Overview of tumours, as a part of cancer.

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- Carcinogens (agents which can cause cancer):

  • e.g.: smoke, radiation;
  • cause mutations in genes which control cell division (oncogenes);
  • divide uncontrollably → small mass of cells (tumour);

- Tumour cells do not respond to signals from nerves and hormons:

  • continue to grow;
  • no programmed cell death occurs (apoptosis);
  • benign → does not spread from origin (not cancerous);
  • malignantcancerous
  • spread, invade and destroy other tissues;
  • cells can break off from primary malignant tumour;
  • spread via lympathic system;
  • cause secondary tumours (metastasis) → hard to find + remove

- Cancers may take years to develop with few/no symptoms (→ but some symptoms are: haemoptysis (coughing up blood), pneumonia).

  • usually advanced when discovered
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Genes & Cancer

- Tendency to develop cancers seems to be inherited.

- Tumours cells in some cancers have abnormal chromosomes.

- Positive correlation between mutations and carcinogens.

- Oncogenes (genes that turn cells into cancers):

  • → found when proto-oncogenes (normal versions of genes) mutate + become over-active.
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RAS Oncogenes

- RAS Oncogenes:

  • G-proteins are found on plasma membranes + enable cells to respond to growth factors;
  • activated by enzymes within cell (GTPase);
  • mutation of RAS gene → GTPase deficient proteins;
  • mutated G-proteins remain active for longer → causing tumours;
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Myc Oncogenes

- Myc Oncogenes:

  • myc gene produces a protein needed for normal cell division;
  • common mutation switches myc proto-oncogene from chromosome 8 to 14;
  • there, acts as oncogene/abnormal cell division/tumour;
  • when both myc and RAS oncogenes present together → malignant cells result;
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Tumour Suppressor Genes

- Tumour suppressor genes:

  • reduce normal activity by inhibiting cell division;
  • initiate cell death (apoptosis) if the cell's DNA is damaged (due to mutations);
  • mutations of this gene → loss of functionreults in tumours
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