Cancer Flashcards

(11 cards)

1
Q

Describe how tumours and cancers form

A

Mutations in genes controlling mitosis can lead to
uncontrolled cell division. A tumour formed if this results in mass of abnormal cells. Malignant tumours are cancerous and can spread by metastasis. Benign tumours are non-cancerous

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1
Q
A
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2
Q

Compare the main characteristics of benign and malignant tumours

A

Benign tumours
* Usually grow slowly (cells divide less often)
* Cells are well differentiated / specialised
* Cells have normal nuclei
* Well defined borders and often surrounded by a capsule so do not invade surrounding tissue
* Do not spread by metastasis (as cell adhesion molecules stick cells together)
* Can normally be removed by surgery and they rarely return

Malignant tumours
* Usually grow faster (cells divide more often)
* Cells become poorly differentiated / unspecialised
* Cells have irregular, larger / darker nuclei
* Poorly defined borders and not encapsulated so can invade surrounding tissues (growing projections)
* Spread by metastasis - cells break off and spread to other parts of the body, forming secondary tumours
(due to lack of adhesion molecules)
* Can normally be removed by surgery and radiotherapy / chemotherapy but they often return

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3
Q

Describe the function of tumour suppressor genes

A

Code for proteins that:
* Inhibit / slow cell cycle (e.g. if DNA damage detected)
* Cause self-destruction (apoptosis) of potential tumour cells (e.g. if damaged DNA can’t be repaired)

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4
Q

Explain the role of tumour suppressor genes in the development of tumours

A
  • Mutation in DNA base sequence results in the production of a non-functional protein due to change in amino acid sequence which changes protein tertiary structure
  • Decreased histone acetylation or increased DNA methylation prevents production of protein by preventing binding of RNA polymerase to promoter region, inhibiting transcription
  • Both lead to uncontrolled cell division
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5
Q

Describe the function of (proto-)oncogenes

A

Code for proteins that stimulate cell division

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6
Q

Explain the role of oncogenes in the development of tumours

A
  • An oncogene is a mutated or abnormally expressed form of the corresponding proto-oncogene
  • A mutation in the DNA base sequence results in overproduction of protein or permanently activated protein, by leading to change in amino acid sequence which changes protein tertiary structure
  • Decreased DNA methylation or increased histone acetylation increases production of the protein, by stimulating binding of RNA polymerase to promoter region, stimulating transcription
  • Both lead to uncontrolled cell division (cell division is permanently stimulated)
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7
Q

Suggest why tumours require mutations in both alleles of a tumour suppressor gene but only one allele of an oncogene

A
  • One functional allele of a tumour suppressor gene can produce enough protein to slow the cell cycle
  • One mutated oncogene allele can produce enough protein to lead to uncontrolled cell division
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8
Q

Explain the relevance of epigenetics in cancer treatment

A

Drugs could reverse epigenetic changes that caused cancer, preventing uncontrolled cell division. For example:
* Increasing DNA methylation or decreasing histone acetylation of oncogene to inhibit transcription / expression
* Decreasing DNA methylation or increasing histone acetylation of tumour suppressor gene to stimulate transcription / expression

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9
Q

Explain the role of increased oestrogen concentrations in the development of some (oestrogen receptor-positive) breast cancers

A
  • Some breast cancers cells have oestrogen receptors, which are inactive transcription factors
  • If oestrogen concentration is increased, more oestrogen binds to oestrogen receptors,
    forming more oestrogen-receptor complexes which are active transcription factors
  • These bind to promoter regions of genes that code for proteins stimulating cell division
  • This increases transcription / expression of these genes, increasing the rate of cell division
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10
Q

Suggest how drugs that have a similar structure to oestrogen help treat oestrogen receptor-positive breast cancers

A

Drugs bind to oestrogen receptors (inactive transcription factors), preventing binding of oestrogen, so no / fewer transcription factors bind to promoter regions of genes that stimulate the cell cycle.

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