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Malignant Rhabdoid Tumor Treatment & Management

  • Author: James I Geller, MD; Chief Editor: Max J Coppes, MD, PhD, MBA  more...
Updated: Dec 05, 2014

Medical Care

After the primary tumor is surgically removed, chemotherapy is indicated as adjuvant treatment for malignant rhabdoid tumor (MRT). Chemotherapy for malignant rhabdoid tumor was historically based on therapy for a Wilms tumor, which included vincristine, actinomycin, and doxorubicin with or without cyclophosphamide. With these agents, the estimated survival rate for patients with malignant rhabdoid tumor was only 23%.

To try to improve these results, investigators in NWTS 5 used a regimen consisting of carboplatin-etoposide alternating with cyclophosphamide. However, this strategy, did not improve outcomes. Recent case reports have documented successful outcomes in patients with metastatic malignant rhabdoid tumor treated with ifosfamide-carboplatin-etoposide (ICE) or ifosfamide-etoposide (IE) alternating with vincristine-doxorubicin-cyclophosphamide (VDC). On the basis of these reports, cyclophosphamide-carboplatin-etoposide (CCE) alternating with VDC is the main treatment in the current COG study.

Insights into the treatment of malignant rhabdoid tumor may be derived from the experience with atypical teratoid/rhabdoid tumors (AT/RT) of the CNS. Like its extra-CNS counterparts, AT/RT results in an unfavorable prognosis and is characterized by resistance to chemotherapy. A review of the AT/RT registry by Hilden and colleagues revealed that 14 (33%) of 42 patients with AT/RT survived disease-free over 9.5-month to 96-month follow-up.[12] Survivors were treated with surgery, radiation therapy, and various chemotherapy regimens that typically included cisplatin, etoposide, vincristine, ifosfamide, doxorubicin, actinomycin, cyclophosphamide, and intrathecal agents. Some survivors received high-dose therapy with autologous stem-cell rescue.

In a separate review by Tekautz et al, AT/RT presenting in older patients demonstrated a 2 year event-free survival of 78% when treated with a combination of radiation and high-dose alkylating therapy.[13] More recently, a multisite study of a multimodal therapy plan incorporating surgery, radiation, and a systemic and intrathecal conventional chemotherapeutic regimen based on a modified IRS-III regimen demonstrated a 2 year progression-free survival of 58%. This later study includes infants younger than 3 years. Considering all data, the COG AT/RT protocol is currently testing a regimen incorporating surgery, conventional chemotherapy, radiation, and tandem high dose chemotherapy with stem cell rescue.

Two reports describe the successful use of high dose chemotherapy with stem cell rescue to treat non-CNS malignant rhabdoid tumor.[14] However, in combination, none of the 4 children described had metastatic disease at presentation. Based on the limited data available at this time, whether high-dose chemotherapy with stem cell rescue is of any added benefit for non-CNS malignant rhabdoid tumor is unclear.

Similarly, anecdotal reports suggest a benefit from the use of radiotherapy as part of multimodal therapy for malignant rhabdoid tumor. However, the lack of treatment uniformity among reported patients makes it difficult to determine if radiotherapy is effective for malignant rhabdoid tumor. In NWTS 1-5, radiation therapy was given to the flank or abdomen at total doses of 1080-3500 cGy. However, the optimal dose remains to be determined. Radiation therapy is a cornerstone of treatment for CNS AT/RT, and some suggest that the high doses delivered to the posterior fossa improve patients' outcomes.

Furtwängler et al conducted a review of 3 prospective studies comparing the change of tumor volume as a result of treatment with either actinomycin D and vincristine combination therapy (AV) or doxorubicin-intensified antinomycin D and vincristine combination therapy (AVD) in all patients with malignant rhabdoid tumor of the kidney who had been treated from 1991 to 2013 in Austria, Switzerland, and Germany. The investigators concluded that a significantly better treatment response is achieved with neoadjuvant AVD than with AV alone.[15]


Surgical Care

Children with a renal tumor or soft tissue mass should be referred to a pediatric surgeon with experience in oncologic surgery.

For renal tumors, a large transabdominal, transperitoneal incision is recommended for adequate exposure. If the mass is unilateral, a radical nephrectomy with subtotal ureterectomy should be performed. The tumor should be removed en bloc to avoid tumoral spillage into the peritoneal cavity because this spillage increases the stage of the tumor. If the mass involves the upper pole of the kidney, the adrenal gland should be removed.

Lymph nodes from the iliac, para-aortic, and celiac areas should be sampled, even if they do not appear abnormal. Lymph node dissection is not indicated. If the tumor is bilateral or unresectable, biopsy should be performed. If a bilateral or unresectable Wilms tumor is diagnosed, preoperative chemotherapy is recommended to shrink the tumor and facilitate subsequent resection. If malignant rhabdoid tumor is diagnosed, complete removal of the tumor is advised.

For extrarenal tumors, the surgical approach depends on the site of disease. Complete resection should be attempted if feasible. If not initially feasible, a preoperative course of chemotherapy is advised.



Therapy for malignant rhabdoid tumor is intensive and requires a multidisciplinary effort.

Practitioners who should be consulted include the following:

  • Pediatric oncologist
  • Pediatric surgeon or urologist
  • Radiation oncologist
  • Pediatric clinical geneticist or genetics counselor
  • Social worker
  • Nutritionist


No dietary restrictions are necessary. The patient's nutritional status should be closely monitored to ensure adequate caloric intake during the intensive chemotherapy. Parenteral nutrition may be required at some point during treatment.



No restrictions on activity are necessary except during periods of thrombocytopenia. Standard neutropenic precautions should be employed when appropriate.

Contributor Information and Disclosures

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 Pediatric Hematology/Oncology, Children's Oncology Group, American Society of Clinical Oncology

Disclosure: Nothing to disclose.


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

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

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, College of American Pathologists, United States and Canadian Academy of Pathology, Children's Oncology Group, Society for Pediatric Pathology

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

Max J Coppes, MD, PhD, MBA Executive Vice President, Chief Medical and Academic Officer, Renown Heath

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

Disclosure: Nothing to disclose.

Additional Contributors

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, Society for Pediatric Research, American Society for Blood and Marrow Transplantation, American Society of Hematology, American Society of Pediatric Hematology/Oncology

Disclosure: Nothing to disclose.


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
Drug Dosage Route Schedule
Carboplatin Target dose to the AUC of 6 mg/mL/min by using the Calvert equation IV Day 1
Etoposide 3.3 mg/kg/dose or 100 mg/m2/dose IV Days 1, 2, and 3
Ifosfamide 65 mg/kg/dose or 2 g/m2/dose IV Days 1, 2, and 3
Mesna 16 mg/kg/dose or 500 mg/m2/dose IV Start immediately after and at 3 h, 6 h, and 9 h after ifosfamide
Filgrastim G-CSF 5 mcg/kg/dose SC Start 24 h after chemotherapy and continue until ANC recovers
Table 2. One Vincristine-Doxorubicin-Cyclophosphamide Regimen for Malignant Rhabdoid Tumor
Drug Dosage Route Schedule
Vincristine 0.05 mg/kg/dose or 1.5 mg/m2/dose; not to exceed 2 mg/dose IV Days 1, 8, and 15
Doxorubicin 1.2 mg/kg/dose or 37.5 mg/m2/dose IV Days 1 and 2
Cyclophosphamide 60 mg/kg/dose or 1.8 g/m2/dose IV Day 1
Mesna 15 mg/kg/dose or 450 mg/m2/dose IV Start immediately after and at 3, 6, and 9 h after cyclophosphamide
Filgrastim G-CSF 5 mcg/kg/dose SC Start 24 h after chemotherapy and continue until ANC recovers
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