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Y3 Biology Of Cancer > Week 3 > Flashcards

Week 3 Flashcards

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1
Q

How many cancer types are there and what do these relate to?

A

The 200 types of cancer are related to the being around 200 differentiated cell types.

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2
Q

Is cancer classified as a genetic disease?

A

Cancer is the most common human genetic disease – there is a transition from normal cells to malignant cancer cells driven by changes within the cellular DNA (mutations). These mutations alter cellular behaviours and pathways, resulting in uncontrollable cellular proliferation and eventually malignancy.

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3
Q

When and why do cancer cells become undifferentiated?

A

Cancer cells progress from differentiated cells to undifferentiated cells. This is because cancer cells are immature. This happens after the progression stage.

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4
Q

What process occurs when DNA is changed to RNA?

A

Transcription

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5
Q

What process occurs when RNA is changed to be a protein?

A

Translation

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6
Q

Name the possible types of chromosomal or mutational changes.

A 
Missense
Nonsense
Frameshift
Insertion
Deletion
Duplication
Repeat expansion
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7
Q

What are somatic muations?

A

Sporadic cancer which occurs within the somatic cells.

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8
Q

What are germline mutations?

A

Familial/ inherited cancer which occurs within the sex cells.

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9
Q

What is a mutator phenotype and what does it lead to?

A

enough mutations within the core genes that might cause cancer. This leads to genomic instability which causes more mutations.

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10
Q

What are driver mutations and what features do they have?

A
  • Confer a fitness advantage to somatic cells in their microenvironment, driving the cell lineage to cancer.
    The mutations that are causing the cancer phenotype within cells.
    Responsible for the survival advantages and loss of regulatory functions in cancer cells.
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11
Q

What are passenger mutations and what features do they have? How do they affect cancer cells?

A
  • Mutations that provide no proliferative benefit or directly contribute to the cancer phenotype.
    o Could be mini/ latent drivers that aid cancer progression by being gnomically instable.
    Mutations that have accumulated in the somatic cell prior or post it becoming malignant. Thought to have no proliferative or survival advantage so don’t increase the lifetime of cancer cells.
  • Add to the hallmark of genomic instability. So, adds to carcinogenesis within the cells.
    o Having an unstable genome may also mean that the cancer can’t progress and metastasise.
    o So we are unsure if passenger mutations are beneficial or detrimental to cancer growth and progression.
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12
Q

What is Aneuploidy?

A

Chromosomal gain or loss of one or many chromosomes) = DNA amplification or duplication

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13
Q

What are the general effects of aneuploidy? Write for both gain or loss of chromosomes.

A

o Regions of the genome increased – many copies of the cancer-related gene – over-expression of gene = increased protein levels.
o OR extra / fewer copies of key regulatory genes

o Regions of the genome deleted – loss of protective anti-cancer-related genes = reduced levels of proteins.
 Important key regulatory genes may be lost. Loss of genes related to anti-cancer mechanisms or proteins related to these processes.

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14
Q

What may be the effects of chromosomal rearrangements on protein products and why?

A

o Loss of function
 Because the gene has been put in a regulatory place that it shouldn’t have been
o Gene fusion leading to novel proteins
 This may have oncogenic properties which could drive the cancer forward
o Chromosome translocations/ substitutions/ inversions etc.

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15
Q

What are pre-neoplastic conditions? And how do they affect cancer malignancy?

A

pre-cancerous conditions. The cancer is not malignant, but it could develop into that. Have a high risk of transforming into a malignant cancer type. There are genomic differences within the environment which drive this. They are high risk. May never be malignant.

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16
Q

What is chromothripsis and what is the result of it?

A

Chromosomes are broken into DNA fragments and the cell attempts to repair itself. However, it doesn’t always construct the chromosomes into the correct order. Rearrangement or loss of chromosomes may occur.
New arrangements mean genes may have moved to areas where they could be expressed more, or they could be shut down and not expressed etc.
Tumour suppressor genes may be lost, amplification of oncogenes could be increased etc.

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17
Q

What are the driver genes in controlling cancer?

A

Oncogenes and Tumour Suppressor genes

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18
Q

Why are oncogenes and tumours suppressor genes driver genes?

A
  • Key regulatory genes that are responsible for controlling the cell cycle, apoptosis, DNA damage, DNA repair, senescence etc.
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19
Q

What happens if function of tumour suppressor genes is lost?

A

can no longer stop and control the cell cycle. The cell will uncontrollably grow and proliferate.

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20
Q

When do oncogenes gain transforming potntial?

A

After mutations occur.

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21
Q

Are proto-oncogenes driver genes?

A

Proto-oncogenes are activated to become oncogenes. Proto-oncogenes are normal versions of the gene. These are not driver genes, only oncogenes are.

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22
Q

What is the overall effect of having mutations within the oncogenes and tumour suppressor genes?

A

This then causes extremely fast, uncontrolled cellular proliferation which is not controlled by TSGs.

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23
Q

What is the most common type of mutation in cancer?

A

Missense

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24
Q

What is gene amplification and what effect does this have?

A

Increase copies of the gene and therefore protein that are expressed. Extra growth signals within the cell.

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25
Q

In what way are oncogenes classified?

A

Subdivide by the site at which they act.

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26
Q

What are the classifications of oncogenes?

A

Growth factors

Receptors for growth factors

Signal transducers

Transcription factors

Regulators of survival

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27
Q

What are the classifications of oncogenes?

A

Growth factors

Receptors for growth factors

Signal transducers

Transcription factors

Regulators of survival

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28
Q

How do growth factor mutations work?

A

a. Mutations which result in extra growth factor signals.

b. Cells receives more signal to grow and proliferate.

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29
Q

How do mutations within receptors for growth factors work?

A

A signalling cascade is caused and amplified.

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30
Q

How do mutations within signal transducers work?

A

a. Nonreceptor membrane associated tyrosine kinases

i. These are linked to the receptor to relay the growth and proliferation signal down.

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31
Q

What are regulators of survival?

A

a. Proteins that work within the nucleus of the cell to control gene expression

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32
Q

What is Ras?

A

Membrane associated, small GTP binding proteins which aid cell growth regulation.
- Involved in most of the pathways for cellular growth.

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33
Q

What is the main mutational hotspot of Ras?

A

KRAS - codon 12

34
Q

What are the purposes and functions of mutational hotspots in Ras?

A

o These regions are responsible for the GTP binding active site. These make the protein constitutively active – protein can’t turn itself off. So is always initiating the signalling cascade for the cell to grow and proliferate.

35
Q

What are the 3 prototypial genes of Ras?

A

HRAS, KRAS and NRAS

36
Q

What hallmark of cancer does Ras complete and how?

A
  • Involved in tumour angiogenesis (formation of new blood vessels).
    o This is a hallmark of cancer – grow its own blood supply. Via KRAS. This is never turned off in cancer gene type so constant blood supply being made and formed.
37
Q

What is B-RAD, what is it’s main function and what activates it?

A

Family of serine/thionine specific protein kinases – so it phosphorylates other proteins.
Initiated by Ras

38
Q

Describe the relationship between Ras and B-RAF

A

Often mutually exclusive (Ras and Raf). Usually, one or the other is mutated.

39
Q

What signalling cascade foes B-RAF participate in that is activated by Ras?

A

MAPK

40
Q

What do mutations of B-RAF case?

A
  • Mutations cause constitutive activity – not able to turn signalling off.Does this by changing shape of protein – the protein lid on the active site cannot close to deactivate the active site. Active site is always available. Signal constant.
41
Q

In what type of cancers are B-RAF a major mutation?

A

Melanomas

42
Q

Where is the mutation of BRAF in melnomas? And what mutation is it?

A

V600E – At the 600th amino acid, valine amino acid changed into glutamic acid.

43
Q

How are B-RAF mutations treated and why?

A

Targeted drug tailored to specific cancers depending on their
Inhibitor molecule sits in active sites and blocks GTP from activating it. Works very effectively at treating melanoma and prevents use of chemotherapy. Reduces side effects and risk of causing secondary cancer.

44
Q

What are MYCs?

A

Super transcription factors which regulate 15% of the entire genome.
- Major effectors involved in proliferation, differentiation, and survival.

45
Q

What is the main functioning process of MYCs?

A
  • Forms Myc/Max heterodimer to bind to E-box. Sequence in transcriptional regulatory regions
46
Q

Outline what occurs when a C-MYC mutation occurs and what effect this has.

A

o C-MYC binds to Max. This leads to extra MYC protein. MYC then activates genes which shouldn’t be activated. De-regulated gene caused by gene amplification or chromosome translocation

47
Q

What is N-MYC amplification?

A

Amplification of neuroblastoma genes (blasts are immature cells).

48
Q

What is the aim of tumour proteins and describe their usual cellular expression.

A

Aim is to try and stop and suppress the cell cycle. Proteins are usually expressed at very low levels.

49
Q

When does tumour suppression inhibition normally occur?

A

Tumour suppressor inhibition usually occurs when the cells have passed all stages of the cell cycle.

50
Q

In general, what does loss of function of tumour suppressor genes lead to?

A

Loss of function = de-sensitises the cells to tumour formation

51
Q

Describe the types of mutations most commonly affecting tumour suppressor genes.

A

• Most of the molecular mutations are nonsense, frameshift and deletion

52
Q

What activates P53?

A

Stress inputs within the cells.

53
Q

DEscribe the usual transcription of P53 in healthy cells.

A

Is usually transcribed in very low levels, all of the time, unless the cell is about to undergo division

54
Q

What happens if P53 is overexpressed?

A

Cell proliferation and transformation is inhibited.

55
Q

Describe the 4 domains of P53 and what each structure does.

A 
. Amino terminal trans-activation
	Activates transcription factors such as DNA repair genes. 
o	2. DNA binding domain
	Core domain
	Recognises specific DNA sequences. 
o	3. Tetramerization domain – OD
	P53 forms tetramer. 
	Connects all P53 proteins together. 
o	4. Carboxy-terminal regulatory domain (RD)
	Recognises DNA damage.
56
Q

What is the most common type of mutation in P53?

A

Missense

57
Q

Where are most mutations of P53 found and how does it work?

A

Within DNA binding regions.

Tags a protein to identify it for proteolysis.

58
Q

What is the main regulator of P53?

A

MDM2

59
Q

Describe what type of feedback loop regulates p53 levels.

A
  • Autoregulatory feedback loop

o Once levels of P53 are low enough, P53 will be expressed again

60
Q

What happens if MDM2 regulation of P53 does not occur?

A

o If excess MDM2 is produced, appropriate levels of P53 are not maintained within the cell and so it can’t do its regulatory job.
o Amplification of MDM2 is diagnostic of liposarcoma in the lab

61
Q

What are the functions of the Retinoblastoma?

A
  • Inhibits cell cycle progression – main job.
  • Binds other proteins to regulate their function
  • Binds and inhibits E2F transcription factor to halt the cell cycle. This stops DNA synthesis.
62
Q

What inactivates Rb (Retinoblastoma) and how?

A

Phosphorylation inactivates Rb by changings its shape.

63
Q

How may mutations affect Rb and what effect does this have?

A

Oncogenetic proteins can bind to and inactivate Rb.

- This means it can’t halt the cell cycle.

64
Q

What are the most common types of mutations that occur in Rb and what effect do these have?

A

Rb is mutated in a number of common cancers. This is mainly due to chromosomal aberrations caused by point mutations (deletions on chromosome 13 for e.g, point mutations are also common).
- This means structure of the protein is affected and so it can’t bind to other proteins and inhibit the cell cycle.

65
Q

What is the main, overall mechanism for epigenetics of cancer?

A

Methylation

66
Q

What is epigenetics in terms of cancer?

A

Control and regulation of gene expression and therefore protein production.

67
Q

By what mechanisms can epigenetic methylation occur?

A

Repetitive sequencing.

CpG island promoters

CpG island shore

Gene Body

68
Q

Describe what happens is repetitive sequence methylation epigenetics in cancer cells?

A

o Usually don’t have function. But some regulate gene production. In cancer cells, different levels of methylation may occur in these areas. This turns on the repetitive sequence (turn on of genes we don’t want on – activation of oncogenes).

69
Q

Describe what happens in the methylation of CpG island promoters in cancer cells?

A

o Indicates start of a coding region.
o Normally, the transcription factor binds to these regions to initiate gene expression.
 Gene turned on = unmethylated
o In cancer, increased methylation of cytosines. Transcription factors can’t bind and so certain genes are turned off. (e.g., in tumour suppressor genes).

70
Q

Describe what happens in the methylation of CpG island shores in cancer cells.

A

o In cancer, increased methylation of cytosines. Transcription factors can’t bind and so certain genes are turned off. (e.g., in tumour suppressor genes).

71
Q

Describe what happens in the gene body in terms of methylation in cancer cells.

A

o Certain regions maybe should be methylated.
o In cancer cell, exons (key coding regions) may be unmethylated and so transcription factors can bind to this. If these are then coded for , oncogenic ability may be activated.

72
Q

How does methylation help in terms of diagnosis of cancer?

A

Methylation levels alter in different types of cancer.

This can give indication of disease progression etc.

73
Q

What is the purpose of ATM gene?

A

Phosphorylates repair proteins

74
Q

What recruits ATM?

A

DSB sensor proteins

75
Q

What happens if ATM genes are mutated?

A

f these genes are mutated, it is usually the promoter region which is hypermethylated. This reduces gene and therefore protein expression.

  • Transcription factors cannot bind. Protein expression reduced.
  • Becomes a silenced tumour suppressor gene.
76
Q

When do errors within DNA repair pathways usually occur?

A

After replication and recombination

77
Q

What repairs mismatch repair issues and how?

A

Proteins are recruited to join DNA and snip mismatched nucleotide out (sometimes snips out some surrounding nucleotides).

78
Q

What is microsatellite instability?

A

repetitive DNA sequences (5-5 base pairs) caused by deletions and random insertions of microsatellites resulting from impaired MMR.

79
Q

What is chromothripsis?

A
  • Chromosome instability
  • Predominant form of genomic instability
  • This means that segregation of chromosomes is often incorrect. This happens because the chromosomes can’t line up correctly during metaphase – the chromosomes are not complementary. This also explains aneuploidy.• Mutations in this gene means that we can’t repair missense mutations or further errors could occur.
80
Q

What does the random insertion of microsatellites do to the genome and how?

A

• Random insertions of microsatellites throughout the genome is caused by unrepaired mismatch repair system. Causes unstable area within microsatellites. If unstable they can increase in size. Can affect the genome greatly.

Y3 Biology Of Cancer (8 decks)

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