cancer pharm Flashcards

0
Q

what enzyme becomes actived so cells can replicated non stop

A

telomerase—- extends telomers so they can replicate many many times without getting shorter

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1
Q

6 hallmarks for ca

A
1- evading apoptosis
2- self sufficent with growth signals
3- insensitivity to anti-growth signals
4- sustained angiogenesis
5- tissue invasion and mets
6- limitless replicative potential
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2
Q

tumor suppressor

A

recessive
stops cell proliferation/stimulates apoptosis when needed
LOSS OF FX

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3
Q

2 hit hypothesis

A

germ line ca- mutations are passed onto kid

somatic- not passed– environmental

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4
Q

proto-oncogene

A

is normal it is when it becomes oncogene that is bad — when the cell’s fx is altered “spontaneous neoplasm”

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5
Q

oncogene

A

dominant

no longer needs a ligand to bind because it turns on some protein that stays on

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6
Q

conventional ca tx

A
  • surgery
  • chemo
  • radiation
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7
Q

how does chemo stop ca

A

1- inhibits synth of dna
- damage dna of the affected ca cells— replication and transcription
3- stops replication of dna in the nucleus
4- effects the mitotic spindles so dna can not pull apart

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8
Q

how does methotrexate work

A

higher affinity to bind with DHFR so DTMP (what we need to make DNA) doesn’t have its precursor FH4 to continue the process

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9
Q

doxorubicin works how

A

by inhibiting topoisomerase 2

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10
Q

what does topoisomerase 2 do

A

it opens up dna for replication and translation

so this becomes damaged when inhibited

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11
Q

cyclophosphamide works how

A

stops replication of DNA in the nucleus

alkylating agent with CL- (attaches alkyl groups to guanine in DNA base)

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12
Q

Vincristine works how

A

binds to tubulin so the mitotic spindles are unable to pull apart the chromatids

class: vinca alkaloid

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13
Q

how do we do targeted tx

A
  • hormone therapy
  • monoclonal antibodies
  • tyrosine kinase inhibitors
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14
Q

tamoxifen works how

A

it is a hormonal tx that binds to estrigen receptors and blocks them so coactivators cannot become active and stops growth

it’s a “pro” drug— meaning the active form is a metabolite

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15
Q

cetuximab works how

A

blocks the ligand binding site— it’s high up in the pathway
— blocks the growth signals

16
Q

monoclonal antibodies have 2 mechanisms of action

A

1- block growth signals

2- stop new blood vessels from forming (angiogenisis)

17
Q

Bevacuzimas works how

A

stops phosphorilation and therefore no more new BV

18
Q

Vemurafenin is an example of ________ and works how?

A

Tyrosine kinase inhibitor and it inhibits specific Braf mutated cells from getting phosphorylated… “wild B600” remains unaffected

19
Q

Gleevac is an example of and works on what dx and how

A

Tyrosine kinase inhibitor
Philadelphia choromosome ca
competitively binds to Bcr-Able to inhibit Kinase activity

20
Q

what is the new trend for CA treatment

A

combo targeted treatment