Cancer

Question 1

What is the etiology of liver cancer?

Answer 1

Chronic alcoholism……
•	Hep C.
•	Chronic Hep. B
•	Alcoholism
•	Aflatoxin B1 (aspergillus flavus)
•	Haemochromatosis
•	Diabetes
•	Obesity
•	Drugs & Medication
•	Steroids
•	Oestrogens

Question 2

Mechanism of proposed theory of liver cancer (5)

Answer 2

Hepatitis infection  becomes chronic if untreated  inflammation  cirrhosis  dysplastic lesions  clonal selection  hepatocellular carcinoma

Question 3

Outline the activation of RAS

Answer 3

EGF binds to receptor protein tyrosine kinase  dimerises and cross phosphorylation occurs  allows recruitment of adaptor proteins e.g. Grb2 that can bind Ras activating factors. Ras is on the cytosolic surface of plasma membrane and is bound to GDP  GDP is exchanged for GTP using exchange factor SOS  Ras with GTP is now active

Question 4

Is SOS a Ras activating factor? Can SOS bind to Grb2?

Answer 4

SOS is always bound to Grb2 and it is an exchange factor- exchanges GDP for GTP on RAS so RAS becomes activated

Question 5

What is the function of Grb2, Sos, Ras (3)

Answer 5

• Grb 2-adaptor protein and binds to the phosphorylated receptor .
• SOS; an exchange factor that is responsible for exchanging the GDP on RAS for GTP .
• RAS; to activate the rest of the ERK pathway after it has been phosphorylated

Question 6

Which 2 are protooncogenes? (2)

Answer 6

Ras, EGF

Question 7

What is an example of initial signalling protein? (1)

Answer 7

Grb2

Question 8

How does actin change in the lamellae?

Answer 8

These undergo polymerization, disassembly, branching, capping, occurring at the leading edge, resulting in net filament assembly - branched and crosslinked.

Question 9

How does actin change in the filopodia + what is their function?

Answer 9

They form tight actin bundles of parallel filaments and crosslinking and there is actin polymerisation at the tip.
There is also retrograde flow but the polymerisation is faster so it grows outwards.
Their function is to form focal adhesion to the substratum

Question 10

How does actin change in stress fibres during retraction at the rear end?

Answer 10

These are the stress fibre, under tension, contraction occurs. (Rho?)

Question 11

How do cells become malignant from benign-4 steps (2)

Answer 11

Disassembly of the cell-cell contact  loss of polarity  Increased motility  Release of MMP to break down the extracellular matrix

Question 12

What are the consequences of metastases? (2)

Answer 12

you probably die harder to treat - can’t cure using surgical resection, worse prognosis

Question 13

Define metaplasia and give an example (3)

Answer 13

Reversible replacement of one differentiated adult cell type to another, in response to a stressful stimuli. E.g sqamous eosophageal to columnar intestinal cells from acid reflux - barrett’s oesophagus

Question 14

What are 3 features of cells showing dysplasia? (3)

Answer 14

• Enlarged hyperchromatic nucleus
• Loss of architectural orientation
• Loss in uniformity of individual cells
• Variability in size and shape
• Mitotic figures abundant

Question 15

Give 2 examples of dysplasia and their causes (4)

Answer 15

• HPV causing CIN

* Acid reflux causing barrett’s oesophagus