Pediatric Seminoma Medication

Updated: Sep 16, 2022
  • Author: Arnold C Paulino, MD; Chief Editor: Cameron K Tebbi, MD  more...
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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.