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Flashcards in Outline of Disease Processes Deck (34)
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1

What is cancer

A carcinoma or disorderly growth of cells (80% originate from epithelial cells and 20% in connective, musculoskeletal or nervous tissue) which invade adjacent tissue and spread by the lymphatics and blood vessels to other parts of the body

2

Most cancers are...

Monoclonal

3

How do cancer cells divide

Mitosis

4

State the features of cancer cell growth

Loss of contact inhibition
Increase in growth factor secretion
Increase in oncogene expression
Loss of tumour suppressor genes
Frequent mitoses

5

State the features of normal cell growth

Few mitoses
Oncogene expression is rare
Intermittent or coordinated growth factor secretion
Presence of tumour suppressor genes

6

Why is cancer sometimes diagnosed late

It cannot be detected until there is 10^9 cancer cells present

7

What are the causes that initiate cancer cell growth

Chemical
Physical
Viral

8

What are the causes that promote cancer cell growth

Growth factors
Oncogenes

9

What are the causes of cancer cell progression

Metastasis

10

Give examples of chemical carcinogens

Aniline dyes in bladder cancer
Aflatoxin in liver
Nitrogen mustard in leukaemia
Alcohol and smoking in lung, head, neck and gastrointestinal cancers

11

Give examples of physical carcinogens

Ionising radiation
Mecanisms (e.g. chromosome translocation, gene amplification and oncogene activation)

12

give examples of viral carcinogens

Herpes virus - Burkitt's lymphoma
Papillomavirus - Cervical cancer
Retroviruses - Adult T-cell leukaemia/lymphoma (HTLV1), Hairy cell leukaemia (HTLV2)
Hep B - Liver cancer

13

What are oncogenes

Transforming genes
Positive regulators of growth
Represent a gain in function to transformed cells (e.g. in follicular lymphoma, BCL2 activation prevents apoptosis and p53 a tumour suppressor gene).

14

What are growth factors

Polypeptide molecules which regulate cell growth and function by binding to cell membrane receptors to stimulate the activation of intracellular signal transduction pathways.

15

How do growth factors and oncogenes work together

Growth factor attaches to the growth factor receptor
Triggers a post receptor signal transduction pathway
Activates oncogenes which promote growth factor and receptor synthesis.
Receptors produced will move to the cell membrane and the receptors can either cause autocrine stimulation (self-stimulating) or paracrine stimulation (adjacent cells)

16

What is autocrine stimulation

When the cell carries the receptor and secretes the growth factor to escape the normal control mechanism

17

What is paracrine stimulation

When the growth factors acting on a cell are produced locally by the cell or its immediate neighbours

18

What is p53

The most commonly altered tumour suppressor gene in human tumours (37% but higher in lung and colon cancers)

19

What is p53's normal function

Act as a transcriptional regulator
Promote DNA repair
Apoptosis
Differentiation

20

How is p53 induced

By DNA damage
Hypoxia

21

What checkpoint does p53 control

G1/S checkpoint

22

State 4 details of metastasis

Its not random
Has a cascade of limited sequential steps
Involves tumour-host interactions
'Survival of the fittest' pertains

23

How does a tumour metastasise

Tumour invades through basement membrane
Moves into the extracellular matrix/connective tissue/surrounding cells
Invades blood vessels allowing tumour cells to be ‘arrested’ in distant organs

24

Which enzymes in the process are present in the ECM

Matrix metalloproteinases (MMPs) which has several subclasses e.g. gelatinases
Plasmin
Cathepsin

25

Which enzymes in the process are present in cell adhesion

Cahedrins (loss correlates with tumour invasion and metastasis)
Integrins
CD44

26

What is angiogenesis

Formation of new blood vessels

27

Why is angiogenesis important for tumour growth

It's a key factor in the maintenance and progression of malignant tumours
New blood vessels must form in order for a tumour mass to exceed 2 mm in diameter

Clinical correlations can be seen between vessel density, tumour malignancy and metastasis

28

What is necessary for angeogenesis

Degradation of the extracellular matrix is necessary for new blood vessel formation to occur

29

How can VEGF releated cancers be treated

Using an anti-VEGF antibody avastin, which binds VEGF
It prevents VEGF interacting with receptors and the activation of downstream signalling pathways Therefore it results in vascular regression and the tumour remaining dormant

30

What does VEGF stand for

Vascular endothelial growth factor