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Role of genetic changes in carcinogenesis Flashcards

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1
Q

What is carcinogenesis?

A

Process of how a normal cell evolves into an invasive cancer cell

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2
Q

How much of carcinogenesis is a genetic process?

A

It is mostly a genetic process

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3
Q

Why is carcinogenesis mostly a genetic process?

A

It results from accumulation of multiple genetic changes

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4
Q

What 2 types of genes undergo genetic changes in carcinogenesis?

A

Oncogenes

Tumour suppressor genes

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5
Q

In the normal cell phenotype, how can cell regulation be described?

A

Highly regulated cell growth and division

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6
Q

What 2 kinds of signals control different stages of the cell-cycle in a normal cell phenotype?

A

Intracellular and extracellular signals

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7
Q

In the normal cell phenotype, how can an extracellular signal from a cell produce a response in another cell?

A

The extracellular signal molecule binds to the complementary receptor on the other cell, producing a response in the other cell

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8
Q

In the normal cell phenotype, does every cell type has the same set of receptors?

A

No, each cell type has a characteristic set of receptors

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9
Q

How do signalling molecules interact in the normal cell phenotype to regulate the cell?

A

Different combinations of extracellular signalling molecules needed to regulate division, differentiation, survival

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10
Q

If appropriate extracellular signals are missing, how does the normal cell phenotype typically respond?

A

Undergoes apoptosis

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11
Q

How is cell growth regulated in the cancer cell phenotype compared to the normal cell phenotype?

A

In cancer cell phenotype there is loss of control of cell growth, but in the normal cell phenotype cell growth is highly regulated

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12
Q

What are the 3 main cancer hallmarks that cause a normal cell to become tumourigenic?

A

Cell immortalisation

Cell fails to follow normal growth constraints

Cell invasion of normal tissues

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13
Q

How does cell immortalisation develop in the cancer cell phenotype?

A

Cell undergoes indefinite growth

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14
Q

How does cancer cell phenotype evade normal growth constraints?

A

Becomes independent of growth factors

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15
Q

How does cancer cell phenotype invade normal tissues?

A

The cancer cell invades basement membrane of origin tissue and spreads to other organs to establish colonies in

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16
Q

What is the name of the process of cancer cell invasion of normal tissues in other organs?

A

Metastasis

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17
Q

What 3 factors occur in carcinogenesis that make it a micro-evolutionary process?

A

Genetic change

Competition between aggressive clones

Natural selection

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18
Q

What is the effect of heritable changes in a cancer cell?

A

Changes function of cell operation

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19
Q

Give 3 examples of functional changes that occur in cellular operation due to heritable changes?

A

Protein underexpressed or overexpressed

Protein changes function

Regulatory pathway changed

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20
Q

What are the 3 main heritable changes that occur in a cancer cell?

A

Dominant driver mutation of oncogenes

Recessive driver mutation of tumour suppressor genes

Epigenetic changes

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21
Q

When dominant driver mutation of an oncogene occurs, how many alleles of the oncogene need to mutate to express the phenotype?

A

One allele of the oncogene, as it is a dominant mutation

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22
Q

What is the effect of the dominant driver mutation of oncogenes?

A

Oncogene products have been altered so have different function

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23
Q

What is the effect of recessive drive mutation of both tumour suppressor genes in the cancer cell phenotype?

A

Tumour suppressor genes undergo loss of function

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24
Q

Does epigenetic change alter the gene sequence of cancer cells?

A

No, it modifies the sequence eg. methylation

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25
Q

What is a driver mutation?

A

Alteration that gives cancer cell a survival advantage for its neoplastic transformation

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26
Q

What is a passenger mutation?

A

Alteration that has no effect on cancer cell fitness but is detected in cells that also have a driver mutation

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27
Q

How do passenger mutations demonstrate the hitch-hiker effect?

A

When cancer cells undergo clonal expansion, passenger mutations are also replicated

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28
Q

What are the 4 types of DNA mutations?

A

Substitution, deletion, insertion, copy number changes

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29
Q

How does DNA substitution occur?

A

A base in the genome is exchanged for another base

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30
Q

How does DNA deletion occur?

A

One base/multiple bases are removed from genome

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31
Q

How does DNA insertion occur?

A

One base/multiple bases are added to genome

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32
Q

How do DNA copy number changes occur?

A

Large section of genome is deleted, duplicated or has many copies

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33
Q

How do translations/chromosomal rearrangements occur?

A

Genome is cut in 2 places and joined, which can also lead to gene fusions

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34
Q

How do genetic changes cause different functional proteins to be synthesised?

A

Transcribed mRNA sequence is different, so codons will be complementary to different amino acids, so a different amino acid sequence is formed in translation

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35
Q

What 3 factors cause genetic change to occur in a cell’s lifetime?

A

Environmental factors

Lifestyle factors

Cell replication

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36
Q

Do all genetic changes that occur in a cell lifetime cause cancer development?

A

No, most changes are repaired but a few persist and develop into cancer

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37
Q

Why do more mutations occur with every stage of cancer development?

A

More mutations make the cancer more aggressive so that it can survive

38
Q

How does a proto-oncogene mutate into an oncogene?

A

One allele of the proto-oncogene undergoes dominant driver mutation, which forms the oncogene

39
Q

What are the 2 features of a protein expressed by an oncogene?

A

Increased activity

No regulation

40
Q

What type of mutation forms the philadelphia chromosome?

A

Translocation

41
Q

What genes are involved in formation of the philadelphia chromosome?

A

ABL proto-oncogene of chromosome 9 and BCR proto-oncogene of chromosome 22

42
Q

What fusion gene in formed in the philadelphia chromosome?

A

ABL-BCR oncogene

43
Q

What is the cancerous effect of the philadelphia chromosome?

A

Uncontrollable division, as ABL-BCR fusion gene is always switched on

44
Q

How does the MYC proto-oncogene mutate in cancer?

A

Amplifies to form multiple copies of the MYC oncogene

45
Q

What is amplification of genes?

A

Same gene has 10-100 copies in the genome

46
Q

What is the cancerous effect of the MYC oncogene being amplified?

A

Increases expression of protein

47
Q

How does the RAS proto-oncogene mutate in cancer?

A

Point mutation (affects single base)

48
Q

What is the effect of the RAS oncogene on the expressed protein?

A

It has different amino acid sequence, so has different functionality

49
Q

How is leukaemia subclassified in terms of disease course?

A

Acute or chronic

50
Q

How is Leukaemia subclassified in terms of predominant abnormal cell type?

A

Lymphoid or myeloid

51
Q

How is Leukaemia subclassified in terms of genetic changes?

A

eg. Translocation, DNA mutation

52
Q

What is the normal role of TS genes?

A

Restrain uncontrollable cell division by activating DNA repair mechanisms or apoptosis in response to DNA damage

53
Q

What kind of cancers can TS gene mutations be associated with?

A

Rare familial cancers

54
Q

What mutation occurs in each TS allele in cancer cell phenotype?

A

One allele undergoes germline mutation or deletion

One allele undergoes deletion or inactivation

55
Q

What chromosome is the RB gene on?

A

Chromosome 13

56
Q

What cancer is caused by loss of both copies of the RB gene?

A

Retinoblastoma, retina tumour in children

57
Q

What are the 2 forms of retinoblastoma?

A

Sporadic and inherited

58
Q

In the sporadic form of retinoblastoma, what mutations occur?

A

Both RB genes undergo somatic (not passed on) mutations

59
Q

In the inherited form of retinoblastoma, what mutations occur?

A

One RB gene undergoes germline (passed on in sperm/ovum) deletion

Other RB gene undergoes somatic mutation

60
Q

What is the function of the TP53 gene?

A

Instructs how to synthesise p53 protein

61
Q

Why is p53 called the ‘guardian of the genome’?

A

Regulates cell-cycle and division to prevent tumour development

62
Q

In what percentage of all cancers is TP53 inactivated?

A

40%

63
Q

What is Li-Fraumeni syndrome?

A

Rare autosomal disorder caused by inherited TP53 mutation

64
Q

How does familial clustering occur in Li-Fraumeni syndrome?

A

Familial clustering of early onset tumour (before age 45)

65
Q

Give 4 types of tumour that are predominant in Li-Fraumeni syndrome?

A

Sarcomas

Breast cancers

Brain cancers

Adrenocortical carcinomas

66
Q

What is the approximate ratio of individuals with Li-Fraumeni syndrome worldwide?

A

1 in 5000 to 1 in 20,000

67
Q

What percentage of people with Li-Fraumeni syndrome develop cancer by age 40?

A

50%

68
Q

What percentage of people with Li-Fraumeni syndrome develop cancer by age 60?

A

90%

69
Q

What is the percentage risk of females with Li-Fraumeni syndrome developing cancer in their lifetime and why?

A

Nearly 100% risk due to increased risk of developing breast cancer

70
Q

How many cancers do many individuals with Li-Fraumeni syndrome develop during their lifetime?

A

2 or more primary cancers

71
Q

What percentage of all UK deaths does cancer cause?

A

28%

72
Q

What percentage of people are diagnosed with cancer in their lifetime in the UK?

A

50%

73
Q

What is a germline mutation?

A

Detectable variation in genome of germ cell (reproductive cell in foetus), that is passed onto offspring when the mutated oocyte/sperm forms a zygote

74
Q

Can germline mutations increase familial risk of cancer?

A

Yes, this is seen when there is a family history of cancer

75
Q

What 2 procedures can patients with potential germline mutations have?

A

Additional screening

Preemptive treatment

76
Q

What 2 genes can have germline mutations that develop ovarian and breast cancer?

A

BRCA1, BRCA2

77
Q

What 2 preemptive treatments can women with BRCA1 and BCRA2 have?

A

Mastectomy (surgical removal of one/both breasts)

Oophorectomy (surgical removal of one/both ovaries

78
Q

What is a somatic mutation?

A

Random genetic change in cell after fertilisation, so can’t be passed onto offspring as it doesn’t involve germline

79
Q

What is the difference between initiator carcinogens and promoter carcinogens?

A

Initiator carcinogens predispose cells to cancer development, but promoter carcinogens stimulate cancer development

80
Q

What are the 3 most preventable causes of cancer from most preventable to least preventable?

A

Smoking (19% preventable cases)

Obesity (7.8% preventable cases)

Alcohol (5.6% preventable cases)

81
Q

What kind of carcinogen is tobacco smoke?

A

Chemical

82
Q

Give 4 examples of cancers that are associated with tobacco smoke?

A

Lung, mouth, throat, bladder

83
Q

Give 3 examples of cancers that are associated with ionising radiation?

A

Leukaemia, skin, bone

84
Q

Give 2 examples of cancers that are associated with sunlight?

A

Skin, lymphomas

85
Q

How does age affect the likelihood of developing cancer?

A

Incidence of cancer increases with age

86
Q

Give 1 example of cancer whose likelihood doesn’t increase with age?

A

Testicular cancer

87
Q

How can driver mutations explain why cancer incidence increases with age?

A

Several driver mutations need to occur over cell lifetime to develop into a cancer

88
Q

How can oncogenes and TS genes explain why cancer incidence increases with age?

A

Up to 11 key changes in oncogenes or TS genes before cancer manifests

89
Q

Why can cancers with familial risk take years to develop?

A

More genetic changes are needed for full expression to develop cancer

90
Q

How many types of cancer is obesity associated with?

A

Up to 13

91
Q

How does obesity lead to cancer development?

A

Fat cells synthesise extra hormones and growth factors, which signal to cell to divide more frequently, which increases chances of mutations occurring

Genetics (2 decks)

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