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Cancer and genetics > Overview of cancer and genetics > Flashcards

Overview of cancer and genetics Flashcards

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Biology 101 flashcards
1
Q

What can cancer lead to?

A

Clonal evolution

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2
Q

What is clonal evolution?

A
  1. One cell ‘goes wrong’ (e.g mutation)
  2. Cancer growth, progression, treatment resistance, disease due to adaptation to changes in cancer environment
    It is an expansion of a population of cancer cells
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3
Q

What does tumour progression involve?

A

Many, independent mutations occur

Triggers parallel clonal expansion

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4
Q

Cancer that is sporadic

A

Happens without a known cause (random)
70% of cancers
Random chance/environmental exposure

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5
Q

Familial cancer

A

20% of cancers
similar genetic background- presence of a genetic mutation?
shared environmental exposure

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6
Q

Hereditary cancer

A

10% cancers
inherited genetic mutation
increased risk of cancer development

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7
Q

How does cancer develop? (4 steps)

A
  1. A cell is mutated= abnormal cell
  2. Cancer develops from a single abnormal cell
  3. Further mutations of descendent cells of abnormal cell accumulate
  4. Muatted descendent cells gain certain capabilities to outgrow normal cells
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8
Q

What is hallmarks of cancer?

A

10 biological capabilities acquired by cells during multistep process of tumour development
Transform normal cell to cancerous cell
Done by mutations

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9
Q

What are the 10 hallmarks of cancer?

A 
Resist cell death
sustain proliferative signalling
Induce angiogenesis 
tumour promoting inflammation
activating invasion and metastasis
genome instability and mutation
evading growth suppressors
avoiding immune destruction
deregulating cellular energetics 
enabling replicative immortality
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10
Q

How do mutations allow cancer cells to evolve?

A

Cancer development and progression= repetition of mutations and proliferation
With each mutation= abnormal cells gain selective advantage over neighboring cells= large clonal population
this process= clonal evolution
as tumour progresses= genetic instability increases

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11
Q

What drives cancer in a cell?

A

Deregulation of cell homeostasis

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12
Q

How does deregulation of cell homeostasis drive cancer?

A

Loss of balance between cell proliferation and apoptosis= rise to cancer
Cancer= deregulation of cell proliferation and apoptosis pathways
Genes that cause disregulation= cancer critical genes

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13
Q

What does cancer depend on?

A

Set of mutations

epigenetic changes

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14
Q

What are cancer-critical genes?

A

Many genes that are altered in human cancers

Cancer risk can arise from too much/too little activity of gene product

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15
Q

What are the 2 types of cancer-critical genes?

A

Proto-oncogenes

Tumour suppressor genes

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16
Q

What are proto-oncogenes?

A

Genes have a gain of function-mutation that drives a cell towards a cancer
Their mutant/overexpressed form= oncogene

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17
Q

What are tumour suppressor genes?

A

Genes have a loss of function mutation

Contribute to cancer

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18
Q

What do mutations in oncogenes and tumour suppressor genes cause?

A

Enhancing cell proliferation, cell survival

Promote tumour development

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19
Q

What do oncogenes do?

A

Uncontrollable cell growth
Promote cell proliferation
Encode growth factors, GF receptors/nuclear proteins

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20
Q

Are oncogenes dominant or recessive?

A

Dominant

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21
Q

An example of a proto-oncogene?

A

Ras

When mutated= oncogene

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22
Q

Mutation of Ras proto-oncogene to Ras oncogene in what proportion of cancers?

A

1 in 5 human cancers

23
Q

What do normal Ras proteins do?

A

Monomeric GTPases

Help transmit signals from cell surface receptors to inside cell

24
Q

How is a ras oncogene made?

A

Point mutation of ras
Creates a hyperactive Ras
Can’t shut itself off by hydrolysing GTP to GDP

25
Q

How is retinoblastoma caused?

A

Deletion of a band on chromosome 13

26
Q

What is Rb gene?

A

Tumour suppressor gene

27
Q

How can tumour suppressor genes be inactivated?

A

Epigenetic changes

28
Q

What are the 4 ways a proto-oncogene can be converted to an oncogene?

A

1) Mutation- point mutation/deletion= hyperactive protein
2) Regulatory mutation- protein overproduction
3) Gene amplification- many copies of the gene- could be error in DNA replication
4) Chromosome translocation

29
Q

What causes retinoblastomas?

A

Mutation of Rb gene

increases cell proliferation

30
Q

Normal key role of Rb

A

Cell cycle inhibitor
Controls cell entering S phase
Acts a brake that restricts entry into S phase by inhibiting genes encoding proteins needed for S phase

31
Q

Examples of oncogenes

A

Myc

Ras

32
Q

What do many critical cancer genes do?

A

Encode for proteins that have a role in cell growth, cell division, cell proliferation and differentiation and apoptosis

33
Q

What is extracellular signal called?

A

Epidermal growth factor

Receptors for EGF can be mutated= still work in absence of EGF= inappropriate stimulatory signal

34
Q

What does Myc do?

A

Acts in nucelus

stimulates cell growth and proliferation

35
Q

What does mutation of Myc result in?

A

Causes cells to proliferate where a normal cell would halt

36
Q

How does burkitt’s lymphoma form?

A

Chromosome translocation that involve mcyc gene

Causes cell to proliferate excessively = tumour

37
Q

A pathway that inhibits cell proliferation?

A

TBF-Beta signalling pathway

38
Q

TGF-Beta pathway cancer

A

Receptor TGF-B Receptor is mutated

Smad4 is mutated

39
Q

What does p16(INK4) protein do?

A

inhibits cell-cycle progression

By inhibiting CcyclinD-CDK4 complexes forming

40
Q

What cuases glioblastomas and breast cancers?

A

Amplified genes encoding CDK4 or cyclin D

41
Q

What stimulates p13Kinase pathway?

A

Extracellular signalling proteins e.g insulin and other growth factors

42
Q

What is PTEN phopshotase?

A

Tumour suppressor gene

Limits AKT activation (p13k pathway) by dephosphorylating molecules that P13Kinase normally phosphorylates

43
Q

What tumour suppressor gene is commonly mutated in cancers?

A

PTEN phosphatase

44
Q

What allows cells to resist apoptosis?

A

Mutations in pro-apoptotic genes

45
Q

How can tumour suppressor genes be inactivated?

A
  1. Mutation to both alleles
  2. Deletion of both alleles (homozygous deletion)
  3. Gene silencing (epigenetics)
  4. Modification of gene expression
  5. Post translational mechanisms
46
Q

What are tumour suppressor genes?

A

Normal genes

Involved in DNA repair, inhibiting cell proliferation, cell cycle arrest, apoptosis

47
Q

Are tumour suppressor genes dominant or recessive?

A

Recessive

48
Q

Herdiatry breast cancers

A

Autosomal, dominant inherited condition

Due to BRCA1/BRCA2 gene mutation

49
Q

What are the consequences of amplification of proto-oncogenes?

A

1) Hyperactivation cell proliferation signalling
2) Rapid cell cycle transition
3) Don’t respond to tumour suppressor genes
4) Tumour suppressor genes are inactivated
5) Levels exceed regulation threshold

50
Q

Meaning of neoplasia (tumour)

A

abnormal mass of tissue that forms when cells grow and divide more than they should or do not die when they should. Neoplasms may be benign (not cancer) or malignant (cancer)

51
Q

Meaning of dysplasia

A

Presence of abnormal cells in tissue (Abnormal changes)

52
Q

Meaning of anaplasia

A

Loss of organisation and differentiation

53
Q

Angiogenesis

A

New blood vessel formation
Cancer cells grow - release angiogenic factors- bind to receptors on epithelial cells in blood vessel= allow new vessel to forms
Allow cancer cells in tumour to enter blood vessel
Encounter immune system in blood
Cancer cells successfully enters bloodstream (as there are so many) and travel to other organs

54
Q

Benign v malignant

A 
Benign= Well differentiated, resemble normal cell, can control cell proliferation
Malignant= Lost ability to control both proliferation and differentiation

Cancer and genetics (3 decks)

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