Exam 3: Cancer Pharmacology Flashcards
“Guardian of the genome”:
P53 tumor suppressor gene
Two-hit hypothesis:
Both alleles for tumor suppressor gene must mutate for gene to lose function
MoA of methotrexate:
Prevents reduction of FH2 to FH4, interfering with DNA synthesis
MoA of doxorubicin:
Inhibits topoisomerase II, which relaxes the DNA coil, thus interfering with DNA replication
MoA of cyclophosphamide:
Attach alkyl groups to guanines, causing guanines on the helix to link and “stick” DNA in its coil, interfering with DNA replication
MoA of vincristine:
Binds to microtubules, preventing their polymerization and arresting the cell in metaphase
MoA of tamoxifen:
Antagonizes estrogen at the receptor level
Two ways monoclonal antibodies work:
Block growth signals
Stop new blood vessels from forming
MoA of cetuximab:
Binds to mutated growth factor receptor and prevents its downstream signalling
MoA of bevacizumab/Avastin:
Inhibits vascular endothelial growth factor A, thus blocking angiogenesis
MoA of tyrosine kinase inhibitors:
Prevent the phosphorylation of the tyrosine kinase, which prevents the signaling cascade that leads to cell proliferation
Define BCR-Abl:
Philadelphia chromosome
Chromosome 22 translocates with chromosome 9
BCR-Abl associated with this cancer:
CML
Example of a tyrosine kinase inhibitor:
Gleevec (imantinib)