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
intravasation is when
primary tumour enters blood vessel
26
extravasation is when
primary tumour leaves vessel to metastasise
27
Anti-VEGF antibody Avastin binds VEGF and prevents
- interaction with receptors | - activation of downstream signalling pathways
28
most lethal gynecological malignancy
ovarian cancer
29
Anti-VEGF therapy normalises
vasculature
30
Why does our immune system not recognise ‘foreign’ cancer cells
- 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
PDL1 is expressed on
cancer cells and precentage of it can give basis for treatment
32
High levels of PD1 or PDL1 protein expression (IHC) may inhibit
Immune response
33
Nivolumab – The First
PD-1 Inhibitor Proven to Significantly Improve Overall Survival vs. Docetaxel1 in NSCLC second line therapy (2015)