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1

what is neoplasia?

an autonomous proliferation of cells with the loss of normal growth control

2

what is a tumour?

it is any swelling that can be benign or malignant

3

what is benign?

when there is no local invasion and no metastasis

4

what is malignant?

when there is local invasion and metastasis

5

what is hypertrophy and hyperplasia?

hypertrophy is an increase in individual cell size and hyperplasia is an increase in the number of cells

6

what is metaplasia?

it is the replacement of mature tissue types

7

what is dysplasia?

commonly it is an abnormality that indicative of the precursor change of malignancy

8

what is anaplasia?

failure to differentiate in malignancy

9

what is the AAA, BCSP, BSP and the CSP programmes?

the abdominal aortic aneurysm, bowel cancer, breast screening and cervical screening programme

10

what are the DES, FASP, IDPS, and NIPE programmes?

the diabetic eye, fetal abnormality, infectious diseases in pregnancy and newborn and infant physical examination programmes

11

what are the NBS, NHSP, SCT?

the newborn blood spot, newborn hearing screening and the sickle cell and thalassaemia programmes

12

what is the name for all programmes and how are they assessed?

the screening and quality assurance programmes

13

what are three characteristics imperative in tumour behaviour?

invasion, metastasis and angiogenesis

14

what is the difference between invasion and metastasis?

invasion is invading the adjacent normal tissue and destroying normal tissue whereas metastasis is when it spreads from the site of origin to distant sites and forms secondary tumours here

15

what is the result of metastasis and invasion?

can result in local disease forming a systemic disease

16

how do clinicians characterise the tumours?

using staging and grading

17

which cancer is unlikely to metastasise?

basal cell carcinoma

18

which cancer is very likely to metastasise?

lung cancer and 1/3 of breast

19

how do paediatric patients present?

majority will already have metastasised

20

what happens with metastasis in adults?

around half of all adult patients will metastasise

21

how does invasion occur?

there is increased motility, decreased adhesion, production of proteolytic enzymes and mechanical pressure

22

how to cells adhere to one another?

cell to cell adhesion molecules called cadherins

23

what happens if there is a mutation in E-cadherin?

there is the loss of cell to cell adhesion and contact inhibition

24

where else can cells adhere to?

the matrix through cell-matrix adhesion molecules

25

what are cell-matrix adhesion molecules and how can changes in these lead to motility changes?

integrins
changes in integrin expression can result in the decreased cell-matrix adhesion

26

what changes happen in epithelial cells in cancer?

epithelial cells are usually tightly connected, polarised and tethered
mesenchymal cells are loosely connected and able to migrate
in cancer epithelial cells with gain mesenchymal cell properties making them able to migrate and invade

27

what changes occur in ECM during caner?

in the ECM there are matrix metalloproteinases and in normal tissue regulation there is a balance between the matrix and the metalloproteins, with tissue inhibitors of metalloproteins. In cancer the balance tips as the inhibitors become more dense and therefore favours ECM breakdown meaning that there is local invasion

28

what role does mechanical pressure play in tumour formation?

the uncontrolled proliferation forms a mass, this puts pressure on vessels and results in occlusion and pressure atrophy. The tumour will spread along the lines of least resistance

29

what are examples of proteolytic enzymes in the ECM?

interstitial collagenases, gelatinases and stomolysins

30

what do stomolysins break down?

collagen type IV and proteoglycans