Disease process of cancer Flashcards

1
Q

Causes of cancer

A
  • Initiation
  • Promotion
  • Progression (metastasis)
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2
Q

Initiation

A
  • Chemical: alcohol, smoking, tar etc.
  • Physical: ionising radiation, mechanism: chromosome translocation, gene amplification, oncogene activation
  • Viral: Herpes virus, papillomavirus, hepatitis B
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3
Q

Promotion

A
  • Growth factors

- Oncogenes

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4
Q

2 methods of stimulation for growth factors

A
  • Autocrine: cell carries receptor and secretes growth factor (GF)
  • Paracrine: GFs acting on a cell are produced locally by the cell or its immediate neighbours
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5
Q

Growth factors

A
  • Polypetide molecule
  • Regulate cell growth and function
  • Bind to cell membrane receptors
  • Stimulate activation of intracellular signal transduction pathways
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6
Q

Oncogenes

A
  • Transforming genes
  • Positive regulators of growth
  • Represent a gain in function to transformed cells
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7
Q

Tumour suppressor genes

A
  • e.g. P53
  • Most commonly altered gene in human tumours
  • Normal function is as transcriptional regulator, promotes DNA repair, apoptosis, differentiation
  • Induced by DNA damage and hypoxia
  • G1/S checkpoint control gene
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8
Q

Metastasis

A
  • Not random
  • Cascade of limited sequential steps
  • Involves tumour-host interactions
  • ‘Survival of the fittest’ pertains. So the healthier you are, the better the outcome
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9
Q

Invasion and metastasis

A
  • Tumour invades through basement membrane
  • Moves into extracellular matrix/connective tissue/surrounding cells
  • Invades blood vessels
  • Tumours cells ‘arrested;’ in distant organ
  • Enzymes involved from the ECM: plasmin, cathepsin
  • Enzyme involved from cell adhesion: integrins and loss of cahedrins correlates with tumour invasion and metastasis
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10
Q

Steps of invasion of metastasis

A
  • Primary tumour -> intravasation -> circulating tumour cell in vessel -> extravsation -> metastases
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11
Q

Angiogenesis

A
  • Formation of new blood vessels is a key factor in the maintenance and progression of malignant tumours
  • For tumour to grow >2mm there needs to be new blood vessels
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12
Q

Example of understanding molecular biology can result in improved treatment methods

A
  • Growth factors
  • Anti-VEGF antbodies can prevent interaction of VEGF with its receptors
  • Can prevent interaction with receptors
  • Activation of downstream signalling pathways
  • Can lead to vascular regression and a dormant tumour
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13
Q

How the immune systems recognise ‘foreign’ cancer cells

A
  • Cancer cells can ‘hide’ from T cells
  • PD1 (programmed death receptors) is present on T lymphocytes
  • Ligand (PGL-1) on tumour cells
  • Interaction of these suppresses T cell action
  • There is a therapeutic opportunity to block PD1 or PDL-1
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