Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Proline-stimulated macs - result?

A

Fibroblast differentiation –> collagen production

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

TGF-B - source

A

Macs!, plts, endothelia, all cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

TGF-B - inhibitor

A

SMAD7/I-SMAD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

TGF-B - family members

A

TGF-B, BMP, activin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

EGF - family members

A

[Epidermal growth factor]
EGF, TGF-a

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

EGF - source

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

EGF - functions

A

granulation, regen/maturation, gastroprotectant

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

TGF-a - specific function

A

hepatocyte regeneration, gastroprotectant

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

PDGF - family members

A

[Plt derived growth factor]
PDGF, VEGF

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

PDGF - source

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

PDGF - functions

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

VEGF - source

A

Mesenchymal cells (secondary to hypoxia)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

VEGF - functions

A

Angiogenesis, lymphogenesis, blood vessel maintenance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

VEGF-A - receptor and result

A

VEGF-R2 - angiogenesis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

VEGF-C - receptor and result

A

VEGF-R3 - lymphogenesis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

VEGF-B - receptor and result

A

VEGF-R1 - blood vessel maintenance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

FGF - family members

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

FGF1 - source

A

ECM (released w/ damage)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

FGF1 - function

A

Neural

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

FGF2 - source

A

Ubiquitous, ECM (released w/ damage)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

FGF2 - function

A

Angiogenesis, mitogen for fibroblasts and epithelial

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

KGF - source

A

[aka FGF10]
Fibroblasts

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

KGF - function

A

[aka FGF10]
Epithelial cell mitogens and differentiation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Canine chondrodysplasia growth factor disease

A

FGF4

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Spider lamb syndrome growth factor disease

A

FGFR3

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Steroid hormones - receptor type

A

Intracellular

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Second messengers

A

cAMP, cGMP, DAG, IP3, inositol phospholipids, Ca2+

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Receptor tyrosine kinase - what signals through this?

A

Growth factors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

G protein-coupled receptor - what signals through this?

A

Inflamm mediators (histamine, leukotrienes, chemokine receptors, bradykinins, tachykinis/substance P, eicosanoid prostaglandins)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Which is completely irreversible in terms of neoplasia? Initiation, promotion, progression

A

Initiation (then has to undergo replication/DNA synthesis for it to stick)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Which is/are considered adaptive changes?
Hypertrophy, dysplasia, hyperplasia, metaplasia

A

Hypertrophy, hyperplasia, metaplasia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Metaplasia is usually a response to what?

A

Chronic inflammation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Define dysplasia

A

Loss of architectural arrangement, increase in cell pleomorphism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Silent mutation

A

Occurs at nucleic acid level, no change at protein level
Least impactful

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Nonsense mutation

A

Encodes a premature stop codon
Most impactful mutation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Missense mutation

A

Changes the sequence of AA and affects the protein
Conservative: AA with similar features (in same family)
Non-conservative: AA with different features

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Frameshift mutations

A

Shift the order of translation, through insertion or deletion

41
Q

Indels

A

Insertion or deletions that result in frameshift mutations

42
Q

List the DNA repair mechanisms:
1. Single stranded break (SSB)
2. Pyrimidine adducts
3. Double stranded breaks
4. Mutations

A
  1. Base excision repair
  2. Nucleotide excision repairs
  3. Recombination repair
  4. DNA mismatch repair
43
Q

Single stranded breaks use what protein to repair?

A

PARP1

44
Q

Major players in homologous recombination

A

ATM/ATR
CHK1/2
BRCA1/2

45
Q

Non-homologous end joining major players

A

Ku proteins
DNA-PKcs
DNA ligase IV

46
Q

Most important effector molecule in DNA Damage Response

A

p53

47
Q

Monosomy

A

Only 1 copy, usually embryonic lethal

48
Q

Mosaicism

A

> 1 cell population with variable chromosomal number
Non-germ line mutation

49
Q

Robertsonian translocation

A

Centered around the centromere and results in loss of genetic material

50
Q

Balanced, reciprocal translocations

A

Equal exchange of genetic material between 2 chromosomes

51
Q

Haploinsufficiency

A

Even if you’re down to 1 copy (“haplo”type), it’s still “insufficient” to prevent cancer
-p53 is an example of this

52
Q

Paternal imprinting

A

Paternal allele is silenced (maternal is expressed)
-ex. mtDNA is paternally imprinted

53
Q

RTKs can activate which pathways?

A

MAPK, PI3K/Akt, PKCy
(All major growth pathways)

54
Q

MAPK signaling pathway - start to finish with examples of each step

A

MAPKKK (MAP3K) (Raf) —> MAPKK (MAP2K) (MEK) —> MAPK (p38, ERK, JNK)

55
Q

AKT function and inhibitor

A

Promotes cell survival (increases cell size, growth, migration, metabolism)
PTEN is inhibitor

56
Q

Activation of PI3K is initiated by what?

A

Binding of Ras and subsequent phosphorylation

57
Q

Phospholipase C (PLCy) function

A

Induces Ca release from ER
Activates protein kinase C (PKC)

58
Q

Main activator of GPCRs

A

Chemokines

59
Q

Major mediator for GPCRs

A

cAMP (cyclic AMP)

60
Q

Receptor for JAK/STAT

A

Cytokines (IL4/10/11/13, TGF-B, IFN-a, etc.)

61
Q

JAK/STAT process

A

JAK phosphorylates STAT —> STAT translocates to nucleus for transcription (only after phosphorylation!)

62
Q

Signal transduction pathway for TGF-B

A

SMAD

63
Q

Inhibition of TGF-B

A

SMAD6/7, SMURFs

64
Q

Growth factor receptor ligand

A

RTKs

65
Q

Tumor suppressor genes

A

Retinoblastoma protein (Rb)
p53
p16/INK4a/ARF
PTEN (inhibits AKT)

66
Q

DNA damage checkpoint in cell cycle

A

G1/S checkpoint

67
Q

Chromosome checkpoint in cell cycle

A

G2/M

68
Q

Which CDK is responsible for each part of the cell cycle listed:
G1 phase
S phase
G2 phase

A

CDK4/6
CDK2
CDK1

69
Q

CDK4/6 functions by…

A

Inhibiting RB

70
Q

Retinoblastoma (Rb) function

A

Inhibits cell cycle at G1/S checkpoint by inhibiting E2F

71
Q

Function of p16

A

Blocks CDK4/6
Major marker of cell senescence

72
Q

Major marker of cell senescence

A

p16

73
Q

Phosphorylation of Rb leads to what?

A

INACTIVATION of Rb —> release of E2F —> activation of transcription

74
Q

Hypophosphorylated Rb leads to what?

A

Sequesters E2F from DNA

75
Q

Function of MDM2/4

A

Inhibit/block p53

76
Q

Functions of ATM and CHK

A

ATM activates CHK which upregulates p53 and inhibits MDM

77
Q

Results of:
DNA methylation
DNA demethylation
Histone methylation
Histone acetylation

A

Gene/transcription silencing
Gene/transcription activation
Closes DNA (condensation; inhibits transcription)
Opens DNA (allows for transcription)

78
Q

DICER function

A

Uses pre-miRNA in the cytoplasm to make miRNA

79
Q

RISC function

A

Mediates the silencing for miRNA using ds-miRNA
•mRNA degradation (perfect match/linear strand)
•inhibition of translation (imperfect/hairpin strand)

80
Q

Location of pri- and pre-miRNA

A

Pri- in nucleus
Pre- made in nucleus and exported to cytoplasm for use to make miRNA

81
Q

Epithelial to mesenchymal transition features

A

•Downregulation of E-cadherin
•Upregulation of SNAIL1/2 (Slug), ZEB1/2, TWIST1 (TFs)
•Inc DNA methylation (shuts of “epithelial genes”)

82
Q

Yamanaka Factors

A

Transcription factors that induce pluripotent stem cells

83
Q

iPS cells/Yamanaka factors

A

Oct4
Sox2
c-Myc
KLF4

84
Q

Triggers of cell senescence

A

Telomere shortening and oncogene induced

85
Q

What allows telomeres to re-lengthen?

A

TERT/telomerase

86
Q

The site of assembly/activation of telomerase and what protects the complex once it is bound to the complex?

A

Cajal body
Shelterin

87
Q

Warburg effect

A

Cancer cell preference in using aerobic glycolysis even in the face of oxygen

88
Q

Is GLUT1 upregulated or downregulated in cancer cells?

A

Upregulated

89
Q

Main immunosuppressive cytokines produced by cancer cells

A

TGF-B and IL10

90
Q

What is constitutively expressed by Tregs cells?

A

CTLA4

91
Q

What controls expression of CTLA4?

A

Foxp3

92
Q

How is the INITIAL activation of a T cell regulated?

A

By engagement of B7 (CD80/86) proteins
•If engaged by CD28 —> TCR activated
•If engaged by CTLA4 —> TCR suppressed

93
Q

CTLA4 function

A

Downregulation of CD4+ TCs and enhances Treg immunosuppressive activity

94
Q

Function of PD1/PDL1

A

Immune checkpoint in peripheral tissue to help downregulate T cells in chronic inflamm and limit collateral damage

95
Q

Production of PDL1 is stimulated by:

A

IFNy or chronic inflamm

96
Q

Where are PD1 and PDL1 expressed?

A

PD1 - lymph
PDL1 - tumor cell

97
Q

Papillomavirus proteins and functions

A

E5: PDGFR-B activation
E6: p53 degradation
E7: sequesters Rb in cytosol

98
Q

What does expression of cMyc do?

A

Blocks activity of p16 and CDKIs by exporting them from the nucleus and degrading them - thus it is an oncogene

Gen Path (8 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions