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Pathology 📖 > Neoplasm > Flashcards

Neoplasm Flashcards

1
Q

Functions of TP53

A

It is a tumor suppressor gene.
• cell cycle progression
• dna repair
• apoptosis
• code protein p53

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2
Q

Location of TP53

A

Chromosome 17p13.1

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3
Q

Mutation of TP53 produces

A

Li Fraumeni syndrome

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4
Q

Causes of Li Fraumeni syndrome

A
  • increased MDM2 levels ( cause degradation of p53)
  • E6 protein of HPV (degradation by transforming proteins of DNA viruses)
  • release of p53 by stressed cells by:
    🪄 DNA DAMAGE AND HYPOXIA
    By protein kinase ATM and ATR
    ⬇️
    Phosphorylation of MDM2 and p53
    ⬇️
    Post translational modifications
    ⬇️
    Separation of p53 and MDM2 bond
    🪄 ONCOGENIC STRESS
    Activation of oncoproteins
    ⬇️
    Progrowth pathways - MAPK, PI3K/AKT
    ⬇️
    Sustained signalling
    ⬇️
    Increased expression of ARF
    ⬇️
    ARF binds to MDM2 and displaces p53
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5
Q

Functions of p53

A

Temporary cell cycle arrest
Permanent cell cycle arrest
Apoptosis

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6
Q

Target genes of p53

A

Genes that cause apoptosis
Genes that cause cell cycle arrest
Genes that induce catabolism / inhibit anabolism

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7
Q

Temporary p53 cell cycle arrest

A

TP53 ➡️ induce protein GADD45
⬇️ ⬇️
p53 DNA repair
⬇️
CDKN1A gene
⬇️
p21
⬇️
Inhibit CDK4 and D cyclins
⬇️
Inhibit progression from G1 to S

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8
Q

Pro apoptotic genes and pathway involved im p53 induced apoptosis

A

BAX, PUMA
intrinsic

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9
Q

APC (adenomatous polyposis coli) is located on chromosome?

A

5q21

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10
Q

Loss of function mutation of APC causes

A

Familial adenomatous polyposis
Autosomal dominant
Later produces colom cancer

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11
Q

Beta catenin binds with ________ to maintain contact inhibition

A

E cadherin - protein that maintains intercellular adhesion

During injury they separate, catenin enters nucleus to stimulate genes for cell repair and join with cadherin once done.

Loss of contact inhibition or loss of E cadherin causes metastasis and invasion of tumor.

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12
Q

Loss of function mutation of CDH1 produces

A

Familial gastric carcinoma

Because CDH1 is associated with E cadherin gene

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13
Q

Proteins coded by CDKN2A

A

P14 - activate p53 pathway (oncogenic stress)
P16 - inhibits CDK4 / cyclin dependent kinase phosphorylatiom of RB

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14
Q

Mutation of CDKN2A - familial carcinoma

A

Melanoma

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15
Q

Mutation of CDKN2A - sporadic

A

Bladder
Head and neck
Acute lymphoblastic leukemia

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16
Q

TGF- ɓ pathway

A

NORMAL
Bind to receptors
⬇️
Stimulate intracellular signals
⬇️
Induce transcriptional regulator
⬇️
Activate SMAD protein
⬇️
Activate anti proliferative genes

17
Q

Protein related to TGF ɓ pathway

A

SMAD

18
Q

Type of mutation in TFG ɓ pathway

A

Loss of function

19
Q

TGF ɓ mutation cancers

A

T - sTomach
G - colon
Fuck - endometrium

20
Q

Mutational inactivation of SMAD causes

A

Pancreatic cancer

21
Q

PTEN full form

A

Phosphatase and tensin homologue

22
Q

PTEN gene code

A

10q23

23
Q

Mutation of 10q23 (PTEN)

A

Cowden syndrome
Frequent benign growths like skin cancer, breast, endometrium, thyroid tumors

24
Q

PTEN acts on

A

PI3K/AKT pathway

25
Q

Types of PTEN mutation

A

Deletion
Point mutation
Epigenetic silencing

26
Q

VHL - von hippel lindau is on chromosome?

A

3p

27
Q

VHL ubiquitin in absence of O2

A

Does not bind to HIF1-alpha
So no degradation of HIF1-alpha
Acculmulates in nuclei of hypoxic cells

28
Q

Accumulation of HIF1-alpha activates

A

Vegf
Pdgf
Glut1
Glycolytic enzymes

29
Q

STK11 (serin/threonine kinase) loss of function produces

A

Peutz jeghers syndrome
Git benign tumor
Pancreatic carcinoma

30
Q

STK11 acts on

A

Glucose uptake
Gluconeogenesis
Protein synthesis
Lipod metabolism

31
Q

Tumor suppressor genes

A

APC
E cadherin
CDKN2A
TGF ɓ
PTEN
VHL
STK11

32
Q

VHL full form

A

Von hippel lindau

33
Q

VHL is on chromosome

A

3p

34
Q

VHL mainly associated with

A

Renal cell carcinoma

35
Q

Warburg effect test

A

Positron emission test
18 flurodeoxyglucose

36
Q

Atp produced by actively growing cells bt glycolysis

A

4
(Normal is 2)

Pathology 📖 (2 decks)

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