Outline Of Cancer Process

Question 1

What is cancer?

Answer 1

A mass, tumour, growth, neoplasm
Disorderly growth of epithelial cells which invade adjacent tissue and spread by lymphatic & blood vessels to other parts of the body

Question 2

What does cancer being monoclonal mean?

Answer 2

Arise from a single cell

Question 3

Differences between cancer and normal cells

Answer 3

Cancer:
Lots of disorderly blood vessels
Frequent mitosis
Large nucleus
Loss of contact inhibition - don’t care that they’re going into adjacent structure
Increased growth factor secretion
Increase in ONCOGENE expression - drives cancer 
Loss of tumour suppressor genes 

Normal:
Oncogene expression rare
Intermittent coordinated growth factor secretion
Presence of tumour suppression

Question 4

Multistage carcinogenesis

Answer 4

Carcinogen - initiation - promotion - tumour growth - progression (spread)

‘Pre-clinical’ and ‘clinical’ cancers.

Question 5

Initiation stage

Answer 5

Chemical

Physical

Viral

Question 6

Promotion stage

Answer 6

Growth factors

Oncogenes

Question 7

Progression

Answer 7

Metastasis

Question 8

Chemical carcinogens

Answer 8

Chimney sweeps

Dyes - industry, hairdressers

Mustard gas - leukaemia

Alcohol& smocking, obesity - lung, head&neck (alcohol), gastrointestinal

Question 9

Physical carcinogens

Answer 9

Ionising radiation:

Smoking, buildings

Mechanism - chromosome translocation, gene amplification, oncogene activation

Question 10

Viral carcinogens

Answer 10

Infection

Question 11

Oncogenes

Answer 11

Transforming genes

Positive growth regulators

Prevention of apoptosis

Question 12

Growth factors

Answer 12

Regulate cell function and cell growth

Question 13

Autocirne and paracrine

Answer 13

??

Question 14

Tumour suppressor gene, P53

Answer 14

Most common: P53

Cancer cells show abnormal P53

Normally: promotes DNA repair, drives cell into apoptosis, differentiation of cells

In cancers: loses normal function, can be over-expressed

G1/S checkpoint control gene

Question 15

Metastasis

Answer 15

Not random

Cascade of limited sequential steps

Tumour-host interactions

Survival of fittest pertains - will immune system pick things up or not?

Question 16

Invasion& metastasis

Answer 16

Tumour invades through basement membrane

Moves into extracellular matrix/ connective tissue

Invades blood cells

Tumour cells ‘arrested’ in distant organ

Lots of things cancer cells will utilise in order to allow them to invade and metastasise

Question 17

Angiogenesis

Answer 17

Formation of new blood vessels

Key factor in maintainance and progression of malignant tumours

Tumours need to grow themselves, but also be able to grow blood vessels to grow. In cancer cells, blood vessels are very disorderly.

Question 18

Pet scans

Answer 18

Cancers ‘glow’

Question 19

VEGF

Answer 19

Vascular endothelial growth factor

Question 20

Anti-VEGF therapy

Answer 20

Stops producing blood vessels

Work sin some cancers

Ultimately causes tumour to go dormant

Question 21

Revelation of Immunotherapy

Answer 21

Not directly toxic to cancer cells

Awaken/ improve immune system using patients own immune system.

Once immune system is activated, no more drugs are needed.

Changing how we look at cancer

Question 22

PD1/ PDL-1 blockage

Answer 22

Takes cloak off of ‘immunoevasive’ cells so that immune system can ‘see’ and act on them.

Question 23

High levels of PD1 and PDL 1 do what?

Answer 23

Inhibit immune response

Question 24

What is NIVOLUMAB?

Answer 24

First PD-1 inhibitor proven to significantly improve overall survival rates.

Question 25

Why is cancer much more common in older people?

Answer 25

More life been lived, more cell repair and potential error mutations

Question 26

Is metastasis an organised process?

Answer 26

YES

Question 27

Stop the primary tumours!

Answer 27

Smoking etc.