Anti-Tumor Agents Flashcards
Adjuvant Chemotherapy
After surgery or radiation to reduce local or systematic recurrence, effects hard to measure
Neoadjuvant Chemotherapy
before surgery or radiation, spares healthy organs and kills micrometastases.
Primary Chemotherapy
No radiation or surgery, used for late stage cancers as palliative measure but can be curative (ALL)
Targeted vs. Conventional Therapy
Conventional is cytotoxic agent that interferes w/ fundamental biology and has slight preference for fast dividing cells.
Targeted are more precise, designated to interfere w/ specific defect that caused cancer
Alkylating Agents
Mechanism: add adducts to DNA or cross-link DNA
Toxicity: injures fast dividing cells, alopecia, additional carcinogenesis
Resistance: inactivation of drug w/in cell (GSH), increase in DNA repair
Cisplatin Analogues
Mech: cross-link/intercalates in DNA
Toxicity: fast dividing cells, nephrotoxicity
Resistance: reduced absorption or increased efflux, inactivation via GSH, increased DNA repair, increase in DNA damage tolerance
Anti-Metabolites
Mech: pyrimidine analogue that stops DNA synthesis
Toxicity: fast dividing cells, alopecia, derm effects major concern
Resistance: increase production of target enzyme, mutation of target enzyme
Topoisomerase Inhibitors
Mech: inhibit DNA re-ligation
Toxicity: cardiotoxicity, carcinogenesis
Resistance: increased efflux, mutation in target enzyme
Anti-Microtubule Agents
Mech: stabilize (taxanes) or destabilize (vinca alkyloids) microtubule dynamics
Toxicity: Bone marrow suppression and neurotoxicity
Resistance: increased efflux, mutation in target enzyme
Hormonal Agents
Mech: used to target specific driver mutations (tamoxifen)
Toxicity: little hormone effect
Resistance: Receptors activated by different mechanism (phosphorylation) or mutation that makes drug agonist
Antibodies
Mech: bind target to inhibit function or bind w/ conjugated toxin
Toxicity: auto-immune possible (little)
Resistance: target no longer expressed
Kinase Inhibitors
Mech: targeted to specific kinase mutations (Imatinib)
Toxicity: Very Little
Resistance: incrased efflux, mutation of drug binding (ATP site), secondary activation of kinase