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Biology of Cancer > Models of Carcinogenesis > Flashcards

Models of Carcinogenesis Flashcards

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1
Q

What are 3 assumptions about carcinogenesis

A
  1. Malignant transformation of a single cell is sufficient to give rise to a tumour
  2. Any cell in a tissue is as likely to be transformed as any other of the same type
  3. Once a malignant cell is generated, the mean time to tumour detection is generally constant
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2
Q

What are 5 different non exclusive models in which cells can become carcinogenic?

A
  1. Mutational
  2. Genome instability
  3. Non-genotoxic
  4. Darwinian
  5. Tissue organisation
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3
Q

What is the mutational model?

A
  • Caused by chemical carcinogens that can mutate DNA and therefore the cancer arises due to accumulation of irreversible DNA damage.
  • They act in a geneotoxic manner
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4
Q

What are the 4 classes of carcinogens?

A
  1. Chemical (eg nitrosamines, carbamates, azo dyes etc)
  2. Physical (radiation from UV/ionising and asbestos)
  3. Heritable (predisposition)
  4. Viral (Hepatitis B/Epstein Barr)
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5
Q

Why does smoking increase the risk of cancer?

A

Cigarettes contain polycyclic hydrocarbon benzo(a)pyrene (BP) as well as 81 other carcinogens. BP is able to easily enter cells

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6
Q

What is the Ames test?

A
  • A test to determine the mutagenic activity of chemicals by observing whether they cause mutations in sample bacteria.
  • A high number of revertants on the plates suggests the mutagen used causes mutations
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7
Q

How do physical carcinogens work?

A

They act by imparting energy into the biological material, using radiation as the primary agent

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8
Q

How does radiation cause cancer?

A
  • Different types of radiation can act as physical carcinogens. Includes ionising radiation (X-rays, nuclear) and UV radiation.
  • If the damage caused isn’t repaired, it can lead to translocations and mutations.
  • UV is leading cause of melanoma
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9
Q

How do heritable carcinogens work?

A
  • It predisposes cancer to offspring.
  • Only accounts for 5% of cancers.
  • Is an inherited germline mutation, allowing increased risk of cancer.
  • Mostly caused by a mutation to a single gene (monogenic hereditary diseases).
  • The risk is increased if a deficiency in DNA repair occurs and the damage accumulates.
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10
Q

Which heritable syndromes are caused through DNA repair defects?

A
  • Ataxia telangiectasia
  • Bloom’s syndrome
  • Lynch type ll
  • Fanconi’s anaemia
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11
Q

Which heritable syndromes are caused through chromosomal abnormalities?

A

Down’s syndrome & Klinefelter’s syndrome

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12
Q

What is Ataxia Telangiectasia

A
  • Causes neuromotor dysfunction and dilation of blood vessels
  • Caused by a mutation in ATM gene which disrupts cell cycle arrest, DNA repair and apoptosis
  • Cancer predisposition = lymphoma, leukaemia, breast cancer
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13
Q

What is Bloom’s syndrome?

A
  • Causes short stature (rarely exceed 5 feet), skin rash due to sun exposure
  • Caused by a mutation in BLM gene which disrupts its ability to maintain structure and integrity of DNA
  • Cancer predisposition = skin cancer, basal cell carcinoma, squamous cell carcinoma
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14
Q

What is Lynch type ll?

A
  • No symptoms
  • Mutations in mismatch repair (MMR) genes
  • Cancer predisposition = colorectal cancer
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15
Q

What is Lynch type ll?

A
  • No symptoms
  • Mutations in mismatch repair (MMR) genes
  • Cancer predisposition = colorectal cancer
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16
Q

How do viral carcinogens work?

A
  • Usually viruses complete the lytic cycle where they multiply inside an infected cell, kill the cell and then go on to infect other cells, eg common cold
  • Some complete the latent cycle where they’re able to transform cells into tumour cells
  • These viruses are tumourigenic viruses
17
Q

What properties do tumourigenic viruses need to function?

A
  • Need stable association with cells through chromosomal intergration
  • Must not kill cells as they require them to live and replicate
  • Must evade immune surveillance of infected cells through not expressing viral antigens on cell surface
18
Q

Which DNA viruses are associated with cancer?

A
  • Burkitt’s lymphoma
  • Nasopharyngeal carcinoma
  • Epstein-Barr virus
  • Hepatitis B/C
19
Q

Which RNA retroviruses are associated with cancer?

A
  • HTLV-l
  • Adult T-cell leukaemia
  • Lymphoma
20
Q

What is Knudson’s hypothesis for hereditary cancers?

A
  • Became the basis of the ‘two-hit’ hypothesis and led to the formation of the tumour suppressor gene theory
  • This led to the discovery of Rb1 (TSG that causes retinoblastoma when both copies are mutated)
  • He found that in inherited type, if the first mutated allele was inherited, the second mutation would lead to cancer
  • In the sporadic type, both mutations had to occur to lead to cancer
  • Therefore, 2 events are needed for carcinogenesis and that the cell with the first event must survive in the tissue long enough to sustain a second event
21
Q

What is the non-genotoxic model of carcinogenesis?

A
  • Characterised by an emphasis on non-genetoxic effects
  • Several important modulators of cancer risk act through a functional change rather than a structural change in the DNA
  • There is a group of carcinogens which induce cancer via non-genotoxic mechanisms
  • These include: tumour promoters, endocrine modifiers, receptor mediators
  • In high proportion of these, multiple pathways can be altered for carcinogenesis
22
Q

What is the Darwinian model of carcinogenesis?

A
  • carcinogenesis through mutation and selection-model of clonal expansion
  • certain cancer cells become resistant to therapy
23
Q

What is the tissue organisation model of carcinogenesis?

A
  • Tissues are groups of cells with similar functions (epithelial, connective muscle, nervous)
  • It consists of the tissue organisation field theory (TOFT)
24
Q

How does the somatic mutation theory (SMT) work?

A
  • Caused by a single catastrophic event
  • Cancer is derived from a single somatic cell that has accumulated multiple DNA mutations
  • these mutations damage genes which control cell proliferation and the cell cycle
  • results in neoplastic lesions
25
Q

How does tissue organisation field theory (TOFT) work?

A
  • Caused by general deterioration of the tissue microenvironment due to extracellular causes
  • Carcinogenesis in this case is primarily due to a problem with tissue organisation
  • carcinogenic agents destroy the normal tissue leading to disruptions of cell signalling which compromises genomic integrity

Biology of Cancer (19 decks)

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