Cancer Flashcards

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1
Q

What cell types does cancer largely occur in?

A

somatic cells

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2
Q

Is cancer a disease?

A

no

rather, it is a family of related complex diseases

this is why there will never be any one cure for cancer

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3
Q

two fundamental properties of cancer

A
  1. unregulated cell proliferation

2. metastatic spread

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4
Q

How does cancer spread?

A

through the bloodstream

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5
Q

How does cancer occur?

A

the accumulation of many mutations

very rarely occurs from a single mutation

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6
Q

How can you determine if cancer in two different locations arose independently from one another or are from the same original tumor?

A
  1. compare base sequences in both areas

2. look for similar chromosomal irregularities in karyotype

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7
Q

Tasmanian devil facial tumor disease (DFTD) case

A

DFTD is a rare transmissible form of cancer

Due to eating together and violently clawing prey, tasmanian devils can transfer cancer through blood on their face

they also have little genetic diversity which gives rise to this

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8
Q

Mutation error rate

A

10^-6 mutations per gene in each division

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9
Q

How many mutations might a person have per gene in a lifetime?

A

10^10

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10
Q

Why does the risk of cancer increase with age?

A

acquire more mutations as more divisions take place and the risk of cancer increases

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11
Q

What happens if cyclins are never degraded?

A

CDK proteins will always be on and cell cycle will progress without control

this can lead to cancer

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12
Q

Retinoblastoma (RB) checkpoint protein

A

ensures that the cell passes from G1 to S only when ready

tumor supressor protein

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13
Q

what happens when RB is on?

A

the cell does not pass from G1 to S

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14
Q

how do you turn RB off? what happens when RB is turned off?

A

RB is phosphorylated to turn off by cyclin-CDK complexes

when RB is turned off, the cell is free to move into the S phase

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15
Q

How does RB work?

A

binds to transcription factor (E2F) that promotes gene expression and prevents it from transcribing certain genes

when RB is not bound to E2F, E2F allows certain genes to be expressed that further the cell from G1 to S

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16
Q

P53 checkpoint

A

evaluates DNA damage and can prevent its replication through stimulating the transcription of the Cdk inhibitor, p21

17
Q

p21

A

inhibits Cdks from phosphorylating RB

this allows RB to stay turned on and the cell cycle does not progress from G1 to S

18
Q

How many copies of the genes have to be mutated for tumor supressors to not work?

A

both copies

19
Q

How many copies of the genes have to be mutated for proto-oncogenes to become oncogenes?

A

just one copy

20
Q

Proto-oncogenes

A

genes whose products promote cell growth and division

21
Q

Tumor supressor genes

A

when both alleles are mutated, cells can keep growing

22
Q

Oncogene

A

proto-oncogene that has been mutated and can lead to uncontrolled cell growth/division

23
Q

What do many oncogenes encode for?

A

constitutively active signal-transduction pathways

constitutively = enzyme/protein that is produced in constant amounts regardless of environmental conditions

24
Q

ABL

A

gene on chromosome 9 that encodes a tyrosine kinase

25
Q

BCR

A

gene on chromosome 22 that encodes an unknown protein

when in the Philadelphia chromosome, provides a docking site for signal transduction proteins

26
Q

BCR-ABL translocation (gives rise to the Philadelphia Chromosome)

A

oncogene caused by fusing of ABL and BCR genes

encodes for a cytosolic nonreceptor kinase

can phosphorylate some substrates that are not normal targets

27
Q

What happens if the BCR-ABL translocation occurs in the blood forming cells of the bone marrow?

A

initial phase of chronic myelogenous leukemia (CML)

expansion of white blood cells

28
Q

Imatinib (Gleevec)

A

binds directly to ABL kinase active site and inhibits kinase activity

29
Q

What was Imatinib the first drug to do?

A

act upon a specific enzyme rather than non-specifically inhibiting and killing all dividing cells

30
Q

What checkpoint does MPF regulate?

A

the G2 checkpoint

31
Q

When do MPF concentrations peak?

A

partially through mitosis

32
Q

How does the BCR-ABL protein differ from the normal ABL protein?

A

Normally, ABL kinase is regulated by other molecules, but the BCR-ABL mutant kinase is constantly active