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MOD Midterm > Neoplasia - Singh > Flashcards

Neoplasia - Singh Flashcards

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

A

GERMLINE

Familial melanomas

25
Q

TSG (good) list them

A
  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
Q

what makes a mutation in TSG different then oncogenes

A

the mutation needs to be a 2 hit

EX: mutated Rb (does not function) = retinoblastoma

27
Q

TP53 function

A

like everything good

  1. senescence
  2. p21 —-I CDK
  3. GADD (DNA repair)
  4. BAX/ PUMA (apoptosis)
28
Q

how to treat X p53

A

MANY CANCERS

TX: chemo, radiation and more needed

29
Q

Li-Fraumeni Syndrome

A

GERMLINE TP53 mutation

many types, diverse and FH tumors

30
Q

Familial Adenomatous Polypsis Coli

A

GERMLINE APC
colon polyps, most get it by age 40yo
(can also happen SOMATICALLY)

31
Q

APC function

A

binds to and inhibits B-catenin (which is a protein that signals proliferation or cells)

32
Q

ATP use and production in cancer cells

A

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
Q

what do cancer cells do to stay alive

A

Autophagy, can stay hibernating in stress conditions (consume own products for energy –> independent)
= provides survival, not growth

34
Q

how is apoptosis avoided

A 
downregulate p53 (overexpressed MDM2)
upregulate BCL2
= effects the intrinsic pathway
35
Q

what determines senescence

A

telomere length

36
Q

how do telomeres work

A

each cell division they get smaller

37
Q

how to telomerases work

A

they are on stem cells and prevent breakdown of telomeres wach division

38
Q

cancer stem cells

A

can divide as many times and become many different types of cells

39
Q

how do tumors grow beyond their boundary

A

angiogensis (to bring them nutrients and O2)

40
Q

how is angiogenesis activated

A
  1. Hypoxia —-> HIF-1a increased
    = increase in VEGF +FGF
  2. RAS/MYC gain or loss of function = high VEGF
41
Q

how to inhibit angiogenesis

A

BLOCK VEGF

= Bevacizumab

42
Q

how do tumors grow past BM

A

they silence the E-cadherins on the (Epithelial-Mesenchymal transition = make themselves look like mesenchymal cells that dont need sticky cadherins)

43
Q

how do tumors grow past ECM

A

degrade ECM , BM, and CT by MATRIX METALLOPROTEINASE

44
Q

when out of BM and ECM where do tumor cells travel and how

A

Carcinoma = lymphatics
Sarcoma = BVs (hematogenous)
go based on location, drainage direction, chemokines attraction, high O2 and nutrition environment (lungs)

45
Q

how do tumor cells evade the bodys immune system

A
  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
Q

how to TX: by targeting the tumor cells making a lot of PD1 ligands

A

drug that has ANTI PD-1/PD-L1, which tells CTL cells to snap out of it and kill this thing

47
Q

how do tumor cells make more mutations

A
  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
Q

Lynch Syndrome

A

GERMLINE
loss of function mutation of DNA mismatch repair gene (high microsatellites)
= in stomach, pancreas, colorectal, ovary, uterus, prostate, GU tract

49
Q

Homologous recombination repair does what

A

BRCA1 and BRCA2 repair strand breaks in DNA

50
Q

tumor micro-environment

A

proinflammatory environment = growth and proliferation to be favored (for body to heal response)

51
Q

5 things that make genes cancer associated

A
  1. Amplification
  2. Deletion
  3. Translocation
  4. Epigenetic Modifications
  5. miRNA
52
Q

Amplification and tumor cells

A

EX: ERBB2,

overexpression

53
Q

Deletion and tumor cells

A

EX: Rb

tumor suppressants removed

54
Q

Translocation and tumor cells

A

unique combinations

55
Q

Translocation and tumor cell EXS:

A

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
Q

TX: acute promyelocytic leukemia

A

ATRA —-> replaces RA and activates RAR = malignant promyelocytes differentiate into mature shortlived myeolcytes

57
Q

Epigenetic mutations and tumor cells

A
  1. methylation = suppresses a gene (low or high)

2. histone tails bound to epigenetic facotrs = suppress genes

58
Q

miRNA and tumor cells

A
  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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