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Renal Transitional Cell Carcinoma Medication

  • Author: Bagi RP Jana, MD; Chief Editor: Jules E Harris, MD, FACP, FRCPC  more...
 
Updated: Mar 26, 2014
 

Medication Summary

The goals of pharmacotherapy are to induce remission, reduce morbidity, and prevent complications. The combination of methotrexate, vinblastine, doxorubicin (Adriamycin), and cisplatin (MVAC) is the best-studied chemotherapy regimen for upper urinary tract TCC. Durable, complete responses were obtained in only 5-10% of patients. Serious complications were encountered in 41% of patients; treatment-related mortality was 2-4%.

Gemcitabine-based combinations (gemcitabine + cisplatin or carboplatin) have activity similar to MVAC in bladder cancer but are associated with less toxicity. Some studies found the combination of gemcitabine and paclitaxel to be as effective as cisplatin-based therapies, with less nephrotoxicity.

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Antineoplastics, Other

Class Summary

Antineoplastic agents inhibit cell growth and proliferation.

Methotrexate

 

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.

Vinblastine

 

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

 

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

 

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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Contributor Information and Disclosures
Author

Bagi RP Jana, MD Associate Professor of Medicine (Genitourinary Oncology), Division of Hematology and Oncology, University of Texas Medical Branch

Bagi RP Jana, MD is a member of the following medical societies: American Cancer Society, American Medical Association, SWOG, American Society of Clinical Oncology

Disclosure: Nothing to disclose.

Coauthor(s)

Kush Sachdeva, MD Southern Oncology and Hematology Associates, South Jersey Healthcare, Fox Chase Cancer Center Partner

Disclosure: Nothing to disclose.

Chief Editor

Jules E Harris, MD, FACP, FRCPC Clinical Professor of Medicine, Section of Hematology/Oncology, University of Arizona College of Medicine, Arizona Cancer Center

Jules E Harris, MD, FACP, FRCPC is a member of the following medical societies: American Association for the Advancement of Science, American Society of Hematology, Central Society for Clinical and Translational Research, American Society of Clinical Oncology

Disclosure: Nothing to disclose.

Acknowledgements

Georgi Guruli, MD, PhD Consulting Staff, Department of Surgery, Division of Urology, University Hospital; Assistant Professor, Department of Surgery, Division of Urology, University of Medicine and Dentistry of New Jersey-New Jersey Medical School

Disclosure: Nothing to disclose.

Wendy Hu, MD Consulting Staff, Department of Hematology/Oncology and Bone Marrow Transplantation, Huntington Memorial Medical Center

Wendy Hu, MD is a member of the following medical societies: American Association for the Advancement of Science, American College of Physicians, American Society for Blood and Marrow Transplantation, American Society of Hematology, and Physicians for Social Responsibility

Disclosure: Nothing to disclose.

Badrinath R Konety, MD Associate Professor, Department of Urology, University of California, San Francisco, School of Medicine

Disclosure: Nothing to disclose.

Michael Perry, MD, MS, MACP Nellie B Smith Chair of Oncology Emeritus, Director, Division of Hematology and Medical Oncology, Deputy Director, Ellis Fischel Cancer Center, University of Missouri-Columbia School of Medicine

Michael Perry, MD, MS, MACP is a member of the following medical societies: Alpha Omega Alpha, American Association for Cancer Research, American College of Physicians, American College of Physicians-American Society of Internal Medicine, American Medical Association, American Society of Clinical Oncology, American Society of Hematology, International Association for the Study of Lung Cancer, and Missouri State Medical Association

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

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CT scan with contrast, vascular phase. Mass can be seen in left renal pelvis (black arrows). Patient underwent nephroureterectomy. Tumor was high-grade urothelial carcinoma invading subepithelial tissue (stage T1) and measuring 7.5 × 3.2 × 3 cm.
CT scan, delayed phase. Enhancing mass can be visualized in left renal pelvis (white arrows).
Retrograde pyelography. Filling defect can be seen in left renal pelvis and lower calyx (black arrows). Patient underwent left nephroureterectomy. Tumor was low-grade urothelial carcinoma measuring 2.5 × 2 × 1 cm.
Right retrograde pyelogram demonstrates large filling defect in midureter due to transitional cell carcinoma (large arrow). Note characteristic appearance of radiographic contrast material just distal to obstruction (small arrow), which gives rise to so-called goblet sign. Contrast is also visible beyond partially obstructed segment of ureter in renal pelvis and collecting system.
Pathology specimen shows urothelial tumor of renal pelvis (white arrows).
 
 
 
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