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Pediatric Seminoma Medication

  • Author: Arnold C Paulino, MD; Chief Editor: Robert J Arceci, MD, PhD  more...
Updated: Apr 16, 2012

Medication Summary

As discussed below, adjuvant moderate-dose pelvic and/or paraaortic radiotherapy remains the standard treatment for patients with early-stage seminoma (stage I, IIA, or IIB) after orchiectomy. However, patients who are found to have more advanced disease (stage IIC, III, IV) have a high risk of systemic relapse if treated with surgery and radiation alone, and the standard treatment for these patients is combination chemotherapy. These patients can be generally divided into good-risk and poor-risk categories. For patients with good risk, several combination chemotherapy regimens are available; one common schedule for adults includes 3 cycles of cisplatin/etoposide/bleomycin (detailed below). Patients with poor risk should be enrolled in clinical trials because the ideal chemotherapeutic strategy has not been determined.


Antineoplastics agents

Class Summary

Adjuvant chemotherapy regimens are for stages I to III disease.

Cancer chemotherapy is based on an understanding of tumor cell growth and how drugs affect this growth. After cells divide, they enter a period of growth (phase G1), followed by DNA synthesis (phase S). The next phase is a premitotic phase (G2), then finally a mitotic cell division (phase M).

The rate of cell division varies for different tumors. Most common cancers increase very slowly in size compared with normal tissues, and the rate may decrease further in large tumors. This difference allows normal cells to recover more quickly than malignant ones from chemotherapy; it is the rationale behind current cyclic dosage schedules.

Antineoplastic agents interfere with cell reproduction. Some agents are cell cycle specific, whereas others (eg, alkylating agents, anthracyclines, cisplatin) are not phase specific. Cellular apoptosis (ie, programmed cell death) is also a potential mechanism of many antineoplastic agents.

Cisplatin (Platinol)


Inhibits DNA synthesis and, thus, cell proliferation by causing DNA crosslinks and denaturation of double helix.

Etoposide (Toposar, VePesid)


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

Bleomycin (Blenoxane)


Glycopeptide antibiotic that inhibits DNA synthesis. For palliative measure in the management of several neoplasms.

Carboplatin (Paraplatin)


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 crosslinks and inhibition of DNA replication. Binds to protein and other compounds containing SH group. Cytotoxicity can occur at any stage of the cell cycle, but cell is most vulnerable to action of these drugs in G1 and S phase. Has same efficacy as cisplatin but with better toxicity profile. Main advantages over cisplatin include less nephrotoxicity and ototoxicity not requiring extensive prehydration, less likely to induce nausea and vomiting, but more likely to induce myelotoxicity.

Dose is based on the following formula: total dose (mg) = (target area under plasma concentration-time curve [AUC]) X (glomerular filtration rate [GFR]+25) where AUC is expressed in mg/mL/min and GFR is expressed in mL/min.

Contributor Information and Disclosures

Arnold C Paulino, MD Professor of Radiation Oncology, Methodist Hospital and Weill-Cornell Medical College; Associate Professor of Pediatrics, Baylor College of Medicine

Arnold C Paulino, MD is a member of the following medical societies: Radiological Society of North America, Children's Oncology Group, American Society of Clinical Oncology, International Society of Paediatric Oncology, American Medical Association, American Radium Society, American Society for Radiation Oncology

Disclosure: Received royalty from Elsevier, Inc for author of book.


Jodi Muscal, MD Assistant Professor of Pediatrics, Division of Hematology-Oncology, Baylor College of Medicine, Texas Children's Hospital

Jodi Muscal, MD is a member of the following medical societies: American Association for Cancer Research, American Society of Pediatric Hematology/Oncology

Disclosure: Nothing to disclose.

Specialty Editor Board

Mary L Windle, PharmD Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Nothing to disclose.

Steven K Bergstrom, MD Department of Pediatrics, Division of Hematology-Oncology, Kaiser Permanente Medical Center of Oakland

Steven K Bergstrom, MD is a member of the following medical societies: Alpha Omega Alpha, Children's Oncology Group, American Society of Clinical Oncology, International Society for Experimental Hematology, American Society of Hematology, American Society of Pediatric Hematology/Oncology

Disclosure: Nothing to disclose.

Chief Editor

Robert J Arceci, MD, PhD Director, Children’s Center for Cancer and Blood Disorders, Department of Hematology/Oncology, Co-Director of the Ron Matricaria Institute of Molecular Medicine, Phoenix Children’s Hospital; Editor-in-Chief, Pediatric Blood and Cancer; Professor, Department of Child Health, University of Arizona College of Medicine

Robert J Arceci, MD, PhD is a member of the following medical societies: American Association for the Advancement of Science, American Association for Cancer Research, American Pediatric Society, American Society of Hematology, American Society of Pediatric Hematology/Oncology

Disclosure: Nothing to disclose.

Additional Contributors

Kathleen M Sakamoto, MD, PhD Shelagh Galligan Professor, Division of Hematology/Oncology, Department of Pediatrics, Stanford University School of Medicine

Kathleen M Sakamoto, MD, PhD is a member of the following medical societies: International Society for Experimental Hematology, American Society of Hematology, American Society of Pediatric Hematology/Oncology, Society for Pediatric Research

Disclosure: Nothing to disclose.

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Radiotherapy fields for stage I seminoma.
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