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1.4 POM Genetics > Cancer Genetics > Flashcards

Cancer Genetics Flashcards

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1
Q

What is intertumour heterogeneity?

A

Cell differences between tumours

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2
Q

What is tumour heterogeneity?

A

Different tumour cells can show different morphological and phenotypic profiles

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3
Q

What are the 6 differences found in tumour heterogeneity?

A
  1. Morphology
  2. Gene expression
  3. Metabolism
  4. Motility
  5. Proliferation
  6. Metastatic potential
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4
Q

What is clonal heterogeneity?

A

Differences between clonal daughter cells

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5
Q

What is intratumour heterogeneity?

A

Cell differences within a tumour

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6
Q

What is the founder clone?

A

First cell with driver mutation

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7
Q

How can genetic changes lead to tumour metastasis?

A

Subclones with different genotypes
—> cloned —> new tumour

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8
Q

What are 2 examples of cancer-risk genes?

A
  1. BRCA 1
  2. BRCA 2
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9
Q

What is a passenger mutation?

A

Mutations not driving cancer initiation and progression

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10
Q

What is a driver mutation?

A

Mutations driving cancer initiation and progression —> result in at least 1 hallmark of cancer

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11
Q

How many genes can driver mutations occur in? (as of 2022)

A

736

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12
Q

What are 2 examples of driver mutations?

A
  1. Proto-onco mutation
  2. Tumour suppressor gene mutation
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13
Q

What are proto-oncogenes?

A

Gene encoding a protein that promotes cell growth and proliferation

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14
Q

What is an oncogene?

A

Proto-onco gene with a driver mutation —> can cause cancer

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15
Q

What is an example of a proto-oncogene?

A

KRAS

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16
Q

What is an example of a tumour suppressor gene?

A

TP53

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17
Q

What are tumour suppressor genes?

A

Gene encoding a protein that limits cell growth and proliferation

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18
Q

What are the 14 hallmarks of cancer?

A
  1. Evading growth suppressors
  2. Non-mutational epigenetic reprogramming
  3. Avoiding immune destruction
  4. Enabling replicative immortality
  5. Tumour-promoting inflammation
  6. Polymorphic microbiomes
  7. Activating invasion and metastasis
  8. Inducing or accessing angiogenesis
  9. Senescent cells
  10. Genome instability and mutation
  11. Resisting cell death
  12. Deregulating cellular metabolism
  13. Unlocking phenotypic plasticity
  14. Sustaining proliferative signalling
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19
Q

What does the Knudson hypothesis state?

A

Tumour suppressor gene issues are recessive —> need 2 mutated alleles

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20
Q

What does the two-hit hypothesis state?

A

Tumour suppressor gene issues are recessive —> need 2 mutated alleles

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21
Q

What is a germline mutation?

A

Mutation in reproductive cells of parent —> cancer in child

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22
Q

What is a somatic mutation?

A

Mutation in non-germ cells

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23
Q

What is the difference between the effect of germline vs somatic mutations in cancer genes?

A

Germline:
- Affect child
- Affect all cells

Somatic:
- Affect person with mutation
- Localised

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24
Q

What is the CGC?

A

Cancer Gene Census:
- List of cancer risk genes

25
Q

What are cancer-risk genes?

A

Genes with the potential to have driver mutations

26
Q

What are hallmarks of cancer?

A

Set of functional capabilities acquired by cells as they become cancerous

27
Q

Why does sustained proliferative signalling act as a hallmark for cancer?

A

Cancerous cells can receive continuous signals —> stimulate growth and division —> proliferate uncontrollably

28
Q

Why does evading growth suppressors act as a hallmark for cancer?

A

Cancerous cells evade mechanisms regulating growth and proliferation

29
Q

Why does non-mutational epigenetic reprogramming act as a hallmark for cancer?

A

Cancerous cells can have epigenetic changes —> change gene expression —> increased survival

30
Q

Why does avoidance of immune destruction act as a hallmark for cancer?

A

Cancerous cells can evade detection and destruction by the immune system
—> no removal of abnormal cells

31
Q

Why does enabling replicative immortality act as a hallmark for cancer?

A

Cancerous cells can bypass the normal limitations on cell division

32
Q

Why does tumour-promoting inflammation act as a hallmark for cancer?

A

Chronic inflammation around tumour —> pro-tumorigenic environment

33
Q

Why do polymorphic microbiomes act as a hallmark for cancer?

A

Microbiome changes —> influence processes eg. inflammation, immune responses —> influence cancer progression

34
Q

Why does inducing or accessing vasculature act as a hallmark for cancer?

A

Cancerous cells can stimulate angiogenesis —> ensure blood supply for growth and survival

35
Q

Why does activation of invasion and metastasis act as a hallmark for cancer?

A

Cancerous cells can invade surrounding tissues and spread —> metastasis

36
Q

Why do senescent cells act as a hallmark for cancer?

A

Cell cycle arrest —> tumour-suppressive mechanism

37
Q

Why does genome instability and mutation act as a hallmark for cancer?

A

Leads to initiation, progression, and heterogeneity of cancerous cells

38
Q

Why does resistance of cell death act as a hallmark for cancer?

A

Cancerous cells can resist apoptosis —> no removal of abnormal cells

39
Q

How does unregulated cellular metabolism act as a hallmark for cancer?

A

Cancerous cells can have metabolic changes —> supplies increased energy needs

40
Q

How does phenotypic plasticity act as a hallmark for cancer?

A

Cancerous cells can adapt to conditions, resist interventions, and promote tumour progression via phenotypic plasticity

41
Q

What is angiogenesis?

A

New blood vessels developing from pre-existing vessels

42
Q

What is senescence?

A

State of irreversible cell cycle arrest

43
Q

What is phenotypic plasticity?

A

Ability for phenotypic adaptation to environment

44
Q

What is genomic instability?

A

Genetic material in a state more prone to changes

45
Q

What is the Warburg effect?

A

Glycolysis inc and TCA dec in cancerous cells even in sufficient oxygen —> for rapid ATP production

46
Q

What is KRAS?

A

A proto-oncogene —> K-Ras (GTPase)

47
Q

How can a KRAS mutation lead to cancer?

A
  1. Driver mutation changes functionality of K-Ras protein
  2. Inhibits proper signalling from cell surface to nucleus
  3. Affects cellular processes —> cancer
48
Q

What is TP53?

A

A tumour suppressor gene —> p53

49
Q

How can a TP53 mutation lead to cancer?

A
  1. Driver mutation changes functionality of p53 protein
  2. Inhibits tumour suppression (at cell cycle checkpoint) —> tumour
50
Q

What is BCR::ABL1?

A

Translocation —> fusion of chromosome 22 p-arm + 9 p-arm
- Cause of leukaemia

51
Q

How can BCR::ABL1 lead to cancer?

A

Driver mutation changes functionality of tyrosine kinase —> uncontrolled cell proliferation

52
Q

What is the Philadelphia chromosome?

A

BCR::ABL1

53
Q

How many driver genes can cause a breast adenocarcinoma?

A

99

54
Q

How many driver genes can cause a lung adenocarcinoma?

A

42

55
Q

How many driver genes can cause a neuroblastoma?

A

20

56
Q

What are the 5 types of cancer treatment?

A
  1. Surgery
  2. Chemotherapy
  3. Radiotherapy
  4. Targeted therapy
  5. Immunotherapy
57
Q

What is an example of a predictive genetic test for cancer risk genes?

A

BRCA gene mutation screening

58
Q

What are the 2 methods of cancer screening?

A
  1. Predictive genetic tests
  2. WGS

1.4 POM Genetics (9 decks)

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