Gallbladder Cancer Medication

Updated: Dec 12, 2019
  • Author: Mary Denshaw-Burke, MD, FACP; Chief Editor: N Joseph Espat, MD, MS, FACS  more...
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Medication

Medication Summary

Historically, chemotherapy has not shown significant activity in gallbladder carcinoma. Typically, 5-fluorouracil (5-FU) has been used with response rates of 10-24% in advanced disease. Often 5-FU is administered either as a bolus or as a prolonged infusion regimen with radiation. Capecitabine is a currently available oral alternative to a prolonged 5-FU infusion.

More recently, gemcitabine has shown activity in gallbladder cancer. Early-phase studies show an increased response rate with gemcitabine combination therapy over historical treatment response rates with 5-FU alone. Gemcitabine has been studied in combination with cis-platinum and capecitabine.

Currently, no clearly defined standard exists for chemotherapy in gallbladder cancer. Patients should be encouraged to participate in clinical trials.

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Antineoplastic agents

Class Summary

These agents inhibit cell growth and proliferation.

Gemcitabine (Gemzar)

Cytidine analog, after intracellular metabolism to active nucleotide, inhibits ribonucleotide reductase and competes with deoxycytidine triphosphate for incorporation into DNA. Cell cycle-specific for S phase.

This drug has been shown to have activity in a phase-2 trial against relapsed germ cell tumors.

Cisplatin (Platinol)

Platinum-containing compound that exerts antineoplastic effect by covalently binding to DNA with preferential binding to N-7 position of guanine and adenosine. Can react with 2 different sites on DNA to cause cross-links. Platinum complex also can bind to nucleus and cytoplasmic protein. A bifunctional alkylating agent, once activated to aquated form in cell, binds to DNA, resulting in interstrand and intrastrand cross-linking and denaturation of double helix.

Modify dose on basis of CrCl. Avoid use if CrCl < 60 mL/min.

Capecitabine (Xeloda)

Prodrug of fluorouracil that undergoes hydrolysis in liver and tissues to form the active moiety (fluorouracil), inhibiting thymidylate synthetase, which in turn blocks methylation of deoxyuridylic acid to thymidylic acid. This step interferes with DNA, and to a lesser degree with RNA synthesis.

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