cancer pharm Flashcards
what enzyme becomes actived so cells can replicated non stop
telomerase—- extends telomers so they can replicate many many times without getting shorter
6 hallmarks for ca
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
tumor suppressor
recessive
stops cell proliferation/stimulates apoptosis when needed
LOSS OF FX
2 hit hypothesis
germ line ca- mutations are passed onto kid
somatic- not passed– environmental
proto-oncogene
is normal it is when it becomes oncogene that is bad — when the cell’s fx is altered “spontaneous neoplasm”
oncogene
dominant
no longer needs a ligand to bind because it turns on some protein that stays on
conventional ca tx
- surgery
- chemo
- radiation
how does chemo stop ca
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
how does methotrexate work
higher affinity to bind with DHFR so DTMP (what we need to make DNA) doesn’t have its precursor FH4 to continue the process
doxorubicin works how
by inhibiting topoisomerase 2
what does topoisomerase 2 do
it opens up dna for replication and translation
so this becomes damaged when inhibited
cyclophosphamide works how
stops replication of DNA in the nucleus
alkylating agent with CL- (attaches alkyl groups to guanine in DNA base)
Vincristine works how
binds to tubulin so the mitotic spindles are unable to pull apart the chromatids
class: vinca alkaloid
how do we do targeted tx
- hormone therapy
- monoclonal antibodies
- tyrosine kinase inhibitors
tamoxifen works how
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