> MAP-kinase
  • ->activated transcription factor (SRF)
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21
Q

Ras mutations that diminish GTPase activity

A

increase ras signaling output (because cant break down GTP)

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22
Q

gene amplification mechanism

A

place proto-oncogene adjacent to powerful tissue-specific promoter, resulting in overexpression

ex-burkit lymphoma

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23
Q

chromosome rearrangement mechanism

A

can create fusion genes–result in unregulated or aberrant activity and transformation

ex-philadelphia chromosome

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24
Q

ex of nuclear regulatory factor

A

persistant expression or overexpression of myc transcription factor in

  • neuroblastoma/glioblastoma (n-myc)
  • small cell lung cancer (l-myc)
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25
philadelphia chromosome
fuses proto-oncogene c-abl with gene bcr, with loss of abl-regulatory domains
26
why are TSG sometimes referred to as recessive oncogenes?
both alleles of a TSG must be "knocked out" for transformation-- knocking a gene that normally inhibits tumor growth
27
loss of heterozygosity
- inheritance of one defective copy of TSG - second hit- transformation occurs one band on PCR- LOH
28
4 mechanisms of LOH
- mitotic recombination - chromosome mis-segregation during mitosis (nondisjunction during G2/M checkpoint-->deletion of WT allele - epigenetic gene inact - random pt mutation (unlikely)
29
four key regulators in cell cycle
p16 cyclin D CDK4 Rb
30
regulator of G1/S phase transition
Rb
31
Rb inhibits by
shutting down E2F-->repress transcription of a number of genes regulated by cyclin D/CDK -->phos and inact Rb-->release E2F
32
why do people only get tumors like retinoblastomas and osteosarcomas with Rb mutation?
we don't know- in most tissue, defective E2f triggers apoptosis in p53 manner, maybe these are resistant
33
p53 mech
Dna damage--P53-->activates CDK inhibitor P21-->induces cell cycle arrest at G1 and G2 to try to repair-->if cant repair, p53 triggers apoptosis
34
MDM2
binds to p53 and inactivates it
35
how do DNA viruses induce neoplasia
encode proteins that bind and inactivate TSGs ex) HPV E6- binds and degrades P53 and HPV E7- binds under-phosed form of RB
36
how many gatekeeper gene does each cell type have
only one or a few
37
caretaker genes
prevent mutation mutation means that if the DNA has a damage, it cant be repaired and may lead to cancer behave genetically like TSG
38
three major types of DNA repair systems
1) Mismatch repair genes 2) Nucleotide excision repair genes 3) recombination repair genes
39
Hereditary non-polyposis colon cancer (HNPCC)
- mismatch repair gene issue - -decreased proofreading capacity-->errors in repetitive nucleotide sequences, so they will have expansions or contractions in DNA (instability)
40
xeroderma pigmentosum
-nucleotide excision repair issue normal skin fibroblasts repair UV radiation dmage to DNA by inserting new pases after ecision of pyrmidine dimers, but if you have this disease you can't do that and can develop skin cancer
41
BRCA1, BRCA2
recombination repair genes issue women have mutations in these have lifetime risks of breast and ovarian cancer - genes are thought to play a role in repair of doble strand DNA breaks, recombination, etc
42
autosomal dominant cancer list
``` retinoblastoma-rb Li-fraumeni syndrome- p53 familial adenomatous polyposis- apc gene familial atypical multiple mole melanoma- p16 neurofibromatosis- neurofibromin breast/ovarian- brca1, brca2 HNPCC- dna mismatch ```
43
autosomal recessive
zeroderma pigmentosum- dna excision repair ataxia-telangiectasia- defective DNA repair sensor Bloom syndrome- recomb repair defect fanconi anemia- recomb repair defect
44
2 methods to evade apoptosis
- dysregulation of anti-apoptotic signals | - loss of pro-apoptotic signals
45
apoptotic signaling pathways
PTEN, Akt, p53, bax, bid
46
Hayflick index
normal cells can divide 50-60 times before telomeric erosion cells that have been transformed go well beyond this and eventualy reach a second phase termed "crisis"
47
crisis stage of cell
a cell in crisis usually dies, but can sometimes escape and reach crisis and become immortalized often will have resumed expression of telomerase, or found another way to avoid senescence
48
in order for tumors to grow, they MUST
induce an accompanying blood supply (angiogenesis)
49
formation of new blood vessels is dependent on
ratio of angiogenic inducers to anti-angiogenic agents | --tipping the balance during tumorgenesis-->angiogenic switch
50
angiogenesis inducers
VEGF, bFGF
51
VEGF
upregulated by hypoxia and often upregulated near areas of tumor necrosis
52
VHL
inhibits VEGF | part of the ubiquitin igase complex--mediates HIF1, resulting in HIF1 degradation
53
if VHL keeps HIF1 levels low..
prevents production of VEGG and other angiogenic factors
54
angiogenesis inhibitors
angiostatin endostatin altered antithrombin III thrombospondin-2
55
what else is also angiogenesis dependent?
metastasis
56
in order to metastasize, tumor cells must have the following properties (8)
``` 1- detachment 2- matrix degradation 3- cell-matrix attachments 4- angiogenesis 5- motility and migration 6- vascular extravasation 7- avoiding immune survellinace 8- survive and proliferate in new foreign microenvironment ```
57
cadherins
transmembrane glycoprotiens that mediate homotypic cell-cell interactions at adherens junctions loss of cadherin gene-->metastatsis therefore, function at tumor/metastasis suppressor
58
TIMPs`
tissue inhibitors of metalloproteinases-- tumor cells destroy local basement membrane and invade stroma -->enter lymphatic or blood vessels if they decrease expression of these it helps
59
integrin switching
tumor cells often show altered integrin expression patterns--> results in decreased adhesion to BM and increased adhesiveness and migrration over alternative ECM components
60
malignant cells and integrins
indifferent to loss of integrin-mediated signaling and resist apoptotic signals generated by detachment from matrix components basis for anchorage independent growth
61
growth factors stimulate
tumor cell motility IGF, FGFs, TGF-b, hepatocyte growth factor
62
what helps protect tumor cells in circulation?
tumor cell interactions with fibrin, platelets, and clotting factors
63
how do tumor cells avoid immune surveillance
"cloak" tumor-specific antigens and inactivate leukocytes in the vicinity
64
3 targets of therapy for metastasis
1) anti-adhesive agents 2) matrix metalloproteinase inhibitors (MMPIs) 3) Anti-motility agents
65
MMPIs
block degradaton of matrix, activation of proteases, and release of matrix-bound growth factors
66
taxanes
block microtubule cycling
67
CAI
inhibits Ca influx through non-voltage gated Ca channels therefore inhibits proliferation, production of MMP2, motility, and signaling of endothelial cells
68
clonal progression
involves successive rounds of mutation adn natural selection repeated rounds of mutation and selection for cells with increasing capacity for proliferation--how they get stronger with time
69
tumor heterogeneity
not all cells in a tumor carry the same genetic defects
70
DNA methylation
methylation of C in Cpg islands--> down regulates gene expression hypermeth around TSG
71
molecular therapeutics
- specific antagonists - cytotoic monoclonal antibodies (binds to specific tuors that overexpress tumor specific antigen) - molecualr therapy targeting oncogene products (TK inhibitors) - antisense oligodeoxynucleotides
72
differentiation therpay
tumor cells are often unable to differnetiate forcible induction of differentiation most effective-ATRA- rearrangement between PML and RAR a genes- activates RARa ligand complexes-->myeloid differentation

Path3 (11 decks)

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