Malignant Rhabdoid Tumor Medication

  • Author: James I Geller, MD; Chief Editor: Max J Coppes, MD, PhD, MBA   more...
 
Updated: Mar 9, 2012
 

Medication Summary

The treatment for malignant rhabdoid tumor (MRT) remains investigational. No accepted standard therapy has been established for this disease. Enrollment of patients on clinical trials is strongly encouraged. The following regimen of ifosfamide-carboplatin-etoposide (ICE) alternating with vincristine-doxorubicin-cyclophosphamide (VDC) has been used to successfully treat malignant rhabdoid tumor.

Due to excessive toxicity in affected infants and young children, chemotherapeutic doses in the current COG protocol, which uses CyCE (rather than ICE) alternating with VDC, have been decreased, and in general, infants and children undergoing intensive chemotherapy for malignant rhabdoid tumor, either VDC/CyCE or VDC/ICE, must be carefully monitored for toxicity, and doses of chemotherapeutic agents must be adjusted as necessary.

Table 1. One Ifosfamide-Carboplatin-Etoposide regimen for Malignant Rhabdoid Tumor (Open Table in a new window)

DrugDosageRouteSchedule
CarboplatinTarget dose to the AUC of 6 mg/mL/min by using the Calvert equationIVDay 1
Etoposide3.3 mg/kg/dose or 100 mg/m2/doseIVDays 1, 2, and 3
Ifosfamide65 mg/kg/dose or 2 g/m2/doseIVDays 1, 2, and 3
Mesna16 mg/kg/dose or 500 mg/m2/doseIVStart immediately after and at 3 h, 6 h, and 9 h after ifosfamide
Filgrastim G-CSF5 mcg/kg/doseSCStart 24 h after chemotherapy and continue until ANC recovers

Note.—AUC = area under the concentration-time curve; IV = intravenous; G-CSF = granulocyte colony-stimulating factor; SC = subcutaneous; ANC = absolute neutrophil count.

Table 2. One Vincristine-Doxorubicin-Cyclophosphamide Regimen for Malignant Rhabdoid Tumor (Open Table in a new window)

DrugDosageRouteSchedule
Vincristine0.05 mg/kg/dose or 1.5 mg/m2/dose; not to exceed 2 mg/doseIVDays 1, 8, and 15
Doxorubicin1.2 mg/kg/dose or 37.5 mg/m2/doseIVDays 1 and 2
Cyclophosphamide60 mg/kg/dose or 1.8 g/m2/doseIVDay 1
Mesna15 mg/kg/dose or 450 mg/m2/doseIVStart immediately after and at 3, 6, and 9 h after cyclophosphamide
Filgrastim G-CSF5 mcg/kg/doseSCStart 24 h after chemotherapy and continue until ANC recovers
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Antineoplastic agents

Class Summary

For children older than 12 months and more than 10 kg, chemotherapy drugs should be dosed according to the child's body surface area. The total number of cycles of ICE or VDC necessary to treat malignant rhabdoid tumor is unknown. Some investigators have advocated for between 8-10 cycles of chemotherapy total. The current COG malignant rhabdoid tumor protocol is exploring the use of VDC and CyCE (5 cycles of each = 10 cycles total).

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Ifosfamide (Ifex)

 

Inhibits DNA and protein synthesis and, therefore, cellular proliferation by causing DNA cross-linking and denaturation of double helix.

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Carboplatin (Paraplatin)

 

Analog of cisplatin. Heavy-metal coordination complex that exerts cytotoxic effect by platinating DNA; mechanism analogous to alkylation, leading to interstrand and intrastrand DNA cross-linking and inhibited DNA replication. Binds to protein and other compounds containing SH group. Cytotoxicity can occur at any stage of cell cycle, but cell most vulnerable in G1 and S phases. Same efficacy as cisplatin but improved toxicity profile. Main advantages over cisplatin include decreased nephrotoxicity and ototoxicity not requiring extensive prehydration and reduced risk of nausea and vomiting, but more likely than cisplatin to induce myelotoxicity.

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Etoposide (VePesid, Toposar, VP-16)

 

Glycosidic derivative of podophyllotoxin that exerts cytotoxic effect by stabilizing normally transient covalent intermediates formed between DNA substrate and topoisomerase II, leading to single- and double-strand DNA breaks. This arrests cell proliferation in late S or early G2 portion of cell cycle.

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Vincristine (Oncovin, Vincasar PFS)

 

Inhibits cellular mitosis by inhibiting intracellular tubulin function, binding to microtubule and spindle proteins in S phase.

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Doxorubicin (Adriamycin)

 

Cytotoxic anthracycline antibiotic isolated from cultures of Streptomyces peucetius var. caesius. Blocks DNA and RNA synthesis by inserting between adjacent base pairs and binding to sugar-phosphate backbone of DNA, inhibiting DNA polymerase. Binds to nucleic acids presumably by specific intercalation of anthracycline nucleus with DNA double helix.

Also powerful iron chelator. Iron-doxorubicin complex induces production of free radicals that can destroy DNA and cancer cells. Can also cause breakage of DNA strands by means of effects on topoisomerase II. Maximum toxicity occurs during S phase of cell cycle.

Multiphasic disappearance curve, with half-lives as long as 30 h. Does not cross blood-brain barrier but taken up rapidly by heart, lungs, liver, kidney, and spleen. Mutagenic and carcinogenic.

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Cyclophosphamide (Cytoxan)

 

Chemically related to nitrogen mustards. Activated in liver to active metabolite 4-hydroxycyclophosphamide, which alkylates target sites in susceptible cells in all-or-none reaction. As alkylating agent, mechanism of action of active metabolites may involve cross-linking of DNA, which may interfere with growth of normal and neoplastic cells.

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Uroprotective antidote

Class Summary

Mesna is a prophylactic detoxifying agent used to inhibit hemorrhagic cystitis caused by ifosfamide and cyclophosphamide. In the kidney, mesna disulfide is reduced to free mesna. Free mesna has thiol groups that react with acrolein, which is the ifosfamide and cyclophosphamide metabolite considered responsible for urotoxicity.

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Mesna (Mesnex)

 

Inactivates acrolein and prevents urothelial toxicity without affecting cytostatic activity.

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Contributor Information and Disclosures
Author

James I Geller, MD  Associate Professor of Clinical Pediatrics, Division of Hematology/Oncology, Cincinnati Children's Hospital Medical Center

James I Geller, MD is a member of the following medical societies: American Academy of Pediatrics, American Society of Clinical Oncology, American Society of Pediatric Hematology/Oncology, and Children's Oncology Group

Disclosure: Nothing to disclose.

Coauthor(s)

Nancy D. Leslie  MD, Professor of Clinical Pediatrics, Cincinnati Children's Hospital

Nancy D. Leslie is a member of the following medical societies: American College of Medical Genetics, American Society of Human Genetics, Society for Inherited Metabolic Disorders, and Society for Pediatric Research

Disclosure: Nothing to disclose.

Hong Yin, MD  Assistant Professor, Department of Pathology and Laboratory Medicine, University of Cincinnati School of Medicine; Staff Pathologist, Department of Pathology, Cincinnati Children's Hospital

Hong Yin, MD is a member of the following medical societies: American Medical Association, Children's Oncology Group, College of American Pathologists, Society for Pediatric Pathology, and United States and Canadian Academy of Pathology

Disclosure: Nothing to disclose.

Specialty Editor Board

Stephan A Grupp, MD, PhD  Director, Stem Cell Biology Program, Department of Pediatrics, Division of Oncology, Children's Hospital of Philadelphia; Associate Professor of Pediatrics, University of Pennsylvania School of Medicine

Stephan A Grupp, MD, PhD is a member of the following medical societies: American Association for Cancer Research, American Society for Blood and Marrow Transplantation, American Society of Hematology, American Society of Pediatric Hematology/Oncology, and Society for Pediatric Research

Disclosure: Nothing to disclose.

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, American Society of Clinical Oncology, American Society of Hematology, American Society of Pediatric Hematology/Oncology, Children's Oncology Group, and International Society for Experimental Hematology

Disclosure: Nothing to disclose.

Helen SI Chan, MBBS, FRCP(C), FAAP  Associate Senior Scientist, Research Institute; Professor, Division of Hematology/Oncology, Department of Pediatrics, The Hospital for Sick Children, University of Toronto Faculty of Medicine, Canada

Helen SI Chan, MBBS, FRCP(C), FAAP is a member of the following medical societies: American Academy of Pediatrics, American Association for Cancer Research, American Society of Hematology, and Royal College of Physicians and Surgeons of Canada

Disclosure: Nothing to disclose.

Chief Editor

Max J Coppes, MD, PhD, MBA  Senior Vice President, Center for Cancer and Blood Disorders, Children's National Medical Center; Professor of Medicine, Oncology, and Pediatrics, Georgetown University School of Medicine; Clinical Professor of Pediatrics, George Washington University School of Medicine and Health Sciences

Max J Coppes, MD, PhD, MBA is a member of the following medical societies: American Association for Cancer Research, American Society of Pediatric Hematology/Oncology, and Society for Pediatric Research

Disclosure: Nothing to disclose.

Additional Contributors

The authors and editors of eMedicine gratefully acknowledge the contributions of previous author Jeffrey Dome, MD, to the original writing and development of this article.

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Nonenhanced CT scan demonstrates linear and curvilinear calcifications outlining tumor lobules in a malignant rhabdoid tumor (MRT) (arrows). A hypoattenuating fluid collection surrounds and separates the lobules. These imaging features are seen with MRT more often than with other childhood renal neoplasms.
Contrast-enhanced CT scan demonstrates a subcapsular fluid collection (arrow) and the lobulated nature of a malignant rhabdoid tumor (MRT). Subcapsular fluid collections are more common with MRTs than with the other renal neoplasms that occur in children.
Histology of malignant rhabdoid tumors (MRTs). This photomicrograph shows the typical large malignant cells with large, vesicular nuclei, prominent red nucleoli, and abundant eosinophilic cytoplasm. Many tumor cells have a distinct, pale, rhabdoid inclusion in the cytoplasm. (Hematoxylin and eosin stain, original magnification x400).
INI1 immunohistochemistry stain shows diffuse loss of INI1 expression in tumor nuclei, with appropriate staining of intratumoral endothelial cells serving as the internal control (original magnification x400).
Table 1. One Ifosfamide-Carboplatin-Etoposide regimen for Malignant Rhabdoid Tumor
DrugDosageRouteSchedule
CarboplatinTarget dose to the AUC of 6 mg/mL/min by using the Calvert equationIVDay 1
Etoposide3.3 mg/kg/dose or 100 mg/m2/doseIVDays 1, 2, and 3
Ifosfamide65 mg/kg/dose or 2 g/m2/doseIVDays 1, 2, and 3
Mesna16 mg/kg/dose or 500 mg/m2/doseIVStart immediately after and at 3 h, 6 h, and 9 h after ifosfamide
Filgrastim G-CSF5 mcg/kg/doseSCStart 24 h after chemotherapy and continue until ANC recovers
Table 2. One Vincristine-Doxorubicin-Cyclophosphamide Regimen for Malignant Rhabdoid Tumor
DrugDosageRouteSchedule
Vincristine0.05 mg/kg/dose or 1.5 mg/m2/dose; not to exceed 2 mg/doseIVDays 1, 8, and 15
Doxorubicin1.2 mg/kg/dose or 37.5 mg/m2/doseIVDays 1 and 2
Cyclophosphamide60 mg/kg/dose or 1.8 g/m2/doseIVDay 1
Mesna15 mg/kg/dose or 450 mg/m2/doseIVStart immediately after and at 3, 6, and 9 h after cyclophosphamide
Filgrastim G-CSF5 mcg/kg/doseSCStart 24 h after chemotherapy and continue until ANC recovers
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