outline of disease processes in cancer Flashcards

1
Q

most cancers are

A

monoclonal; arise form single cell

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2
Q

cancers invade

A

adjacent tissue and are spread by lymphatics nad blood vessels to other parts of the body

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3
Q

cancer cell features

A
  • loss of contact inhibition
  • increase in growth factor secretion
  • increase in oncogene expression
  • loss of tumour suppressor genes
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4
Q

normal cell features

A
  • oncogene expression is rare
  • intermittent or co-ordinated growth factor secretion
  • presense of tumour suppressor genes
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5
Q

things that initiate cancers are

A

chemical
physical
iral

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6
Q

things that promote cancers are

A

growth factors

oncogenes

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7
Q

things that allow progression of cancers

A

metastasis

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8
Q

aniline dyes can cause

A

bladdar cancer

- chemical carcenogenesis

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9
Q

nitrogen mustard can cause

A

leukaemia

- chemical carcenogenesis

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10
Q

aflatoxin can cause

A

liver damage

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11
Q

physical carcinogens

A
  • ionising radiation
    - dose response relationship
    - radon source is mainly buildings
    - ventillation reduces risk
  • mechanism
    - chromosome translocation
    - gene amplification
    - oncogene activation
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12
Q

oncogenes function

A

transforming genes

  • positive regulators of growth
  • represent gain in function to transformed cells
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13
Q

growth factors function

A

polypeptide molecules

  • regulate cell growth and function
  • bind to cell membrane receptors
  • stimulate activation of intracellular signal transduction pathways
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14
Q

oncogene stimulation may be

A
  • autocrine

- paracrine

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15
Q

autocrine stimulus is when

A
  • cell carries receptor and secretes growth factor

- cell escapes normal control mechanism

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16
Q

paracrine stimulus is when

A
  • growth factors acting on cell are produced locally the cell or its intermediate neighbours
17
Q

P53 normal function

A

tumour suppressor gene

  • normal function is as transcriptional regulator
  • promotes DNA repair, apoptosis, differentiation
18
Q

p53 is induced by

A

DNA damage and hypoxia.

- G1/S checkpoint control gene

19
Q

metastasis features

A
  • non random
  • cascade of limited sequental steps
  • involves tumour-host interactions
  • survival of the fittest pertains
20
Q

invasion and metastasis

A
  • tumour invades through basement membrane
  • moves into extracellular matrix/connective tissue/surrounding cells
  • invades blood vessels
  • tumour cells arrested in distant organ
21
Q

enzymes involved in invasion and metastasis:

In ECM

A
  • Matrix metalloproteinases (MMPs) – several subclasses eg gelatinases
  • Plasmin
  • Cathepsin
22
Q

enzymes involved in invasion and metastasis:

cell adhesion

A
  • Cahedrins (loss correlates with tumour invasion and metastasis)
  • Integrins
  • CD44
23
Q

angiogenesis is

A

the formation of new blood vessels.

  • key factor in maintenance and progression of malignant tumours
  • is a must for tumours that want to grow past 2mm in diameter
24
Q

degradation of the extracellular matrix is necessary for

A

new blood vessel formation to occur

25
Q

intravasation is when

A

primary tumour enters blood vessel

26
Q

extravasation is when

A

primary tumour leaves vessel to metastasise

27
Q

Anti-VEGF antibody Avastin binds VEGF and prevents

A
  • interaction with receptors

- activation of downstream signalling pathways

28
Q

most lethal gynecological malignancy

A

ovarian cancer

29
Q

Anti-VEGF therapy normalises

A

vasculature

30
Q

Why does our immune system not recognise ‘foreign’ cancer cells

A
  • Cancer cells can ‘hide’ from T cells
  • PD1 (programmed death receptor) present on T lymphocytes
  • Ligand (PDL-1) on tumour cells
  • Interaction of these suppresses T cell action
31
Q

PDL1 is expressed on

A

cancer cells and precentage of it can give basis for treatment

32
Q

High levels of PD1 or PDL1 protein expression (IHC) may inhibit

A

Immune response

33
Q

Nivolumab – The First

A

PD-1 Inhibitor Proven to Significantly Improve Overall Survival vs. Docetaxel1 in NSCLC second line therapy (2015)