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MOD Midterm > Neoplasia - Singh > Flashcards

Neoplasia - Singh Flashcards

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1
Q

germline mutations

A

from embryo made form egg and sperm, all cells effected

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2
Q

Driver vs Passenger mutations

A

Driver mutation is the mutation causing the tumor

Passenger mutations are mutations that are there only dont cause the tumor

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3
Q

Protoocogene
oncogene
pncoprotein

A

normal gene
mutated causes excessive growth
protein formed from mutation

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4
Q

coding mutations leads to

A

Abnormal protein

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5
Q

Regulatory mutations leads to

A

Excessive protein

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6
Q

Translocation mutations leads to

A

new protein made

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7
Q

Gene amplification leads to

A

Excessive protein

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8
Q

Self-sufficiency (hallmark 1)

A

what gets uppregulated or downregulatated by mutations for the cells to grow

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9
Q

Her2neu

A

the HER2 gene (part of a growth receptor) gets amplified

= breast carcinoma

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10
Q

what happens when Her2neu is amplified and TX:

A

a bunch of HER2 receptors get on cell surfaces
= high signaling for cells to grow and divide
= TX: Herceptin (Trastuzumab) that blocks these receptors

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11
Q

RAS mutation is what and locations

A

point mutation —-> KRAS (or any other XRAS, lung, Colon, Pancrease)
= causes Gprotien to be stuck in GTP phase**

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12
Q

function of RAS

A 
activate PI3K (AKT, mTOR for increase growth and proteins)
activate RAF (MAPK (MEK, ERK) for transcription)
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13
Q

PTEN function

A

INHIBIT PI3K = tumor suppressant gene

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14
Q

X PTEN causes

A

endometrial carcinoma , due to high RAS activity

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15
Q

Abl kinase

A

when there is a translocation from chr 9 to chr 22 (Philadelphia chr)
= BCR and Abl are next to eachother = TYROSINE KINASE constantly activated = GFs activated

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16
Q

Abl-BCR leads to

A

Chronic Myeloid Leukemia

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17
Q

what makes the ABL-BCR special

A

in is an ocogene addiction
= this mutation has to happen for this CML to happen
VERY EASY TO TREAT

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18
Q

TX for CML

A

Tyrosine kinase inhibitors (gleivic)

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19
Q

MYC

A

master transcriptor regulator

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20
Q

MYC amplification leads to

A

Neuroblastoma = common in children (extracranial - adrenal medulla, Paraspinal ganglion, Thoracic posterior)
N-MYC amplification

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21
Q

Cyclin D and CDK function

A 
activate pRB (phosphorylates)
= cell enters cell cycle from G1 to S
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22
Q

overexpressed Cyclin D1

A

Mantel cell lymphoma

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23
Q

what inhibits Cyclin and CDKs

A

p16

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24
Q

X p16 causes

Study These Flashcards
A

GERMLINE

Familial melanomas

25
TSG (good) list them
1. RB- hypophosphorylated 2. TP53 3. APC ----I B-catenin 4. p16 5. PTEN 6. TGF-B 7. miRNA : degrade mRNA, inhibit translation 8. GADD45 9. p21 ----I cell cycle 10. BAX/ PUMA
26
what makes a mutation in TSG different then oncogenes
the mutation needs to be a 2 hit | EX: mutated Rb (does not function) = retinoblastoma
27
TP53 function
like everything good 1. senescence 2. p21 ----I CDK 3. GADD (DNA repair) 4. BAX/ PUMA (apoptosis)
28
how to treat X p53
MANY CANCERS | TX: chemo, radiation and more needed
29
Li-Fraumeni Syndrome
GERMLINE TP53 mutation | many types, diverse and FH tumors
30
Familial Adenomatous Polypsis Coli
GERMLINE APC colon polyps, most get it by age 40yo (can also happen SOMATICALLY)
31
APC function
binds to and inhibits B-catenin (which is a protein that signals proliferation or cells)
32
ATP use and production in cancer cells
they do Aerobic glycolysis (WARBURG EFFECT) make small amounts of NET ATP, since they use most energy on making new proteins and proliferation =NO OXPHOS
33
what do cancer cells do to stay alive
Autophagy, can stay hibernating in stress conditions (consume own products for energy --> independent) = provides survival, not growth
34
how is apoptosis avoided
``` downregulate p53 (overexpressed MDM2) upregulate BCL2 = effects the intrinsic pathway ```
35
what determines senescence
telomere length
36
how do telomeres work
each cell division they get smaller
37
how to telomerases work
they are on stem cells and prevent breakdown of telomeres wach division
38
cancer stem cells
can divide as many times and become many different types of cells
39
how do tumors grow beyond their boundary
angiogensis (to bring them nutrients and O2)
40
how is angiogenesis activated
1. Hypoxia ----> HIF-1a increased = increase in VEGF +FGF 2. RAS/MYC gain or loss of function = high VEGF
41
how to inhibit angiogenesis
BLOCK VEGF | = Bevacizumab
42
how do tumors grow past BM
they silence the E-cadherins on the (Epithelial-Mesenchymal transition = make themselves look like mesenchymal cells that dont need sticky cadherins)
43
how do tumors grow past ECM
degrade ECM , BM, and CT by MATRIX METALLOPROTEINASE
44
when out of BM and ECM where do tumor cells travel and how
Carcinoma = lymphatics Sarcoma = BVs (hematogenous) go based on location, drainage direction, chemokines attraction, high O2 and nutrition environment (lungs)
45
how do tumor cells evade the bodys immune system
1. tumor gets rid of Ag on surfaces (makes it look normal) or MHC1 receptor so CTL cells cant bind or recognize 2. tumor cells have PD1 Ligand that they get out when CTL binds to it (binding to CTL PD1 R and inhibiting it)
46
how to TX: by targeting the tumor cells making a lot of PD1 ligands
drug that has ANTI PD-1/PD-L1, which tells CTL cells to snap out of it and kill this thing
47
how do tumor cells make more mutations
1. downregulated p53 = no dna repair = more mutations able to come 2. X mismatch repair = high microsatellites (instability) ----> more mutations 3. X HRR (double strand breaks)
48
Lynch Syndrome
GERMLINE loss of function mutation of DNA mismatch repair gene (high microsatellites) = in stomach, pancreas, colorectal, ovary, uterus, prostate, GU tract
49
Homologous recombination repair does what
BRCA1 and BRCA2 repair strand breaks in DNA
50
tumor micro-environment
proinflammatory environment = growth and proliferation to be favored (for body to heal response)
51
5 things that make genes cancer associated
1. Amplification 2. Deletion 3. Translocation 4. Epigenetic Modifications 5. miRNA
52
Amplification and tumor cells
EX: ERBB2, | overexpression
53
Deletion and tumor cells
EX: Rb | tumor suppressants removed
54
Translocation and tumor cells
unique combinations
55
Translocation and tumor cell EXS:
EX: 1. MYC/IgH translocation = Burkitt's lymphoma (the MYC is overexpressed when placed next to promoter gene IgH) 2. PML/RARa translocation = Acute Promyelocytic leukemia (normal ---> RA binds to RAR and activated differentiation into mature myelocytes) (RAR next to PML----> RA cant activate RAR and makes accumulation of leukemic malignant blasts undifferentiated)
56
TX: acute promyelocytic leukemia
ATRA ----> replaces RA and activates RAR = malignant promyelocytes differentiate into mature shortlived myeolcytes
57
Epigenetic mutations and tumor cells
1. methylation = suppresses a gene (low or high) | 2. histone tails bound to epigenetic facotrs = suppress genes
58
miRNA and tumor cells
1. non-coding ssRNAs that cleave and degrade mRNA and inhibits translation 2. ----I BCL2 (heme malignancies)

MOD Midterm (9 decks)

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