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Gen Path > Growth Factors, Cell Signaling, Neoplasia > Flashcards

Growth Factors, Cell Signaling, Neoplasia Flashcards

1
Q

Genes that promote cell proliferation and survival

A

Proto-oncogenes

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2
Q

Proline-stimulated macs - result?

A

Fibroblast differentiation –> collagen production

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3
Q

TGF-B - source

A

Macs!, plts, endothelia, all cells

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4
Q

TGF-B - functions (promotion, inhibition)

A

Promotion: fibrosis/scarring, mac chemotaxis, TIMPs, angiogenesis (myofibroblast), keratinocyte migration
Inhibition: MMP, immune cell proliferation (neuts and lymphs), epithelial cell cycle

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5
Q

TGF-B - signaling pathway

A

SMAD
Binding to receptor –> ligamerization –> R-SMAD and Co-SMAD –> R-SMAD-P and Co-SMAD-P –> act on DNA to induce transcription of ECM deposition, myofibroblast transdifferentiation, and fibroblast activation

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6
Q

TGF-B - inhibitor

A

SMAD7/I-SMAD

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7
Q

TGF-B - family members

A

TGF-B, BMP, activin

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8
Q

EGF - family members

A

[Epidermal growth factor]
EGF, TGF-a

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9
Q

EGF - source

A

macs, epithelial tissues, kidney, plts, mammary, etc.

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10
Q

EGF - functions

A

granulation, regen/maturation, gastroprotectant

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11
Q

TGF-a - specific function

A

hepatocyte regeneration, gastroprotectant

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12
Q

PDGF - family members

A

[Plt derived growth factor]
PDGF, VEGF

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13
Q

PDGF - source

A

Plt alpha granules, macs, activated endothelia, fibroblasts, keratinocytes

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14
Q

PDGF - functions

A

Fibrosis (chemotaxis of PMNs, macs, fibroblasts), angiogenesis

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15
Q

VEGF - source

A

Mesenchymal cells (secondary to hypoxia)

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16
Q

VEGF - functions

A

Angiogenesis, lymphogenesis, blood vessel maintenance

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17
Q

VEGF-A - receptor and result

A

VEGF-R2 - angiogenesis

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18
Q

VEGF-C - receptor and result

A

VEGF-R3 - lymphogenesis

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19
Q

VEGF-B - receptor and result

A

VEGF-R1 - blood vessel maintenance

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20
Q

FGF - family members

A

FGF1/aFGF, FGF2/bFGF, FGF3-6, FGF7/keratinocyte growth factor, FGF10/KGF2

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21
Q

FGF1 - source

A

ECM (released w/ damage)

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22
Q

FGF1 - function

A

Neural

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23
Q

FGF2 - source

A

Ubiquitous, ECM (released w/ damage)

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24
Q

FGF2 - function

A

Angiogenesis, mitogen for fibroblasts and epithelial

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25
KGF - source
[aka FGF10] Fibroblasts
26
KGF - function
[aka FGF10] Epithelial cell mitogens and differentiation
27
Canine chondrodysplasia growth factor disease
FGF4
28
Spider lamb syndrome growth factor disease
FGFR3
29
Steroid hormones - receptor type
Intracellular
30
Second messengers
cAMP, cGMP, DAG, IP3, inositol phospholipids, Ca2+
31
Receptor tyrosine kinase - what signals through this?
Growth factors
32
G protein-coupled receptor - what signals through this?
Inflamm mediators (histamine, leukotrienes, chemokine receptors, bradykinins, tachykinis/substance P, eicosanoid prostaglandins)
33
Which is completely irreversible in terms of neoplasia? Initiation, promotion, progression
Initiation (then has to undergo replication/DNA synthesis for it to stick)
34
Which is/are considered adaptive changes? Hypertrophy, dysplasia, hyperplasia, metaplasia
Hypertrophy, hyperplasia, metaplasia
35
Metaplasia is usually a response to what?
Chronic inflammation
36
Define dysplasia
Loss of architectural arrangement, increase in cell pleomorphism
37
Silent mutation
Occurs at nucleic acid level, no change at protein level Least impactful
38
Nonsense mutation
Encodes a premature stop codon Most impactful mutation
39
Missense mutation
Changes the sequence of AA and affects the protein Conservative: AA with similar features (in same family) Non-conservative: AA with different features
40
Frameshift mutations
Shift the order of translation, through insertion or deletion
41
Indels
Insertion or deletions that result in frameshift mutations
42
List the DNA repair mechanisms: 1. Single stranded break (SSB) 2. Pyrimidine adducts 3. Double stranded breaks 4. Mutations
1. Base excision repair 2. Nucleotide excision repairs 3. Recombination repair 4. DNA mismatch repair
43
Single stranded breaks use what protein to repair?
PARP1
44
Major players in homologous recombination
ATM/ATR CHK1/2 BRCA1/2
45
Non-homologous end joining major players
Ku proteins DNA-PKcs DNA ligase IV
46
Most important effector molecule in DNA Damage Response
p53
47
Monosomy
Only 1 copy, usually embryonic lethal
48
Mosaicism
>1 cell population with variable chromosomal number Non-germ line mutation
49
Robertsonian translocation
Centered around the centromere and results in loss of genetic material
50
Balanced, reciprocal translocations
Equal exchange of genetic material between 2 chromosomes
51
Haploinsufficiency
Even if you’re down to 1 copy (“haplo”type), it’s still “insufficient” to prevent cancer -p53 is an example of this
52
Paternal imprinting
Paternal allele is silenced (maternal is expressed) -ex. mtDNA is paternally imprinted
53
RTKs can activate which pathways?
MAPK, PI3K/Akt, PKCy (All major growth pathways)
54
MAPK signaling pathway - start to finish with examples of each step
MAPKKK (MAP3K) (Raf) —> MAPKK (MAP2K) (MEK) —> MAPK (p38, ERK, JNK)
55
AKT function and inhibitor
Promotes cell survival (increases cell size, growth, migration, metabolism) PTEN is inhibitor
56
Activation of PI3K is initiated by what?
Binding of Ras and subsequent phosphorylation
57
Phospholipase C (PLCy) function
Induces Ca release from ER Activates protein kinase C (PKC)
58
Main activator of GPCRs
Chemokines
59
Major mediator for GPCRs
cAMP (cyclic AMP)
60
Receptor for JAK/STAT
Cytokines (IL4/10/11/13, TGF-B, IFN-a, etc.)
61
JAK/STAT process
JAK phosphorylates STAT —> STAT translocates to nucleus for transcription (only after phosphorylation!)
62
Signal transduction pathway for TGF-B
SMAD
63
Inhibition of TGF-B
SMAD6/7, SMURFs
64
Growth factor receptor ligand
RTKs
65
Tumor suppressor genes
Retinoblastoma protein (Rb) p53 p16/INK4a/ARF PTEN (inhibits AKT)
66
DNA damage checkpoint in cell cycle
G1/S checkpoint
67
Chromosome checkpoint in cell cycle
G2/M
68
Which CDK is responsible for each part of the cell cycle listed: G1 phase S phase G2 phase
CDK4/6 CDK2 CDK1
69
CDK4/6 functions by…
Inhibiting RB
70
Retinoblastoma (Rb) function
Inhibits cell cycle at G1/S checkpoint by inhibiting E2F
71
Function of p16
Blocks CDK4/6 Major marker of cell senescence
72
Major marker of cell senescence
p16
73
Phosphorylation of Rb leads to what?
INACTIVATION of Rb —> release of E2F —> activation of transcription
74
Hypophosphorylated Rb leads to what?
Sequesters E2F from DNA
75
Function of MDM2/4
Inhibit/block p53
76
Functions of ATM and CHK
ATM activates CHK which upregulates p53 and inhibits MDM
77
Results of: DNA methylation DNA demethylation Histone methylation Histone acetylation
Gene/transcription silencing Gene/transcription activation Closes DNA (condensation; inhibits transcription) Opens DNA (allows for transcription)
78
DICER function
Uses pre-miRNA in the cytoplasm to make miRNA
79
RISC function
Mediates the silencing for miRNA using ds-miRNA •mRNA degradation (perfect match/linear strand) •inhibition of translation (imperfect/hairpin strand)
80
Location of pri- and pre-miRNA
Pri- in nucleus Pre- made in nucleus and exported to cytoplasm for use to make miRNA
81
Epithelial to mesenchymal transition features
•Downregulation of E-cadherin •Upregulation of SNAIL1/2 (Slug), ZEB1/2, TWIST1 (TFs) •Inc DNA methylation (shuts of “epithelial genes”)
82
Yamanaka Factors
Transcription factors that induce pluripotent stem cells
83
iPS cells/Yamanaka factors
Oct4 Sox2 c-Myc KLF4
84
Triggers of cell senescence
Telomere shortening and oncogene induced
85
What allows telomeres to re-lengthen?
TERT/telomerase
86
The site of assembly/activation of telomerase and what protects the complex once it is bound to the complex?
Cajal body Shelterin
87
Warburg effect
Cancer cell preference in using aerobic glycolysis even in the face of oxygen
88
Is GLUT1 upregulated or downregulated in cancer cells?
Upregulated
89
Main immunosuppressive cytokines produced by cancer cells
TGF-B and IL10
90
What is constitutively expressed by Tregs cells?
CTLA4
91
What controls expression of CTLA4?
Foxp3
92
How is the INITIAL activation of a T cell regulated?
By engagement of B7 (CD80/86) proteins •If engaged by CD28 —> TCR activated •If engaged by CTLA4 —> TCR suppressed
93
CTLA4 function
Downregulation of CD4+ TCs and enhances Treg immunosuppressive activity
94
Function of PD1/PDL1
Immune checkpoint in peripheral tissue to help downregulate T cells in chronic inflamm and limit collateral damage
95
Production of PDL1 is stimulated by:
IFNy or chronic inflamm
96
Where are PD1 and PDL1 expressed?
PD1 - lymph PDL1 - tumor cell
97
Papillomavirus proteins and functions
E5: PDGFR-B activation E6: p53 degradation E7: sequesters Rb in cytosol
98
What does expression of cMyc do?
Blocks activity of p16 and CDKIs by exporting them from the nucleus and degrading them - thus it is an oncogene

Gen Path (8 decks)

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