Which medications in the drug class Antineoplastics, Other are used in the treatment of Renal Transitional Cell Carcinoma?

Updated: Nov 05, 2019
  • Author: Bagi RP Jana, MD, MBA, MHA, FACP; Chief Editor: E Jason Abel, MD  more...
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Antineoplastics, Other

Antineoplastic agents inhibit cell growth and proliferation.


Methotrexate inhibits dihydrofolate reductase (DHFR), causing a block in the reduction of dihydrofolate to tetrahydrofolate. This inhibits the formation of thymidylate and purines and arrests DNA, RNA, and protein synthesis.


A vinca alkaloid with cytotoxic effect via mitotic arrest, vinblastine binds to a specific site on tubulin, prevents polymerization of tubulin dimers, and inhibits microtubule formation. Intrathecal (IT) administration may result in death.

Doxorubicin (Adriamycin)

Doxorubicin is an anthracycline antibiotic that causes DNA strand breakage through effects on topoisomerase II and direct intercalation into DNA, which causes DNA polymerase inhibition. This drug is both mutagenic and carcinogenic.


Cisplatin is a platinum-containing compound that exerts an antineoplastic effect by covalently binding to DNA, with preferential binding to N-7 position of guanine and adenosine. It can react with 2 different sites on DNA to produce cross-links. The platinum complex also can bind to nucleus and cytoplasmic protein.

Gemcitabine (Gemzar)

Gemcitabine is a cytidine analog. After intracellular metabolism to its active nucleotide, it inhibits ribonucleotide reductase and competes with deoxycytidine triphosphate for incorporation into DNA.


Carboplatin is an analog of cisplatin. This is a heavy metal coordination complex that exerts its cytotoxic effect by platination of DNA, a mechanism analogous to alkylation, leading to interstrand and intrastrand DNA cross-links and inhibition of DNA replication. It binds to protein and other compounds containing an SH group. Cytotoxicity can occur at any stage of the cell cycle, but the cell is most vulnerable to the action of these drugs in the G1 and S phase. Carboplatin has the same efficacy as cisplatin but with a better toxicity profile. The main advantages over cisplatin include less nephrotoxicity and ototoxicity (not requiring extensive prehydration) and a lower likelihood of inducing nausea and vomiting; however, it is more likely to induce myelotoxicity.

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