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Pathology Midterms > Neoplasia: Proto Oncogen > Flashcards

Neoplasia: Proto Oncogen Flashcards

1
Q

Growth factors receptors oncoproteins that are activated by mutations in various cancer

A

RAS
PI3K
MYC
D cyclins

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2
Q

Signaling nodes that have to the greatest impact on the malignant phenotype

A

Darwinian selections

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3
Q

Operates immediate downstream from receptor tyrosine kinase

A

RAS

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4
Q

Apply brakes to RAS activation

A

GAPs

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5
Q

Same function of PI3K

A

PTEN

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6
Q

Downstream of RAS
Arms
Important in promoting cancer cell growth

A

MAPK

PI3K

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7
Q

MAPK

A

Mitogen activated protein kinase

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8
Q

Normal cells + growth factors

A

Proliferation

Paracrine action

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9
Q

Cancer cells + growth factors

A

Autocrine loop

Eg.
PDGF
TGF-a
EGFR

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10
Q

Important pathogenic element in tumors

A

Autocrine loop

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11
Q

Tyrosine kinase receptor

A

Extracellular ligand binding domain

Cytoplasmic tyrosine kinase domain

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12
Q 
Encodes EGFR (point mutation)
Found in a subset of lung adenocarcinoma
A

ERBB1

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13
Q

Encodes tyrosine kinase family HER2

Breast carcinoma

A

ERBB2

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14
Q

Gene rearrangement

A

ALK, EML4

EML4- ALK protein

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15
Q

Encodes yet another receptor tyrosine kinase

Hindi na tumatalab yung ibang gamot dahil dito, lalo na pag advanced na yung cancer.

A

MET

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16
Q

When RAS mutation are present in tumor

A

Absent mutations in receptor tyrosine kinase

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17
Q

Tumor activated RAS can completely substitute for

A

Tyrosine kinase activity

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18
Q

Most common type of abnormality involving proto oncogene

A

RAS mutations

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19
Q

RAS in humans

A

HRAS
KRAS
NRAS

This are retrovirus

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20
Q

Mutated RAS

A

15-20%

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21
Q

RAS 90%

A

Pancreatic adenocarcinoma

Cholangiocarcinoma

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22
Q

RAS 50%

A

Colon
Endometrial
Thyroid

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23
Q

RAS 30%

A

Lung adenocarcinoma

Myeloid leukemia

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24
Q

Excited signal transmitting state RAS bound

A

GTP

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25
Q

Quiescent state of RAS bound

A

GDP

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26
Q

During tyrosine kinase growth factors in RAS

A

GDP to GTP

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27
Q

Prevents uncontrolled RAS activity

A

GAP

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28
Q

Gain of function on RAS

A

GTP

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29
Q

Lost of function in RAS

A

GAP

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30
Q

BRAF

100%

A

Hairy cell leukemias

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31
Q

BRAF

> 60%

A

Melanoma

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32
Q

BRAF

80%

A

Benign novi

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33
Q

BRAF

A

Serine/threonine protein kinase

Top of MAPK family

34
Q

PI3K

Key signaling node

35
Q

PI3K activates cascade of serine threonine kinases

36
Q

PI3K

Activated by AKT
Sensor of cellular nutrient status stimulate protein and lipid synthesis

37
Q

PI3K

Pro apoptotic protein that inactivated by AKT

38
Q

PI3K

Bracking factor
PI3K is negatively regulated

39
Q

PI3K

Most frequently mutated than RAS/MAPK pathways

40
Q

PI3K

Gain of function

41
Q

PI3K

Lost of function
Lost through mutation or Epigenetic silencing

42
Q

No treatment

43
Q

Identical melanomas without BRAF mutations never respond to BRAF inhibito.

This is just example

A

Oncogene addiction

44
Q

Alterations in Nonreceptor Tyrosine Kinases

ABL tyrosine kinase

A

Chronic myelogenous leukemia

Acute lymphoblastic leukemia

45
Q

Alterations in Nonreceptor Tyrosine Kinases

Translocate chromosome 9 to chromosome 22

46
Q

Alterations in Nonreceptor Tyrosine Kinases

Fuse to chromosome 22

47
Q

Alterations in Nonreceptor Tyrosine Kinases

Fusing of C22 to BCR genes produce

A

BCR-ABL tyrosine kinase

48
Q

Alterations in Nonreceptor Tyrosine Kinases

Most important contribution of the BCR

A

Unleash tyrosine kinase activity of ABL

Promotes self association of BCR-ABL complex

49
Q

Alterations in Nonreceptor Tyrosine Kinases

Treatment for CML

A

BCR - ABL inhibitors

50
Q

Alterations in Nonreceptor Tyrosine Kinases

Addiction with BCR-ABL inhibitor doesn’t lead to cure

A

Because of CML stem cells. Kaya kailanagan lang tuloy tuloy ang gamot para hindi mag return ang CML

51
Q

Alterations in Nonreceptor Tyrosine Kinases

Activated by point of mutations that abrogate the function of negative regulatory domains

A

Nonreceptor kinase JAK2

52
Q

Alterations in Nonreceptor Tyrosine Kinases

JAK2 participate in

A

JAK/STAT signaling pathway

53
Q

Alterations in Nonreceptor Tyrosine Kinases

Associated with JAk2 mutations

A

Polycythemia Vera
Thrombocytosis
Myelo fibrosis

Affected by erythropoietin

54
Q

Signaling pathways that drive proliferation

A

Proto oncogene

55
Q

Transcription factors

A 
MYC
MYB
JUN
FOS
REL
56
Q

Transcription factors

Most common involved in human tumors

A

MYC oncogenes

57
Q

Transcription factors

MYC oncogenes

A

Immediate early response genes

Induced by RAS/MAPK

58
Q

Transcription factors

SNP, MYC on chromosome 8

A

Induced by RAS/MAPK

Prostate, ovarian carcinoma

59
Q

Transcription factors

MYC target genes

60
Q

Transcription factors

MYC up regulates

A 
Expression of rRNA genes
rRNA processing
Gene expression
Metabolic reprogramming
Warburg effect
Multiple Glycolytic enzymes
Glutamine metabolism
61
Q

Transcription factors

MYC considered as

A

Master transcriptional regulator of cell growth

62
Q

Transcription factors

Highest level of MYC

A

Burkitt lymphoma

Fastest growing human tumor

63
Q

In some context MYC up regulates expression of

A

Telomerase

64
Q

MYC transcription factor

A

Reprogramming somatic cells into pluripotent stem cells

65
Q

Transcription factors

Neuroblastomas
Chromosome 2p

66
Q

Transcription factors

Cancer of the lungs

67
Q

Cyclin and cyclin dependent kinase

Progression of cells through the cell cycle

68
Q

Cyclin and cyclin dependent kinase

Bind to CDK’s to become active

69
Q

Cyclin and cyclin dependent kinase

Negative control over the cell cycle

A

CDK inhibitors

70
Q

Cyclin and cyclin dependent kinase

CDK inhibitors down regulated by

A

Mitogenic signaling pathway

71
Q

Cyclin and cyclin dependent kinase

Promote cell cycle

A

CDK- cyclin inhibitors

72
Q

2 main cell cycle checkpoints

A

G1/S more important in cancer

G1/M

73
Q

Cyclin and cyclin dependent kinase

Gain of function G1/S

A

D cyclin - lymphoid tumors
- solid tumors

CDK4- melanomas
- sarcomas

74
Q

Cyclin and cyclin dependent kinase

Loss of function - tumor suppressor genes

A

CDKIs- germ line mutation of p16

CDKN2A

75
Q

Cell cycle inhibitors

A

CIP/KIP family
P21
P27 CDKN1A-D

INK4/ARF family
(CDKN2A-C)

76
Q

CIP/KIP family
P21
P27 CDKN1A-D

A

Block the cell cycle by inhibiting to cyclin CDK complexes

77
Q

Binds to cyclin D-CDK4 and promotes the inhibitory effects of RB

A

INK4/ARF family

CDKN2A-C

78
Q

Most important tumor suppressor genes

79
Q

Pocket protein that binds E2F transcription factors in its hypo phosphorylated state.
Preventing G1S transition

80
Q

Acts mainly through p21 that causes cell cycle arrest

Causes apoptosis by transcription of pro apoptotic genes like BAX

81
Q

P53 is required for

A

G1/S checkpoint

82
Q

P53 is main component of the

A

G2/M checkpoint

Pathology Midterms (5 decks)

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