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Pathology Midterms > Neoplasia: Proto Oncogen > Flashcards

Neoplasia: Proto Oncogen Flashcards

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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
Quiescent state of RAS bound
GDP
26
During tyrosine kinase growth factors in RAS
GDP to GTP
27
Prevents uncontrolled RAS activity
GAP
28
Gain of function on RAS
GTP
29
Lost of function in RAS
GAP
30
BRAF 100%
Hairy cell leukemias
31
BRAF >60%
Melanoma
32
BRAF 80%
Benign novi
33
BRAF
Serine/threonine protein kinase | Top of MAPK family
34
PI3K Key signaling node
AKT
35
PI3K activates cascade of serine threonine kinases
AKT
36
PI3K Activated by AKT Sensor of cellular nutrient status stimulate protein and lipid synthesis
mTOR
37
PI3K Pro apoptotic protein that inactivated by AKT
BAD | FOXO
38
PI3K Bracking factor PI3K is negatively regulated
PTEN
39
PI3K Most frequently mutated than RAS/MAPK pathways
PI3K | PTEN
40
PI3K Gain of function
PI3K
41
PI3K Lost of function Lost through mutation or Epigenetic silencing
PTEN
42
No treatment
RAS
43
Identical melanomas without BRAF mutations never respond to BRAF inhibito. This is just example
Oncogene addiction
44
Alterations in Nonreceptor Tyrosine Kinases ABL tyrosine kinase
Chronic myelogenous leukemia | Acute lymphoblastic leukemia
45
Alterations in Nonreceptor Tyrosine Kinases Translocate chromosome 9 to chromosome 22
ABL gene
46
Alterations in Nonreceptor Tyrosine Kinases Fuse to chromosome 22
BCR genes
47
Alterations in Nonreceptor Tyrosine Kinases Fusing of C22 to BCR genes produce
BCR-ABL tyrosine kinase
48
Alterations in Nonreceptor Tyrosine Kinases Most important contribution of the BCR
Unleash tyrosine kinase activity of ABL | Promotes self association of BCR-ABL complex
49
Alterations in Nonreceptor Tyrosine Kinases Treatment for CML
BCR - ABL inhibitors
50
Alterations in Nonreceptor Tyrosine Kinases Addiction with BCR-ABL inhibitor doesn't lead to cure
Because of CML stem cells. Kaya kailanagan lang tuloy tuloy ang gamot para hindi mag return ang CML
51
Alterations in Nonreceptor Tyrosine Kinases Activated by point of mutations that abrogate the function of negative regulatory domains
Nonreceptor kinase JAK2
52
Alterations in Nonreceptor Tyrosine Kinases JAK2 participate in
JAK/STAT signaling pathway
53
Alterations in Nonreceptor Tyrosine Kinases Associated with JAk2 mutations
Polycythemia Vera Thrombocytosis Myelo fibrosis Affected by erythropoietin
54
Signaling pathways that drive proliferation
Proto oncogene
55
Transcription factors
``` MYC MYB JUN FOS REL ```
56
Transcription factors Most common involved in human tumors
MYC oncogenes
57
Transcription factors MYC oncogenes
Immediate early response genes | Induced by RAS/MAPK
58
Transcription factors SNP, MYC on chromosome 8
Induced by RAS/MAPK | Prostate, ovarian carcinoma
59
Transcription factors MYC target genes
D cyclins
60
Transcription factors MYC up regulates
``` Expression of rRNA genes rRNA processing Gene expression Metabolic reprogramming Warburg effect Multiple Glycolytic enzymes Glutamine metabolism ```
61
Transcription factors MYC considered as
Master transcriptional regulator of cell growth
62
Transcription factors Highest level of MYC
Burkitt lymphoma Fastest growing human tumor
63
In some context MYC up regulates expression of
Telomerase
64
MYC transcription factor
Reprogramming somatic cells into pluripotent stem cells
65
Transcription factors Neuroblastomas Chromosome 2p
NMYC
66
Transcription factors Cancer of the lungs
LMYC
67
Cyclin and cyclin dependent kinase Progression of cells through the cell cycle
CDK's
68
Cyclin and cyclin dependent kinase Bind to CDK's to become active
Cyclins
69
Cyclin and cyclin dependent kinase Negative control over the cell cycle
CDK inhibitors
70
Cyclin and cyclin dependent kinase CDK inhibitors down regulated by
Mitogenic signaling pathway
71
Cyclin and cyclin dependent kinase Promote cell cycle
CDK- cyclin inhibitors
72
2 main cell cycle checkpoints
G1/S more important in cancer | G1/M
73
Cyclin and cyclin dependent kinase Gain of function G1/S
D cyclin - lymphoid tumors - solid tumors CDK4- melanomas - sarcomas
74
Cyclin and cyclin dependent kinase Loss of function - tumor suppressor genes
CDKIs- germ line mutation of p16 | CDKN2A
75
Cell cycle inhibitors
CIP/KIP family P21 P27 CDKN1A-D INK4/ARF family (CDKN2A-C)
76
CIP/KIP family P21 P27 CDKN1A-D
Block the cell cycle by inhibiting to cyclin CDK complexes
77
Binds to cyclin D-CDK4 and promotes the inhibitory effects of RB
INK4/ARF family | CDKN2A-C
78
Most important tumor suppressor genes
RB | p53
79
Pocket protein that binds E2F transcription factors in its hypo phosphorylated state. Preventing G1S transition
RB
80
Acts mainly through p21 that causes cell cycle arrest | Causes apoptosis by transcription of pro apoptotic genes like BAX
P53
81
P53 is required for
G1/S checkpoint
82
P53 is main component of the
G2/M checkpoint

Pathology Midterms (5 decks)

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