Cancers Flashcards

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1
Q

Meta plastic

A

Replacement of one cell lineage with another

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2
Q

Dysphasia

A

Abnormal tissue architecture

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3
Q

Cancers neoplasia

A

Forms new tissues / neoplasm

Benign mild dysplasia restricted to one location

Malignant cells invade other tissue highly dysplastic

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4
Q

Chronic myeloid leukaemia

A

Philadelphia chromosome

Chromosome 22 cut and bound to 9

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5
Q

BCR and ABL rearrangement and expression of fusion protein

A

The fused product is deregulated stimulation the production of leukaemia cells.

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6
Q

Gleevec

A

Treatment for CML

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7
Q

RB knock out

A

Requires 2 hits of mitosis recombination

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8
Q

Hyperplasia

A

Excessive growth

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9
Q

RTK

A

Receptors dimerise causing a conformational change and transphosphorylate together at the c terminal removing the activation loop from the catalytic cleft

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10
Q

Deregulation of RTK

A

Mutations can cause it to not require a stimulus to signal causing the cell to constantly grow

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11
Q

Raw

A

Cell cycle control

Allows the cell to proliferate if no mitogen is present

Small gtpase catalysed by GEF and inactivates by GAP

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12
Q

GEF

A

Catalyse exchange of gdp for gtp

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13
Q

GAP

A

Catalyse exchange of gtp for gdp

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14
Q

Ras mutations

A

Mutation at gly12 causes valine to be there instead so gtp cannot be hydrolysed

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15
Q

SH2

A

Binds to the RTK phosphate before binding sh3 and sos to plasma membrane

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16
Q

SOS

A

Ras GEF

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17
Q

RAS induced proliferation

A

GTP bound form exposes a loop which binds molecules such as RAF p13k
RAF induces the MAPK pathway

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18
Q

GF RTK RAS RAF MEK ERK pathway

A

Brings cells out of G0 and into the cell cycle

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19
Q

Rb

A

Regulates cell cycle at the R point

20
Q

TGF beta

A

Regulates cell cycle until Rpoint as a growth inhibitor

21
Q

P53

A

Tumour suppressor gene

Monitors three stages of cell cycle

G1
S
G2

Blocks continuation if DNA damage is detected or if replication is incomplete

22
Q

Cycling and CDK

A

Conserved alpha helix binding

Responsible for substrate recognition

23
Q

Cyclin D

A

Present when mitogens bind

24
Q

Inactivation of RB

A

Cyclin CDK hyper phosphorylated

25
Q

P13K

A

Stimulated by IGFR RTK

Generates second messenger pip3
Which phosphorylated akt at the membrane by

26
Q

P53 mutations

A

Missense

Often in dna specific binding domain

27
Q

Mdm2

A

Conjugated ubiquitin to p53 which is then degraded

Blocked by atm and atr

28
Q

Nutlin

A

Mdm2 mimetic

29
Q

SV40

A

Codes for oncoprotein that inhibits p53 and pRB

30
Q

Tolomerase

A

TTAGGG enzyme

Prevent Philadelphia chromosome

31
Q

GRN 163l

A

Prevents telomerase extension

32
Q

Hypoxia

A

Hif1 alpha binds beta causing transcription of VEGF

33
Q

Normoxia

A

Proline hydroxylase adds oxygen to th proline residues on hif1 alpha then pvhl poly ubiquitylation then causes it degradation

34
Q

Angiogenesis

A

Peri sites move away from the capillary before the basement membrane breaks down and migrate to the peri vascular space before proliferating and adhering to each other then everything adds itself to it again

35
Q

Treatment for angiogenesis

A

Inhibit the cascade or block the ability of endothelial cells to break down the matrix

Or anti VEGF antibodies block its binding

Endostatins inhibit cell growth

36
Q

Sources of energy I. Tumour cells

A

Glycolysis

Gluatmineolysis replenishes citric acid intermediates

37
Q

E cadherin

A

Present in epithelial cells crosslinking actin by the c terminus

Very low level present in carcinoma

38
Q

Invadapodia

A

Actin polymerisation forms a protrusion into the basement membrane mediated by arp23 and cdc42

Matrix metala pro teases then released from the ends of the filaments and expand the gap in the basement membrane

39
Q

RGD

A

Interferes with integrin binding to the ecm preventing metastasis

40
Q

Rho GTPase

A

Members of the Ras superfamily

Can be sequestered in membrane by GDI

41
Q

Intrinsic inflammatory pathway

A

Activated by various oncogenes such as RAS or EGFR

Chromosomal rearrangement in the absence of a suppressor gene and create a inflammatory micro environment

42
Q

Extrinsic

A

Inflammatory conditions augment the risk of cancer

43
Q

Pathways convergence

A

Activate transcription factors such as Nfkb and hif1 and produce cox2 resulting in activation of leukocytes and the cytokines then activate the inflammatory pathway

44
Q

Chronic liver inflammation

A

NSAIDs and anti TNF alpha drugs highly reduce incidence

45
Q

Veclade

A

Inhibits the proteasome by interfering with the degradation of iKB triggering apoptosis as the Nfkb cannot be broken down

46
Q

NSAIDs such as aspirin

A

Reduce incidence of cancer as prostaglandins cannot be formed properly