Tumour Pathology

Question 1

What is a tumour?

Answer 1

Abnormal growing mass of tissue
Uncoordinated with surrounding normal tissue
Growth continues after stimulus removal, meaning it is an irreversible change

Question 2

What are benign tumours of the glandular epithelium/squamous epithelium called?

Answer 2

Adenoma/Squamous papilloma

Question 3

Malignant of glandular epithelium/squamous epithelium?

Answer 3

Adeno-carcinoma/Squamous carcinoma

Question 4

Benign of bone/fat/fibrous tissue?

Answer 4

Osteoma/Lipoma/Fibroma

Question 5

Malignant of bone/fat/fibrous tissue?

Answer 5

Osteo-sarcoma/Lipo-sarcoma/Fibro-sarcoma

Question 6

What are tumours of the white blood cells/lymphoid tissue called?

Answer 6

Leukaemia/Lymphoma

Question 7

Tumours of the CNS/PNS?

Answer 7

Astrocytoma/Schwannoma

Question 8

Tumours of the germ cells?

Answer 8

Ovarian teratoma (usually benign)
Testicular treatoma (usually malignant)

Question 9

Give features of benign tumours

Answer 9

Non-invasive growth
Well differentiated
Encapsulated
No metastases
Rarely cause death

Question 10

Give features of malignant tumours

Answer 10

Invasive growth
Poorly differentiated
Not encapsulated
Metastases present
Frequently cause death

Question 11

Give feature of cancer cells

Answer 11

• altered genetics (tumour suppressor genes and oncogenes)
• altered cellular function (caused by tumour-related proteins)
• abnormal morphology
• loss of cell/cell and cell/matrix adhesion (for movement)

Question 12

What are tumour related proteins?

Answer 12

Biomarkers whose presence predict the type of cancer present/prognosis/appropriate therapy

Question 13

How is the presence of tumour biomarkers detected?

Answer 13

A specific cancer drug will only work when the biomarker is active in the body

Question 14

Give some examples of tumour biomarkers and the cancers they can be used to predict

Answer 14

Kras - colorectal
EGFR - lung
Her2 - breast/gastric
Braf - melanoma
Alpha-fetoprotein - testicular/liver

Question 15

What is angiogenesis?

Answer 15

Formation of new blood vessels to supple the tumour

Provides a mechanism for metastasis

Question 16

What is metastasis?

Answer 16

Spreading of cancer cells following capsule degradation and transport in the blood/lymph

Question 17

What is the term given to the special spread of cancer across a body cavity?

Answer 17

Trans-coelomic spread

Question 18

What are common sites of metastasis?

Answer 18

Places of high blood flow;

Liver/lungs/brain/axial skeleton

Question 19

What are uncommon sites of metastasis?

Answer 19

Spleen/heart/kidney

Question 20

Where do the following tumours specifically metastasise to?

Breast
Colorectal
Prostate

Answer 20

Bone
Bone
Liver

Question 21

What are the local effects of benign tumours?

Answer 21

Pressure and obstruction

Question 22

What are the local effects of malignant tumours?

Answer 22

Pressure
Obstruction
Tissue destruction (ulceration and infection)
Bleeding (anaemia and haemorrhage)
Pain (pressure on nerves/pathological bone fractures)

Question 23

What are the systemic effects of malignant tumours?

Answer 23

Normal and abnormal hormone secretion

Question 24

What is ‘normal’ hormone secretion in relation to the systemic effects of malignant tumours?

Answer 24

Secretion by cancer cells where it is normally expected in physiology, but at an abnormal level

Question 25

What is 'abnormal' hormone secretion in relation to the systemic effects of malignant tumours?

Answer 25

Secretions of unexpected origin; e.g. ADH/ACTH

Question 26

What is dysplasia?

Answer 26

a pre-malignant change (organ/tissue enlargement), the earliest change in the malignancy process that can be detected - in epithelium - no invasion - can progress to cancer

Question 27

Give some features of dysplasia?

Answer 27

Increased nuclear size Increased mitotic activity Abnormal mitoses

Question 28

How is the cell cycle externally controlled?

Answer 28

by: - hormones - growth factors - cytokines - stroma

Question 29

How is the cell cycle intrinsically controlled?

Answer 29

by restriction points (R)

Question 30

When does external control of the cell cycle occur?

Answer 30

before the restriction point

Question 31

How is the cell cycle controlled after the restriction point?

Answer 31

autonomous control

Question 32

What happens during the G0 stage of the cell cycle?

Answer 32

resting phase, no division occurring

Question 33

G1 stage?

Answer 33

- cells increase in size | - G1 checkpoint control occurs

Question 34

S stage?

Answer 34

DNA replication occurs

Question 35

G2 stage?

Answer 35

- cells continue to increase in size | - G2 checkpoint control occurs

Question 36

M stage?

Answer 36

- no more cell growth - mitosis occurs - metaphase checkpoint control occurs (to ensure cell is ready to complete division

Question 37

What causes G1 to stop?

Answer 37

- inadequate cell size - inadequate nutrient supply - no external stimuli present - DNA damage isn't detected

Question 38

What causes G2 to stop?

Answer 38

- inadequate cell size | - DNA damage isn't detected

Question 39

What causes S to stop?

Answer 39

- DNA isn't replicated

Question 40

What causes M to stop?

Answer 40

- chromosomes mis-align

Question 41

What are checkpoints?

Answer 41

- cyclically active/inactive enzymes (CDK/cyclin complex) | - catalytic sub-units activated by regulatory sub-units

Question 42

What are the catalytic sub-units called?

Answer 42

Cyclin-dependent kinases (CDKs)

Question 43

What are the regulatory sub-units called?

Answer 43

Cyclins

Question 44

What is the function of the CDK/cyclin complex?

Answer 44

- phosphorylates target proteins - causes activation/inactivation of substrates - regulates the next phase in the cell cycle

Question 45

How are CDKs expressed?

Answer 45

constitutively in inactive form

Question 46

What happens to cyclins in the cell cycle?

Answer 46

accumulate and are destroyed as the cycle progresses

Question 47

What is the function of the retinoblastoma gene?

Answer 47

- encodes pRb (phosphoprotein) in almost every cell - pRb is hypophosphorylated by CDK/cyclin complexes - E2F transcription is inactivated by Rb

Question 48

What is the function of active E2F?

Answer 48

- activates viral target genes | - stimulates cell cycle entry (potent; leads to cancer)

Question 49

What causes carcinogenesis?

Answer 49

- mutation of genetic material that unbalances proliferation and apoptosis - in genes that regulate division/apoptosis/DNA repair - uncontrolled proliferation leads to cancer

Question 50

How can this genetic damage occur?

Answer 50

- environmental | - inherited

Question 51

How does environmental genetic damage occur?

Answer 51

- chemicals - radiation - oncogenes

Question 52

How can chemicals give rise to carcinogenesis?

Answer 52

- DNA bases damaged by oxidising and alkylating agents - chemical carcinogens/active metabolites react with DNA to form DNA adduct (covalent bonds) - adducts at certain chromosomes can lead to cancer

Question 53

How can radiation give rise to carcinogenesis?

Answer 53

- damages DNA bases | - when received in high doses e.g. UV rays/X-rays/Gamma radiation

Question 54

What two pathways can carcinogenesis disrupt?

Answer 54

- cyclin D-pRb-E2F pathway (retinoblastoma) | - p53 pathway

Question 55

What is the physiological function of p53?

Answer 55

- usually present in higher levels in damaged cells - stops cell cycle at G1 - facilitates DNA repair/induces apoptosis