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BDS Module 4 > Biochemistry 3 > Flashcards

Biochemistry 3 Flashcards

1
Q

What does cancer depend upon the accumulation of?

A

changes in somatic cells

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2
Q

What can give rise to cancerous cell behaviour?

A

mutations and epigenetic changes

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3
Q

What does ‘cancer-critical’ refer to?

A

all genes whose alteration contributes to, causing or evolution of, cancer by driving tumourigenesis (tumour development)

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4
Q

How do tumours develop?

A
  • cancer cells grow and proliferate, unregulated by normal control mechanisms
  • they may become able to invade surrounding tissues and remove organs - metastasis
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5
Q

Where are cancers thought to originate from?

A
  • a single cell that has mutated and then acquired additional abnormalities
  • these changes increase the ability of the cancer cells to survive, grow and divide and then to metastasise, grow at other sites
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6
Q

What is selected for in the clones of aberrant cells able to produce tumours, and why?

A
  • genetic and/or epigenetic instability
  • the instability accelerates accumulation of genetic and/or epigenetic changes required for tumour progression
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7
Q

In what 2 ways can a genome be disrupted?

A
  1. in some cases the karyotype at mitosis appears normal - indicating there must be point mutations in individual genes - therefore failure of repair mechanism
  2. karyotype severely abnormal with chromosome breaks and rearrangements
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8
Q

What are the 2 main classes of cancer-critical genes?

A
  1. proto-oncogenes
  2. tumour-suppressor genes
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9
Q

What are proto-oncogenes?

A
  • where a gain-of-function mutation can drive a cell towards cancer
  • mutant, overactive or over-expressed forms of these genes are called oncogenes
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10
Q

What are tumour-suppressor genes?

A
  • where loss of function mutation(s) can contribute towards cancer

e.g. TP53

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11
Q

How many of the genes in the human genome are cancer critical?

A

approximately 1% (~300)

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12
Q

What does ‘loss of function’ mean?

A

generally refers to the tumour suppressor genes, where loss of function leads towards cancer development

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13
Q

What does ‘gain of function’ mean?

A

generally refers to a situation where gain of function leads towards cancer development
e.g. when proto-oncogenes are mutated, overactive or over-expressed (now called oncogenes)

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14
Q

What 3 key pathway are often found to be damaged in tumours?

A
  1. p53 pathway
  2. Rb pathway
  3. RTK/Ras/PI3K
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15
Q

What is the importance of the p53 pathway?

A

genes within the pathway that regulate responses to stress and DNA damage
- protective function over the genome

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16
Q

What is the importance of the Rb pathway?

A

Rb itself and genes that regulate Rb (retinoblastoma)
- involved in initiation of the cell division cycle

17
Q

What is the importance of the RTK/Ras/PI3K pathway?

A

this pathway transmits signal for cell growth and division from the outside of the cell into the cell

18
Q

What is the protein function of TP53 gene (a tumour suppressor gene)?

A

transcription factor

19
Q

What is the protein function of RB1 gene (a tumour suppressor gene)?

A

transcriptional Co-Repression

20
Q

What is the protein function of PTEN gene (a tumour suppressor gene)?

A

Lipid phosphotase (phosphoinositide metabolism)

21
Q

What is the protein function of BRCA1 gene (a tumour suppressor gene)?

A

DNA repair, cell cycle control, genomic stability

22
Q

What is the protein function of ARF gene (a tumour suppressor gene)?

A

MDM2 Antagonist (p53 stability)

23
Q

What is the protein function of NF1 gene (a tumour suppressor gene)?

A

GTPase Activating Protein for Ras

24
Q

What gene is p53 encoded by?

A

TP53

25
Q

Where was TP53 mapped within?

A

a region of DNA consistently deleted in human tumours

26
Q

What is one of the most frequently mutated genes in human cancers?

A

TP53

27
Q

What is the protein products of TP53 and what does it do?

A

p53, a transcription factor - controlling gene expression

28
Q

What is often reffered to as ‘Guardian of the Genome’?

A

p53

29
Q

When is p53 induced?

A

in response to stress including DNA damage,activated oncogenes, telomere shortening, spindle damage, hypoxia and metabolic stress

30
Q

What can p53 activation result in?

A

Cell Cycle Arrest (G1/G2), Sensescence or Apoptosis

31
Q

What do cell cycle arrest, sensescence, and apoptosis prevent?

A

prevent propagation of damaged DNA within a cell population, or give cells time to repair damage

32
Q

What may cells lacking function p53 do?

A

may continue to replicate damaged DNA, increasing the chances of accumulating potentially oncogenic mutations

33
Q

What were loss of function mutations in TP53 linked to?

A

Li-Fraumeni syndrome - a dominantly inherited condition that predisposed individuals to a number of cancers, typically including breast cancer

BDS Module 4 (65 decks)

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