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Extragonadal Germ Cell Tumors Medication

  • Author: Kush Sachdeva, MD; Chief Editor: Jules E Harris, MD, FACP, FRCPC  more...
 
Updated: Apr 16, 2015
 

Medication Summary

The goals of pharmacotherapy are to induce remission, reduce morbidity, and prevent complications.

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Chemotherapeutic agents

Class Summary

Regardless of the tumor location and whenever chemotherapy is considered, a BEP combination (bleomycin, etoposide, and cisplatin) is the treatment of choice (BEP for 4 cycles at 3-wk intervals). VIP (etoposide, ifosfamide, and cisplatin) has been used as salvage therapy for progressive disease or as postoperative therapy following resection of residual mass containing viable tumor. Vinblastine has occasionally replaced etoposide if the latter was used in the initial regimen.

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 produce cross-links. Platinum complex also can bind to nucleus and cytoplasmic protein. A bifunctional alkylating agent, once activated to aquated form in cell it binds to DNA, resulting in interstrand and intrastrand cross-linking.

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

Etoposide (Toposar, VePesid)

 

Inhibits topoisomerase II and causes DNA strand breakage, causing cell proliferation to arrest in late S or early G2 portion of cell cycle. Prodrug activated by dephosphorylation.

Reduce dose in hepatic (increased total bilirubin [TB]) and renal (decreased CrCl) impairment.

Bleomycin (Blenoxane)

 

Glycopeptide antibiotic that acts by intercalating and binding to guanosine and cytosine portions of DNA. May induce single- or double-stranded DNA breaks by ability to form oxygen free radicals.

Test dose is optional: 1-2 U IV/IM prior to full dose.

Ifosfamide (Ifex)

 

Alkylating agent—2 major metabolites are produced after its activation in liver. Ifosfamide mustard, by its ability to cross-link DNA strands, responsible for therapeutic effect. Acrolein related to bladder toxicity.

Vinblastine (Velban)

 

Vinca alkaloid, inhibits microtubule formation, which in turn disrupts formation of mitotic spindle, causing cell proliferation to arrest at metaphase.

Reduce dose by 50% in patients with TB > 3 mg/dL. Dose reduction not required in impaired renal function.

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Contributor Information and Disclosures
Author

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

Disclosure: Nothing to disclose.

Coauthor(s)

Brendan Curti, MD Director, Genitourinary Oncology Research, Robert W Franz Cancer Research Center, Earle A Chiles Research Institute, Providence Cancer Center

Brendan Curti, MD is a member of the following medical societies: American College of Physicians, American Society of Clinical Oncology, Oregon Medical Association, Society for Immunotherapy of Cancer

Disclosure: Serve(d) as a speaker or a member of a speakers bureau for: Prometheus Pharmaceuticals<br/>Received research grant from: Prometheus Pharmaceuticals.

Issam Makhoul, MD Associate Professor, Department of Medicine, Division of Hematology/Oncology, University of Arkansas for Medical Sciences

Issam Makhoul, MD is a member of the following medical societies: American Society of Clinical Oncology, American Society of Hematology

Disclosure: Nothing to disclose.

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.

Specialty Editor Board

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

Disclosure: Received salary from Medscape for employment. for: Medscape.

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.

Additional Contributors

Robert C Shepard, MD, FACP Associate Professor of Medicine in Hematology and Oncology at University of North Carolina at Chapel Hill; Vice President of Scientific Affairs, Therapeutic Expertise, Oncology, at PRA International

Robert C Shepard, MD, FACP is a member of the following medical societies: American Association for Cancer Research, American Association for Physician Leadership, European Society for Medical Oncology, Association of Clinical Research Professionals, American Federation for Clinical Research, Eastern Cooperative Oncology Group, Society for Immunotherapy of Cancer, American Medical Informatics Association, American College of Physicians, American Federation for Medical Research, American Medical Association, American Society of Hematology, Massachusetts Medical Society

Disclosure: Nothing to disclose.

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