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Year 2 EMS MoD > Behaviours of Tumours > Flashcards

Behaviours of Tumours Flashcards

1
Q

What are the main characteristics of malignant tumours? (3)

A
  • Invasion
  • Metastasis
  • Angiogenesis
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2
Q

What is invasion?

A

Tumour invades adjacent tissue and destroys it.

-local disease

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3
Q

What is metastasis?

A

Tumour spreads from site of origin to distant sites&raquo_space; 2* tumour.
-systemic disease

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4
Q

What proportion of metastases lead to death?

A

50%.

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5
Q

What causes invasion? (3)

A
  • Increased motility
  • Decreased adhesion
  • Proteolytic enzyme production
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6
Q

What are Cadherins?

A

Transmembrane proteins.

|&raquo_space; cell to cell adhesion

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7
Q

What does a mutation of E-cadherin lead to?

A

Loss of cell-cell adhesion and contact inhibition.

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8
Q

What are integrins?

A

Proteins that attach cells to extra-cellular matrix.

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9
Q

What does a change in integrin expression lead to?

A

Decreased cell-matrix adhesion.

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10
Q

What are the main properties of epithelial cells? (3)

A
  • Tightly connected
  • Polarised
  • Restricted movement
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11
Q

What are the main properties of mesechymal cells? (2)

A
  • Loosely connected

- Able to migrate

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12
Q

What happens to cancer epithelial cells that enables them to have an increased motility?

A

Epithelial-Mesenchymal properties.

  • cancer epithelial cells gain mesenchymal properties.
  • can invade and migrate
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13
Q

What are metalloproteinases?

A

Proteolytic enzymes.

|&raquo_space; break down proteins / degrade ECM

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14
Q

What type of proteolytic enzyme breaks down collagen types I-III?

A

Interstitial collagenases.

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15
Q

What type of proteolytic enzyme breaks down collagen type IV and gelatin?

A

Gelatinases.

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16
Q

What type of proteolytic enzyme breaks down collagen type IV and proteoglycans?

A

Stomolysins.

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17
Q

Proteolytic enzymes; how are they regulated in normal tissues?

A

Matrix metalloproteinases = tissue inhibitors of metalloproteinases.

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18
Q

Why do proteolytic enzymes favour ECM breakdown in cancer?

A

Matrix metalloproteinases > tissue inhibitors of metalloproteinases.

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19
Q

How do tumours cause mechanical pressure?

A

Uncontrolled proliferation&raquo_space; mass.

-pressure occludes vessels / tissues

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20
Q

What are the main metastatic routes of spread? (4)

A
  • Lymphatic
  • Blood
  • Transcoelomic
  • Implantation
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21
Q

What is transcoelomic spread?

A

Spread across peritoneal / pleural / pericardial cavities, or in CSF.

22
Q

What is implantation?

A

Spread of tumour during biopsy / surgery.

23
Q

What are the main sites that tumours spread to in the blood?

A
  • Liver
  • Lungs
  • Brain
  • Bone
24
Q

Via what route do carcinomas normally spread first?

A

Lymphatic spread.

25
Q

Via what route do sarcomas normally spread first?

A

Blood.

26
Q

Where do bone metastases tend to originate from?

A 
Breast
Prostate
Lung
Kidney
Thyroid
27
Q

What are the main types of bone metastases? (2)

A
  • Lytic (lung)

- Sclerotic (prostate)

28
Q

Where do transcoelomic metastases often originate from?

A

Ovaries.

29
Q

Where do lung tumours often metastasise to?

A

Brain

Adrenal

30
Q

What is thought to affect sites of metastases?

A

Tissue environment.

-different tissues are more susceptible

31
Q

What is angiogenesis?

A

Formation of new blood vessels.

-essential if metastases are to grow > 1-2mm

32
Q

An increase in what type of molecule causes angiogenesis?

A

Promoters.

33
Q

What type of cells produced promoters&raquo_space; angiogenesis? (3)

A
  • Tumour cells
  • Stromal cells
  • Inflammatory cells
34
Q

What are the main promoters produced&raquo_space; angiogenesis? (3)

A
  • VEGF
  • PDGF
  • TGF-beta
35
Q

What normally prevents angiogenesis?

A

Inhibitors.

36
Q

What are the main inhibitors that prevent angiogenesis?

A
  • ECM PROTEINS
  • thrombospondin
  • Canstatin
  • Endostatin
37
Q

What is stage?

A

How advanced a tumour is.

-whether it has spread, and to what extent

38
Q

What is grade?

A

How aggressive a tumour is.

  • how different it looks from tissue of origin
  • how fast it develops
39
Q

What staging system is generally used?

A

TMN staging (I-IV).

  • Tumour, Metastasis, Node
  • differs for each organ
40
Q

TMN; what does T stand for?

A

Tumour.

-size +/- extent of 1* tumour

41
Q

TMN; what does M stand for?

A

Metastases.

-presence and extent

42
Q

TMN; what does N stand for?

A

Nodes.

-presence and number of lymph node metastases

43
Q

What are the T stages for breast cancer?

A 
Tis = in situ
T1 = 5cm
T4 = involving skin/chest wall
44
Q

What are the M stages for breast cancer?

A 
M0 = no distant metastases
M1 = distant metastases
45
Q

What are the N stages for breast cancer?

A 
N0 = no nodes
N1 = ipsilateral nodes
N2 = >node involvement
46
Q

What are the simplified stages of breast cancer?

A 
0 = Tis
I = T1, N0, M0
II = T1-2 + M1 or T3
III = T(any) + N2, or T4
IV = T(any), N(any), M1
47
Q

What type of cancer uses Dukes staging?

A

Colorectal cancer.

48
Q

What are the Dukes stages? (4)

A

A - invades into bowel wall
B - invades through bowel wall, but no lymph nodes metastases
C - local lymph nodes
D - distant metastases

49
Q

What is the 5 year survival for Dukes staging?

A 
A = >90%
B = 70%
C = 30%
D = 5-10%
50
Q

What are the main components of grading? (4)

A
  • Differentiation (from tissue of origin)
  • Nuclear polymorphism and size
  • Mitotic activity
  • Necrosis

Year 2 EMS MoD (20 decks)

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