Cancers

Question 1

Meta plastic

Answer 1

Replacement of one cell lineage with another

Question 2

Dysphasia

Answer 2

Abnormal tissue architecture

Question 3

Cancers neoplasia

Answer 3

Forms new tissues / neoplasm

Benign mild dysplasia restricted to one location

Malignant cells invade other tissue highly dysplastic

Question 4

Chronic myeloid leukaemia

Answer 4

Philadelphia chromosome

Chromosome 22 cut and bound to 9

Question 5

BCR and ABL rearrangement and expression of fusion protein

Answer 5

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

Question 6

Gleevec

Answer 6

Treatment for CML

Question 7

RB knock out

Answer 7

Requires 2 hits of mitosis recombination

Question 8

Hyperplasia

Answer 8

Excessive growth

Question 9

RTK

Answer 9

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

Question 10

Deregulation of RTK

Answer 10

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

Question 11

Raw

Answer 11

Cell cycle control

Allows the cell to proliferate if no mitogen is present

Small gtpase catalysed by GEF and inactivates by GAP

Question 12

GEF

Answer 12

Catalyse exchange of gdp for gtp

Question 13

GAP

Answer 13

Catalyse exchange of gtp for gdp

Question 14

Ras mutations

Answer 14

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

Question 15

SH2

Answer 15

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

Question 16

SOS

Answer 16

Ras GEF

Question 17

RAS induced proliferation

Answer 17

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

Question 18

GF RTK RAS RAF MEK ERK pathway

Answer 18

Brings cells out of G0 and into the cell cycle

Question 19

Rb

Answer 19

Regulates cell cycle at the R point

Question 20

TGF beta

Answer 20

Regulates cell cycle until Rpoint as a growth inhibitor

Question 21

P53

Answer 21

Tumour suppressor gene

Monitors three stages of cell cycle

G1
S
G2

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

Question 22

Cycling and CDK

Answer 22

Conserved alpha helix binding

Responsible for substrate recognition

Question 23

Cyclin D

Answer 23

Present when mitogens bind

Question 24

Inactivation of RB

Answer 24

Cyclin CDK hyper phosphorylated

Question 25

P13K

Answer 25

Stimulated by IGFR RTK Generates second messenger pip3 Which phosphorylated akt at the membrane by

Question 26

P53 mutations

Answer 26

Missense Often in dna specific binding domain

Question 27

Mdm2

Answer 27

Conjugated ubiquitin to p53 which is then degraded Blocked by atm and atr

Question 28

Nutlin

Answer 28

Mdm2 mimetic

Question 29

SV40

Answer 29

Codes for oncoprotein that inhibits p53 and pRB

Question 30

Tolomerase

Answer 30

TTAGGG enzyme Prevent Philadelphia chromosome

Question 31

GRN 163l

Answer 31

Prevents telomerase extension

Question 32

Hypoxia

Answer 32

Hif1 alpha binds beta causing transcription of VEGF

Question 33

Normoxia

Answer 33

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

Question 34

Angiogenesis

Answer 34

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

Question 35

Treatment for angiogenesis

Answer 35

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

Question 36

Sources of energy I. Tumour cells

Answer 36

Glycolysis Gluatmineolysis replenishes citric acid intermediates

Question 37

E cadherin

Answer 37

Present in epithelial cells crosslinking actin by the c terminus Very low level present in carcinoma

Question 38

Invadapodia

Answer 38

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

Question 39

RGD

Answer 39

Interferes with integrin binding to the ecm preventing metastasis

Question 40

Rho GTPase

Answer 40

Members of the Ras superfamily Can be sequestered in membrane by GDI

Question 41

Intrinsic inflammatory pathway

Answer 41

Activated by various oncogenes such as RAS or EGFR Chromosomal rearrangement in the absence of a suppressor gene and create a inflammatory micro environment

Question 42

Extrinsic

Answer 42

Inflammatory conditions augment the risk of cancer

Question 43

Pathways convergence

Answer 43

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

Question 44

Chronic liver inflammation

Answer 44

NSAIDs and anti TNF alpha drugs highly reduce incidence

Question 45

Veclade

Answer 45

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

Question 46

NSAIDs such as aspirin

Answer 46

Reduce incidence of cancer as prostaglandins cannot be formed properly