Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
24 Cards in this Set
- Front
- Back
|
Mechanism of Action: Alkylating Agents
|
In presence of H20, activated via ring formation and chlorine release.
Activated ring, nucleophilic attach of S, N, or O of protein/DNA onto the ring = DNA adduct. Has two "activation zones" (2Cl) and can make additional adduct to "crosslink" |
|
|
Mechanism of Action: Platinums
|
Crosslinks N7 guanine on DNA to form DNA adduct
|
|
|
Mechanism of Resistance: Alkylating Agents
|
DNA repair, decreased uptake, and detoxification via Glutathione
|
|
|
Mechanism of Resistance: Platinums
|
DNA excision repair, decreased uptake, increased efflux
|
|
|
Cisplatin vs Carboplatin vs Oxaliplatin
|
All are Platinums - form DNA adducts
Cisplatin - broad range against solid tumors (esp. squamous cell carcinomas) BUT nephrotoxicity Carboplatin - Similar spectrum LESS nephrotoxicity. Can lead to mylosuppression Oxaliplatin (Eloxatane) - Good for tumors resistant to Cisplatin and Carboplatin via DACH subunit. Can lead to neurotoxicity |
|
|
Cyclophosphamide
|
Alkylating Agent - nitrogen mustard. Can form 2 DNA adducts via ring formation and Cl removal
Must be activated by liver (prodrug) |
|
|
Ifosamide
|
Alkylating Agent - nitrogen mustard. Can form 2 DNA adducts via ring formation and Cl removal
Must be activated by liver (prodrug) |
|
|
Temozolomide
|
Alkylating Drug - adds methyl groups or larger. Penetrates blood brain barrier and good for brain tumors
|
|
|
Mechloroethamine
|
Alkylating Agent - Nitrogen Mustard - first one historically
|
|
|
Melphalan
|
Alkylating Agent - Nitrogen Mustard
|
|
|
Chlorambucil
|
Alkylating Agents - Nitrogen Mustards
|
|
|
Mechanism of Action: Antimetabolites
|
Inhibit nucleotide synthesis (DNA and RNA): Antagonists of Purines, Folic Acid, and Pyrimidines
G1 to S phase most sensitive; G1 Arrest |
|
|
Mechanism of Resistance: Antimetabolites
|
Decreased HGPRT activity; HGPRT activates antimetabolites
|
|
|
Mechanism of Action: Vinca Alkaloids
|
Inhibit microtubule polymerization, disrupt mitotic spindle and chromosome separation. M phase arrest
|
|
|
Mechanism of Resistance: Vinca Alkaloids
|
Increased export via P-glycoprotein
|
|
|
Mechanism of Action: Taxanes
|
Stabilize GDP-bound tubulin, inhibit mitosis and cell division. M phase arrest.
|
|
|
Mechanism of Resistance: Taxanes
|
Increased P-glycoprotein export; Tubulin mutations
|
|
|
Paclitaxel
|
Taxol. Broad spectrum activity taxane against solid tumors (primarily breast). Stabilize GDP-tubulin. M phase arrest
|
|
|
Docetaxel
|
Broad spectrum taxane. Stabilize GDP-tubulin. M phase arrest
|
|
|
Topotecan
|
DNA topoisomerase poison
|
|
|
Irinotecan vs Topotecan Indication and Toxicity
|
Irinotecan - Colorectal Cancer, tox - bone marrow suppression
Topotecan - Ovarian cancer, small lung cancer; tox - GI Both are topoisomerase inhibitors |
|
|
Vinca Alkaloids Indication
|
Hematological malignancies, breast and pediatric cancers
|
|
|
Mechanism of Action: Antitumor Antibiotics
|
Inhibition topoisomerase II, DNA intercalation, alteration in membrane fluidity and ion transport, free radical generation
|
|
|
-mycin ending is
|
Antitumor antibiotics
|
