Lecture 31 Flashcards Preview

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Flashcards in Lecture 31 Deck (17)
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1

What causes tumours to form

Tumours are created by cells that have lost the ability to assemble and create tissue of normal form and function

2

The plasias occur independently of each other and in a sequential manner, T or F

F – plasia’s often occur together or can develop over time

3

What is the overall trend of cancer progression

Hyperplasia --> Metaplasia --> Dysplasia --> Neoplasia

4

What is the major risk factor in acquiring cancer

Age – on average the older you are, the higher your risk of cancer

5

The likelihood of developing cancer increases in with age for every cancer, T or F

F – the age/incidence prolife varies with different cancer – for example testicular cancer reaches its peak incidence during puberty and adolescence

6

The incidence of cancer is increasing, T or F

T – 80% of patients that die of other causes will be found to have a tumour too

7

Explain the results of the Japanese/Hawaii migrant studies in explaining the environmental influence in cancer influence

Amongst Japanese nationals living in Japan, stomach and liver cancer levels were elevated. After moving to Hawaii though, the rates of both stomach and liver cancer decreased. However the levels of colon and prostate cancer in these migrants did see an increase towards the higher levels seen in Caucasian Hawaiians. This shows that migrants acquire a cancer spectrum depending on their environment not just their genetic heritage

8

Explain Richard Doll’s contribution to cancer research

Doll linked the carcinomas of the lung to smoking. He was deemed the father of epidemiology for correlating of the number of cigarettes smoked to the incidence of lung cancers. He also identified the lag phase after taking up smoking due to the time taken for the induction of genetic instability

9

How long is the lag phase after taking up smoking before lung carcinomas usually begin to present

20 years

10

Give examples of cancers that have a genetic or familiar basis of inheritance

Colon cancer – FAP/APC, Retinoblastoma, Kidney Cancer – Wilms’ Tumour, Breast Cancer – Hereditary (BRCA1/2)

11

A single mutation is enough to cause cancer, T or F

F

12

What is the equation that links the probability of tumorigenesis with the number of mutations and age

LogP(T)=nLogA+k where P(T) is the probability of a tumour forming, n is the slope or the number of mutations required, A is age and k represents a constant

13

Which residues do cdks phosphorylate in target proteins

Serine/Threonine

14

What prevents the inactive cdks from acting

Their active site is occluded by the T loop

15

What happens in response to cyclin binding to cdk and the subsequent activation of the kinase

Cyclin binding to Cdk pulls the T loop away from the active site and exposes the bound ATP which allows it to access to target proteins and phosphorylate them

16

What other protein is required for the full activation of cdk and why is this

Cdk activating kinase phosphorylates a crucial threonine in the T loop of the protein. This enables cdk to bind and phosphorylate its target proteins

17

What is the role of cdk inhibitor proteins (CKIs)

Cdk inhibitor proteins (CKIs) help regulate the rise and fall of cyclin-Cdk activity. Some inhibitors bind directly at the kinase active site and block kinase activity by interfering with ATP binding