Introduction to molecular therapies Flashcards
side effects of standard cancer therapy? why does this occur?
hair loss
sickness and diarrhoea
weakened immune system
targets rapidly dividing cells
what drug is gleevex
imatinib
imatinib MOA
blocks TK activity of the oncogenic Bcr-abl fusion protein
imatinib is licensed for use in?
CML
what does imatinib have additional activity against? so can be used in?
against cKIT- highly expressed in gastrointestinal stroll tumours
chromosome _____ between which chromosomes in CML
translocation
between Chromosome bar 22 and all 9
there’s a breakpoint at the 2 genes
fusion gene product bcr-abl effects?
increased TK activity compared to its protooncogene.
= uncontrolled proliferation of myeloid cells as they become hypersensitive to GF’s
what is the name of the bcr-abl fusion protein
philadelphia chromosome
Philadelphia chromosome if found in ___% of CML cases
95
philadelphia chromosome is ____ then normal. what is this information used for
smaller
diagnosing- a diagnostic marker
gleevex mechanism of action?
binds to kinase pocket of bcr-abl and prevents it binding its associated protein and hence no signal occurs so no proliferation
which pathway is good to block in colorectal cancer?
PI3K
diagnostic marker of colorectal cancer? what happens if treated properly
pAKT is a protein biomarker of PI3K activity- is high in uncontrolled tumours- if treated pAKT will be low meaning you’ve hit the target pathway
how can resistance occur in colorectal cancer when the PI3K is blocked. how do we know if this has happened/ how can be monitor if this has happened?
MAPK pathway is switched on instead- produced pERK, so if this increases we know its resistant now
