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Foundation - Cancer > Carcinogen's, Mutations and DNA repair > Flashcards

Carcinogen's, Mutations and DNA repair Flashcards

1
Q

Conversion of DNA to RNA is…

A

Transcription

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2
Q

Production of a protein from RNA is…

A

Transcription

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3
Q

What is DNA damage?

A

• DNA damage is the alteration of the chemical structure of the DNA.

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4
Q

What is DNA mutation?

A

Mutation is the alteration of the information that DNA carries.

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5
Q

What is the key difference between DNA damage and DNA mutation?

A

DNA damage is the alteration of the chemical structure of the DNA.

Mutation is the alteration of the information that DNA carries.

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6
Q

What is known as the dogma of biology?

A

DNA copies itself, makes RNA which then produces a protein.

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7
Q

Regarding DNA damage and DNA mutation, which can cells repair?

A

Cells can repair DNA damage but cannot repair DNA mutation.

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8
Q

Proto-oncogene

A

A normal gene which, when altered by mutation, becomes an oncogene that can contribute to cancer.

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9
Q

What functions can proto-oncogenes have in a cell?

A

Some proto-oncogenes provide signals that lead to cell division. Other proto-oncogenes regulate programmed cell death (apoptosis).

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10
Q

What are the cancer promoting mutations that can occur?

A
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11
Q

Types of DNA damage and their repair mechanisms:

Understand

A
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12
Q

Bulky adducts

A

DNA adducts are covalent modifications of the DNA that result from exposure to specific carcinogens and thus, the level of DNA adducts in normal cells can serve as a biomarker for a significant exposure to carcinogens.

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13
Q

Outside of cancer what is the relevance of DNA repair to other medical conditions?

A

Conditions such as Xeroderum pigmentosum, Fanconi’s anaemia, and neurological conditions such as Ataxia and telangiectasia.

Syndromes such as Bloom syndrome, Werner syndrome.

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14
Q

Mismatch repair fixes which DNA mutations?

A

Mismatchs, insertions and deletions.

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15
Q

Hereditary nonpolyposis colorectal cancer

A

Hereditary nonpolyposis colorectal cancer (HNPCC) or Lynch syndrome is an autosomal dominant genetic condition that is associated with a high risk of colon cancer as well as other cancers including endometrial cancer, ovary, stomach, small intestine, hepatobiliary tract, upper urinary tract, brain etc.

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16
Q

What repairs bulky adducts?

A

Nucleotide excision repair

17
Q

Nucleotide excision repair

A

In nucleotide excision repair (NER), damaged bases are cut out within a string of nucleotides, and replaced with DNA as directed by the undamaged template strand. This repair system is used to remove pyrimidine dimers formed by UV radiation as well as nucleotides modified by bulky chemical adducts.

18
Q

What causes bulky adduct mutations?

A

Carcinogens such as those in smoking and UV light.

19
Q

What causes double strand DNA breaks?

A

Ionising radiation

20
Q

What are the two repair mechanisms for double strand DNA breaks?

A

Homologous recombination

Non-homologous end joining

21
Q

A deficiency in mismatch repair leads to what condition?

A

Hereditary Nonpolyposis colorectal carcinoma aka Lynch syndrome

22
Q

A deficiency in nucleotide excision repair can lead to which condition?

A

Xeroderma pigmentosum (Cockayne syndrome).

23
Q

Xeroderma pigmentosum

A

Xeroderma pigmentosum (XP) is a genetic disorder in which there is a decreased ability to repair DNA damage such as that caused by ultraviolet (UV) light. Symptoms may include a severe sunburn after only a few minutes in the sun, freckling in sun exposed areas, dry skin and changes in skin pigmentation.

24
Q

A deficiency in DBS (double strand breaks) repair can lead to what conditions?

A

Ataxia-telangiectasia, Fanconi anaemia, Bloom and Werner syndromes. Importantly: BRCA1/2 genes and breast cancer predisposition.

25
Q

Ataxia telangiectasia

A

Ataxia telangiectasia (A-T) is an autosomal recessive disorder primarily characterized by cerebellar degeneration, telangiectasia, immunodeficiency, cancer susceptibility and radiation sensitivity.

26
Q

Telangiectasia

A

Telangiectasia is a condition in which widened venules (tiny blood vessels) cause threadlike red lines or patterns on the skin.

27
Q

Outline Werner and Bloom syndromes and their cause.

A

The premature aging and cancer-prone diseases Werner and Bloom syndromes are caused by loss of function of WRN and BLM proteins

28
Q

What type of protein are WRN and BLM proteins?

A

They are helicases part of the RecQ family - they facilitate pairing of complementary DNA strands.

Involved in double strand break DNA repair.

29
Q

What is the role of tumour supressor genes?

  • What are the tumour supressor genes associated with each role?
A
  1. Gatekeepers: Regulate cell cycle progression.

(P53, Rb, APC)

  1. Caretakers: Promote DNA repair.

(XPA-G, MSH1, ATM)

30
Q

What is the essential difference regarding pathology between gatekeeper and caretaker tumour supressor genes?

A

Gatekeepers: Re-introduction of wild-type version can revert tumour phenotype.

Caretakers: Re-introduction of wild-type version cannot revert tumour phenotype.

31
Q

What is meant by wild type in genetics?

A

Wild type (WT) refers to the phenotype of the typical form of a species as it occurs in nature.

‘normal alelle’

32
Q

In what way can mutations accelerate the formation of cancer?

  • what are the mutations that would cause this to occur?
A

• Divide faster (more divisions per unit time)

Gatekeeper TSG failure

• Mutate faster (more mutations per cell division)

Caretaker TSG failure

33
Q

Are tumour supressor gene mutations dominant or recessive?

  • what is the significance of this regarding inheritance?
A

TSG mutations are recessive for a cell to become cancerous, so we need both alleles mutated (Knudson’s two-hit hypothesis).

  • Inheritance of a mutated allele increases the probability of having both alleles mutated (we only need to mutate the remaining wild-type one).
34
Q

APC gene

  • what may mutations of this gene cause?
A

Adenomatous polyposis coli

Mutations in the APC gene may result in colorectal cancer. APC is classified as a tumor suppressor gene.

35
Q

What is the role of K-RAS?

A

K-RAS is an oncogene that promotes cell division.

36
Q

Proto-oncogenes are

A

Genes commonly mutated in cancer

37
Q

Histone H3 acetylation and methylation is an example of what?

A

Epigenetic change.

38
Q

Dysplasia is the

A

Replacement of one differentiated cell type with a less differentiated cell type

39
Q

TERT gene promoter mutations observed in melanomas can be best mapped to which of the following hallmarks of cancer?

A

Enabling replicative immortaliy.

Foundation - Cancer (10 decks)

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