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Respiratory > Neoplasia 2 - Molecular Aspects of Cancer and Carcinogenesis > Flashcards

Neoplasia 2 - Molecular Aspects of Cancer and Carcinogenesis Flashcards

1
Q

What are the 6 hallmarks of cancer?

A
  • sustaining proliferative signalling
    • evading growth suppressors
    • activating invasion and metastasis
    • enabling replicative immortality
    • inducing angiogenesis (independent vasculature)
    • resisting cell death
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2
Q

What are the 4 emerging hallmarks of cancer?

A
  • avoiding immune destruction
    • tumour promoting inflammation
    • genome instability and mutation
    • deregulating cellular energetics
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3
Q

What are the 4 classes of genes that are the principal targets of genetic damage in carcinogenesis?

A
  • growth promoting proto-oncogenes
    • growth inhibiting tumour suppressor genes
    • genes that regulate programmed cell death
    • genes involved in DNA repair
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4
Q

What are genes involved in DNA repair?

A

Genes which normally repair mutated DNA but if the gene is mutated will allow further mutations to develop

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5
Q

What is an example of genes involved in DNA repair?

A

BRCA1 and BRCA2

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6
Q

What are growth promoting proto-oncogenes?

A

Genes which normally regulate growth and when mutated are overly activated to cause accelerated growth

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7
Q

What are the different types of oncogenes?

A

growth factors, growth factor receptors, proteins in signal transduction, transcription factors, cell cycle regulators

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8
Q

What are examples of growth promoting proto-oncogenes?

A

Her2-neu, Ras, Mac

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9
Q

What happens if Ras is mutated?

A

It loses its ability to be dephosprylated and inactivated

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10
Q

What are growth inhibiting tumour suppressor genes?

A

Genes which normally suppress cell division and when mutated this function is inhibited and leads to continuous growth

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11
Q

What are the different types of tumour suppressor genes?

A

Either regulate cell cycle directly or inhibit oncogenic pathways

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12
Q

What are examples of growth inhibiting tumour suppressor genes?

A

P53, Rb, APC, PTEN

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13
Q

How many alleles need to be mutated in growth promoting proto-oncogenes?

A

1 allele - because that is sufficient to create accelerated growth

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14
Q

How many alleles need to be mutated in growth inhibiting tumour suppressor genes?

A

2 alleles - because if one allele is still making the product then there will be enough product to still suppress cell division - this most often occurs when 1 allele that is inherited is mutated and then another mutation develops in the other allele

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15
Q

What are the four types of mutations in cancer?

A
  • errors in DNA replication not repaired
    • point mutations
    • amplification of oncogenes
    • chromosomal rearragnement
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16
Q

What are the ‘hotspots’ for errors in DNA replication not being repaired?

A

oncogenes, tumour supressor genes and their regulatory regions

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17
Q

What are the two types of point mutations?

A

A mutation where the gene function is altered or a polymorphism (SNP) which leads to a genetic predisposition

18
Q

Which genes commonly have polymorphisms leading to a genetic predisposition?

A

RB, p53, APC, BRCA1, BRCA2

19
Q

What are the different types of SNPs?

A

Causative SNPs in coding or non coding regions and linked SNPs in regions with no known role in protein production

20
Q

What happens in the amplification of oncogenes?

A

There are many copies of the gene on the chromosome which results in much more expression as each one acts like an independent allele - there may also be the formation of double minutes which act like mini chromosomes with only the amplified allele and can replicate independently of the chromosome

21
Q

Which gene is commonly amplified?

A

N-MYC

22
Q

What happens in chromosomal rearrangement?

A

Part of one chromosome attaches to part of another chromosome which may result in the formation of a novel hybrid gene

23
Q

What is an example of a novel hybrid gene?

A

BCL-ABL which is a tyrosine kinase

24
Q

How long would it take for a tumour of 1 cell to become a 1g tumour if no cells were shed or lost?

A

90 days

25
Q

How long does a detectable tumour take to double in size?

A

2-3 months

26
Q

What limits tumour growth?

A

Inability of nutrients to be supplied

27
Q

Do all tumours grow at the same rate?

A

No

28
Q

What are some high growth fraction tumours?

A

leukaemias, lymphomas, small-cell carcinoma

29
Q

What are some low growth fraction tumours?

A

colon, breast adenocarcinoma

30
Q

How does cell proliferation occur under normal circumstances?

A

A growth factor binds to a receptor with intrinsic tyrosine kinase activity. The receptor links to signal transduction via PI3 kinase pathway, PLC/IP3 pathway and the MAP-kinase pathway. There are also GPCRs which activated the cAMP pathway and cytokines which activate the JAK/STAT pathway.

31
Q

What is retinoblastoma?

A

A single gene mutation in Rb which causes a loss of a tumour suppressor gene and leads to a white pupil - usually doesn’t metastasise so prognosis is good after eye removal

32
Q

What is p53?

A

A transcription factor which regulates many aspects of the genome - causes apoptosis in response to mutations - if p53 is mutated then tumorgenic cells won’t be able to undergo apoptosis

33
Q

What are miRNAs?

A

non coding single stranded RNAs that function as negative regulators of genes

34
Q

How are miRNAs involved in cancer?

A

reduced miRNAs may lead to over expressed oncoproteins and increased miRNAs may lead to reduced expression of tumour suppressor proteins

35
Q

What is epigenetics?

A

Changes in genomic structure not at the level of the nucleotide - e.g. methylation

36
Q

How is epigenetics involved in cancer?

A

Inappropriate methylation of a promoter region may lead to increased expression of oncoproteins or decreased expression of tumour suppressor proteins

37
Q

What are the 6 ways in which tumour cells can evade apoptosis?

A
  • reduced CD95 (Fas) levels
    • inactivation of death induced signalling complex by FLICE protein
    • up regulation of BCL2 (anti apoptotic protein)
    • reduced levels of pro apoptotic BAX from loss of p53
    • loss of APAF-1
    • up regulation of inhibitors of apoptosis
38
Q

How do tumour cells achieve immortality?

A

By reactivating telomerase

39
Q

What are the molecular mechanisms of metastasis?

A

cadherins, beta-catenin, connexin - adherence molecules

40
Q

What causes angiogenesis?

A

vascular endothelial growth factor

41
Q

What is tumour cell heterogeneity?

A

Tumour cell variants - different types of tumour cells with different functions in the same tumour

42
Q

What are cancer stem cells?

A

The tumour cells which act like stem cells in that they are able to under limitless proliferation. These cells are more resistive to treatment so may be the basis behind the relapse.

Respiratory (31 decks)

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