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302: Scientific basis of medicine > Hallmarks of cancer > Flashcards

Hallmarks of cancer Flashcards

1
Q

The 6 cellular hallmarks of cancers

A
  1. Can evade inhibitory growth signals.
  2. Grows without growth signals
  3. Angiogenesis
  4. Invasion and metastasis
  5. Evades apoptosis
  6. Unlimited replication
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2
Q

Oncogenes

  • Definition
  • Examples
A

Normal genes that is pro-malignant when mutated.

Mutations lead to:

  • Unregulated angiogenesis
  • Continuous replication/ growth
  • Invasion, metastasis

Genes are dominant

  • Only one allele mutation required for oncogenic effect
  • But it is not inherited like this

Examples

  • erB2/ Her2 (epidermal growth factor)
  • Ras
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3
Q

Tumour suppressor genes

  • Definition
  • Examples
A

Definition

  • Genes that regulate anti-malignant processes
  • Involved in: apoptosis, DNA repairs, cell cycle regulation, growth inhibition.

Genes are recessive

  • Requires two alleles to be mutated
  • Can be inherited.

Examples

  • p53
  • APC
  • BRCA1, 2
  • retinoblastoma (Rb)
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4
Q

Viruses and cancer

A

Certain viruses predisposes to certain cancers.

HPV 16, 18

  • Viral DNA inserts itself into host DNA
  • Stimulates production of proteins that makes cells pro-malignant

Adult T cell lymphoma
- HTLV-1

Burkitt’s lymphoma
- EBV

Hepatocellular cancer
- Hep B, C

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5
Q

HPV and cervical carcinoma

A

HPV 16, 18

viral dna inserts itself into host DNA and stimulates proteins that make cell pro-malignant

E6
- degrades p53

E7
- inactivates Rb by phosphorylating it

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6
Q

Virus associated with Adult T cell lymphoma

A

HTLV-1 (human T cell leukaemia virus type 1)

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7
Q

Virus associated with Burkitt’s lymphoma

A

EBV

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8
Q

ErbB-1

A

Epidermal growth factor gene

Protein

  • Transmembrane, activated by EGF
  • Tyrosine kinase receptor- autophosphorylation
  • Stimulates downstream signalling–> RAS-MAPK (mitogen activated protein kinase)

Oncogene when mutated
- Stimulates persistent replication and growth

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9
Q

erB2/ her2

A

Human epidermal growth factor receptor
- Oncogene

When mutated, predisposes to breast cancer (25%)

Cancer is more resistant to treatment and more aggressive.

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10
Q

Ras

A

GTPase that is involved in cell proliferation
- When mutated, becomes oncogenic

In mutation:

  • GTPase loses function and RAS is constantly active
  • Found in 1/3 of all cancers
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11
Q

p53

A

Tumour suppressor protein involve in regulate cell growth
- Mutated in half of cancers

Involved in

  • apoptosis
  • cell cycle crest
  • DNA repair
  • Angiogenesis

Mutation leads to

  • Increased mutation rate of cell’s DNA
  • Reduced apoptosis
  • Persistent angiogenesis
  • increased tumour growth
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12
Q

Li-Fraumeni syndrome

A

Autosomal dominant condition
- Germline mutation of p53

Predisposes to several cancers (SBLA)

  • Sarcoma
  • Breast
  • Leukaemia
  • Adrenal
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13
Q

APC

A

Tumour suppressor protein
- Pro-oncogene

Germline mutation associated with familial adenomatous polyposis
(FAP)
- Predisposes to colorectal cancer

Spontaneous mutation associated with colorectal cancer.

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14
Q

Familial adenomatous polyposis (FAP)

A

Autosomal dominant inheritance

Predisposes to developing colorectal cancer through formation of colonic polyps

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15
Q

Multistep carcinogenesis of colorectal cancer

A

Non-hereditary mutations and environmental stresses leading to development of cancer

  1. APC mutation= small adenoma
  2. K-ras/ DCC mutation= large adenoma
  3. p53 mutation= carcinoma
  4. Aneuploidy= metastasis
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16
Q

Hallmark: Grows without influence of growth signals

A

EGFR is stimulated despite lack of ligand due to mutation.

17
Q

Examples of inhibitory growth signals

A

Down regulation of growth receptors.

Inactivation/ degradation of signalling proteins

Inhibition of kinase signalling (phosphates)

Competition with growth-mediating proteins

Inhibition of transcription

18
Q

Tumour’s ability to evade apoptosis

A

Pro-apoptotic signals are deficient

  • i.e Caspases, cytokines
  • Bax, p53

Anti-apoptotic signals upregulated
- Bcl-2

19
Q

Unlimited replication in tumours

A

Telomerase is upregulated

- Telomeres are longer so becomes anti-apoptotic

20
Q

Angiogenesis in tumours

A

VEGF is unregulated
- Can produce vessels as it grows.

Anti-angiogenesis factors are down regulated

21
Q

Tumours Invasion and metastasis into other tissues.

A

Tumour cells express abnormal integrins
- breaks from inter/extracellular connections

Matrix metalloproteases facilitates invasion

TIMPsi nhibits invasion

MMP-TIMPs balance is abnormal in tumours

22
Q

Evidence for cancer clonality

A

All cells in a cancer carry the same founding mutation
- Philadelphia mutation in CML

Lyonisation of the same X chromosome in cancer cells, in women
- G6PD polymorphism

Multiple myeloma patients

  • Monoclonal Ig on protein electrophoresis
  • Light chain restriction

Cancer stem cells can reproduce the cancer
- Transplantation study of cancer cells in animals.

23
Q

Darwinian selection of cancer cells

A

Increasingly malignant sub-clones of cancer cells arise from ‘selective pressures’ (i.e chemothreapy)
- Selects out cells with additional mutations and growth advantages.

This further leads to invasion and metastasis
- Due to increased genetic and chromosomal instability.

24
Q

Where is p53 gene located?

A

Short arm (p) of chromosome 17.

25
Q

Factors that trigger P53 (5)

A

DNA damage

Abnormal growth signals

Oncogene activation

Cell stress

  • Hypoxia
  • Nucleotide depletion
26
Q

Function of P53 (4))

A

Cell cycle arrest

Apoptosis

DNA repair

Inhibition of angiogenesis

302: Scientific basis of medicine (28 decks)

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