Primary Malignant Rhabdoid Tumor of the Central Nervous System

Meenakshi Bhattacharjee, MBBS, MB, MRCPath John Hicks, MD, DDS, PhD

Department of Pathology, Texas Children’s Hospital, Baylor College of Medicine, Houston, Texas, USA

Robert Dauser, MD

Department of Neurosurgery, Texas Children’s Hospital, Baylor College of Medicine, Houston, Texas, USA

Douglas Strother, MD Murali Chintagumpala, MD Marc Horowitz, MD

Department of Hematology and Oncology, Texas Children’s Hospital, Baylor College of Medicine, Houston, Texas, USA

Linda Cooley, MD

Department of Pathology, University of Texas-Houston Health Science Center Medical School, Houston, Texas, USA

Hannes Vogel, MD

Department of Pathology, Texas Children’s Hospital, Baylor College of Medicine, Houston, Texas, USA

Since the initial description of malignant rhabdoid tumor (MRT) of the kidney by Beckwith in 1978, MRTs have been established as a distinct clinicopathologic entity lacking nephrogenic and myogenic differentiation. MRTs are highly aggressive neoplasms with characteristic histopathologic, immunocytochemical, and ultrastructural features. Many reports have appeared documenting primary extrarenal rhabdoid tumors (ERRTs) occurring at diverse sites, including infratentorial and supratentorial compartments of the central nervous system (CNS). The authors report 2 cases of primary CNS-MRT in young male children (6.5 and 7 years of age) and review the literature on CNS-MRTs. Neuroimaging studies showed an inhomogeneous parasagittal mass in the left anterior parietal region involving the motor strip and attached to the lateral aspect of the superior sagittal sinus in one case, and a right parietal parasagittal tumor with a cystic component in the other case. Metastatic workup, including abdominal CT, was negative in both cases. Histologic examination of the resected tumors showed irregular clusters and nests of cells with variable desmoplasia in both cases. Large areas of tumor necrosis and apoptotic tumor cells were present. Prominent eosinophilic cytoplasmic inclusions and eccentric, indented nuclei with conspicuous nucleoli characterized many of the tumor cells. Diffuse strong vimentin reactivity and focal strong reaction for epithelial membrane antigen (EMA) were demonstrated. Cyto- genetic analyses reported a normal male karyotype in one case and an abnormal male karyotype with loss of both normal copies of chromosome 22 and gain of one structurally rearranged chromosome 22 in the other case. Ultrastructural examination displayed tumor cells with ovoid to indented nuclei, marginated chromatin, and prominent nucleoli. Intercellu- lar junctions were not found. Masses of cytoplasmic intermediate filaments in a characteristic whorled configuration were present. CNS-MRTs are consistently vimentin positive (100%) and usually EMA positive (90%). Glial fibrillary acidic protein, neuron-specific enolase, and S-100 protein are variably expressed. Markers for myogenous differentiation are invariably absent. Ultrastructural characteristics include aggregates of intermediate filaments. Monosomy 22 occurs in some CNS rhabdoid tumors, while most renal rhabdoid tumors are cyto- genetically normal with only isolated cases having del(l3q), del(1 Ip), deI(22Hql I), and unbalanced reciprocal translocation involving chromosomes 8 and 22. The prognosis for CNS rhabdoid tumors is dismal and almost two-thirds of patients are dead of disease shortly after diagnosis; one-third have been reported to be alive with disease, but have been fol- lowed for only short periods; and a single patient is reported to be free of disease at 5 years.

Keywords central nervous system, immunocytochemistry, pediatrics, rhabdoid tumors, ultrastructure

Received 3 January 1997, accepted 22 January 1997

The authors acknowledge the technical expertise of B Antalffy, J Barrish, B Smith, and S -H Zhu

Presented at UltraPath VIII, Society for Ultrastructural Pathology, Oaxaca, Mexico, August 1996

Address correspondence to Dr John Hicks, Department of Pathology MC1-2261, Texas Children’s Hospital, 6621 Fannin Street, Houston, TX 77030-2399, USA E-mail ]hicksQmsmail path tch tmc edu

Ultrastructural Pathology, 2 1 :361-368, 1997 Copyright 0 1997 Taylor €4 Francis

361 0191-3123197 $12.00 + .OO

362 M. Bhattachajee et al.

Malignant rhabdoid tumor (MRT) of the kidney was first described by Beckwith and Palmer [I1 in 1978 as a rhabdomyosarcomatoid variant of Wilms' tumor with unfavorable histology and a grave prognosis with a high risk for early metastasis. This par- ticular renal tumor resulted in a mortality rate of 80% despite aggressive multimodality therapy and was noted to be resistant to radiotherapy [I-31. With further investigation 11-31, it was realized that this highly aggressive neoplasm did not represent a nephrogenic or myogenic tumor, but rather was a distinct clinicopathologic entity characterized by a diffuse proliferation of polygonal cells resembling rhabdomyoblasts, but lacking the expression of myofilaments and muscle proteins. Abundant eosinophilic cytoplasm with hyaline-like inclusions displacing the nuclei is often seen and by ultrastructural examination proves to be masses of intermediate filaments arranged in a concentric whorling pattern. The tumor tends to have a diffuse proliferation pattern with focal trabecular and alveolar architecture. Characteristically, these tumors are immunoreactive for vimentin and epithelial membrane antigen.

Extrarenal rhabdoid tumors have been described in many organ systems and in soft tissue 13-51. The central nervous system (CNS) is a relatively common site and tumor may involve either infratentorial or supratentorial compartments [6-171. The signs and symptoms of CNS-MRT are similar to other primary CNS tumors, with irritability, apathy/lethargy, ataxia, neck stiffness, and seizures. Differentiation from other tumors is based on histopathologic evaluation.

We report two pediatric cases of primary CNS malignant rhabdoid tumor and review the literature on these neoplasms.

CASE HISTORIES

Case 1 A 6.5-year-old Caucasian male presented with recent onset of irritability, lethargy, and ataxia. Magnetic resonance imaging (MRI) and com- puter-assisted tomography (CT) scans revealed an inhomogeneous parasaggital mass in the left anterior parietal region. The tumor involved the motor strip and was attached to the lateral aspect of the superior sagittal sinus. A subtotal resection of the mass was performed and a diagnosis of rhabdoid tumor was made. A metastatic workup including abdominal CT scan was negative and no renal mass was identified. The child underwent multiagent chemotherapy and radiation therapy. He has subsequently undergone two repeat surgical procedures to remove residual and recurrent tumor. The initial diagnosis of CNS-MRT has been confirmed with tissue obtained at the repeat surgeries. Localized radiotherapy has also been

attempted to control microscopic and gross tumor within the residual tumor bed. The child is alive with tumor 30 months after diagnosis.

Case 2 A 7-year-old Caucasian male presented with acute onset of seizures and ataxia. A parasagittal mass with a cystic component was identified by MRI and CT scan. Following a subtotal resection of the tumor, a diagnosis of MRT was made. Metastatic workup including CT scan of the abdomen failed to show any disease outside the cranium. Aggres- sive multiagent chemotherapy was instituted and the child is alive without definite evidence of disease 12 months following diagnosis.

MATERIALS AND METHODS The histopathologic features of the two cases were similar. The tumor cells diffusely infiltrated and re- placed the surrounding cerebral tissue (Figure 1) with only occasional areas showing trabecular or alveolar architecture. The tumor had pushing margins which displaced adjacent cerebral tissue, as well as focal insinuation of cords and nests of neoplastic cells between neurons, astrocytes, and other supporting cells. Frequent areas of necrosis and apoptosis were apparent. There was a brisk mitotic rate with 10 to 15 typical mitotic figures per 10 high-power fields. Tumor cells lay within a markedly edematous stroma with a fine vascular- ity. The cytologic features of the rhabdoid cells were somewhat variable. Many possessed eccentrically located, somewhat indented nuclei, while others were round to oval. Most nuclei had one or more prominent nucleoli and the chromatin pattern varied from dispersed with condensed peripheral chromatin to diffuse condensed chromatin. There was relatively abundant eosinophilic cytoplasm with inclusions in frequent cells. The cytoplasm was diffusely immunoreactive with vimentin (Fig- ure 2A) and focally, but strongly reactive for epithelial membrane antigen (Figure 26) and low molecular weight cytokeratin (Figure 2C). These immunostains highlighted the cytoplasmic areas occupied by the eccentrically placed eosinophilic inclusions. Ultrastructural evaluation (Figure 3) showed neoplastic cells with varying quantities of intermediate filaments, arranged in a concentric, whorling pattern, often entrapping organelles. The nuclear morphology varied from smooth and regu- lar to sharply indented and convoluted. Nuclei with dispersed chromatin and infrequent nucleoli, and nuclei with relatively condensed chromatin and prominent nucleoli were also present. Occasional binucleate tumor cells with several whorled masses of intermediate filaments were identified. In tumor areas without stromal edema, rudimen- tary cytoplasmic attachments could be seen.

Primary Rhabdoid Tumors of CNS 363

FIG. 1. Primary rhabdoid tumors of the CNS: histopathologic appearance. (A) Diffuse proliferation of rhabdoid cells with frequent mitotic figures (arrows). (B) Rhabdoid cells in an edematous background efface the normal cerebral architecture. (C) Blunt, pushing margins char- acterize the interface between the tumor and adjacent normal cerebral tissue. (D, E) Eosin- ophilic cytoplasmic inclusions displace and indent nuclei in rhabdoid cells (arrows mitotic figures). Hematoxylin and eosin stain, original magnifications: (A, B, and C) x200; (D and E l x 7,000.

Tissue from both tumors was submitted for flow cytometric ploidy studies and cytogenetic analysis. Both tumors were diploid with increased prolifera- tive fractions (S + G2M) of 21.7% in the first case and 7.1% in the second case. A normal karyotype (46, XY) was identified in the first case. An abnor- ma1 karyotype with loss of both normal copies of chromosome 22 and gain of one structurally rearranged chromosome 22 occurred in the second

case (45XY,-22, der(22)t(22;22)?(qter -sp12:: p12 ->q13::?).

DISCUSSION Malignant rhabdoid tumor is an unusual neoplasm that may involve the central nervous system 13, 5-171 predominantly in the pediatric age group (Table 1). The diagnosis of primary CNS-MRT is

364 M. Bhattacharjee et al.

FIG. 2. Primary rhabdoid tumors of the CNS: immunocytochemical features. Rhabdoid cells im- munoreact diffusely with vimentin (A), frequently with epithelial membrane antigen (B), and occasionally with low molecular weight cytokeratin (C), Original magnifications: (A and B) x200; (C) ~7,000.

dependent on a thorough metastatic workup to eliminate other primary tumor sites where MRTs more commonly occur, particularly the kidney. Relatively few cases 13, 5-171 of primary CNS-MRT have been reported. The majority occur in children under 6 years of age, although the tumor may be seen from the neonatal period into young adult- hood. There is a slight male predilection. The brainstem and ventricular system are affected in a small percentage of cases, while the cerebrum and posterior fossa, including the cerebellum, are involved in over 80%. Meningeal and cerebrospinal fluid involvement are common, and ventriculoperitoneal shunting necessary to relieve increased intracranial pressure may act as a conduit for peritoneal cavity tumor seeding. Surgical treatment is directed to- ward total or gross subtotal resection, but as with any infiltrative brain tumor, surgical resection may be limited by the proximity of vital structures. Oc- casionally, the diagnosis is made only at necropsy. Multimodal aggressive chemotherapy alone or in conjunction with radiotherapy is instituted in most cases (Table 2) 13, 5-171. In 15% of cases, therapy may be considered to be of limited benefit based on the location or extent of the tumor, and neither chemotherapy nor radiotherapy is initiated 13, 5-171. Despite aggressive surgical and oncologic

management, almost two-thirds of patients suc- cumb within 16 months and the vast majority (95%) of survivors are alive with disease [3, 5-171.

Because the clinical presentation and imaging studies are not specific for MRT, the diagnosis de- pends on histopathologic, immunocytochemical, and ultrastructural evaluation (Tables 3 and 4) [3, 5-171. All tumors will have a diffuse round cell infiltrative pattern composed of classic rhabdoid cells mimicking rhabdomyoblasts; however, the tumor cells in CNS-MRT tend to have eosinophilic inclusions which indent or eccentrically displace the nuclei. Occasionally, these tumors may resemble the small round blue cell tumors frequently seen in the pediatric age group, and especially when confined to the CNS may be confused with medulloblas- toma. Areas of tumor necrosis and a high mitotic index are prevalent. Ultrastructural examination is the optimal method for eliminating other consider- ations in the differential diagnosis [3,7, 10, 141. The cytoplasm contains concentric whorls of intermediate filaments that correspond to the eosinophilic inclusions seen on routine light microscopy and these are considered to be diagnostic for rhabdoid cells. It must be recognized that cells with a rhabdoid appearance may be present in many neoplastic processes and represent primitive or undif-

Primary Rhabdoid Tumors of CNS 365

FIG. 3. Primary rhabdoid tumors of the CNS: ultrastructural features. Cytoplasmic intermediate filaments arranged in a whorling pattern (A-E) displace the nuclei to the periphery of the cell. These cytoplasmic masses of intermediate filaments often engulf cytoplasmic organelles. Binucleate rhabdoid cells are frequently identified (E). Original magnifications: (A) ~3,600; (B) ~6,500; (C) ~6,200 (D) ~6,200 (E l ~3,200.

ferentiated cells. A search for other cell types is mandatory to eliminate a rhabdoid component arising in another type of malignant tumor. The lack of definitive structures, such as myofi la- ments, neurofilaments, neurosecretory granules, or melanosomes in the neoplastic cells, should be

ascertained before defining a tumor as a primary CNS-MRT. A recently described and uncommon CNS tumor of infancy and early childhood that also possesses rhabdoid cells is the atypical teratoidl rhabdoid tumor [181. In this tumor, a number of structural elements are present, one of them rhab-

M. Bhattacharjee et al.

TABLE 3 Primary rhabdoid tumor of CNS: histopathologic and ultrastructural characteristics

TABLE 1 Primary rhabdoid tumors of CNS: clinical characteristics

Number of cases Gender ratio Age range

5 1 year of age 56 years of age

Cerebrum Cerebellum/posterior fossa Cerebropontine angle Brainstem/fourth ventricle Intraventricular/trigone Spinal cord

Metastatic disease pattern Meningeal Cerebrospinal fluid involvement Peritoneal cavity via VP shunt Brainstem

Lesion site

31 1.2M:lF Neonate to 21 years 45% 93%

52% 33% 6% 3% 3% 3% 45% 78% 14% 7% 7%

Treatment Total resection 32% Subtotal resection 42% Partial resection 14% Biopsy only 7% None (diagnosis at autopsy) 7%

Note. Data compiled from references 3-19 and include present 2 cases.

doid. Both CNS-MRT and the atypical teratoidl rhabdoid tumor tend to be aggressive tumors with dismal prognoses.

lmmunophenotyping of CNS-MRTs indicates that certain antibodies 13, 5-171 may provide sup- portive evidence of the rhabdoid character of the neoplasm when ultrastructural evaluation is not available. Vimentin is universally positive and high- lights the eosinophilic inclusions seen by routine light microscopy. These intermediate filament inclusions are also immunoreactive for epithelial membrane antigen and cytokeratin, but to a lesser degree than for vimentin. Other markers are less frequently positive in CNS-MRTs. Desmin is re-

TABLE 2 Primary rhabdoid tumor of the CNS: therapy and outcome

Tumor therapy Chemotherapy and radiotherapy Chemotherapy alone Radiotherapy No therapy

Died of disease Survival

65% 13% 6%

65% (Survival range from 2 weeks to 6 years) (87% died of disease in 5 18 months)

(Followup period range from 5 to 18 months) Alive with disease 32%

No evidence of disease 1%

Light microscopic features Diffuse round cell pattern Small blue cell pattern Cytoplasmic inclusions Necrosis Mitotic activity, increased

Intermediate filament whorls Large pleomorphic nuclei with

Ultrastructural features

marginated chromatin

100% 8%

100% 90% 94%

100% Most

Note. Compiled from references 3-19 and includes present 2 cases.

ported to be expressed in a small percentage of cases 181. Expression of such a marker may warrant a further search, especially ultrastructural examination of multiple tissue blocks, in order to determine the reason for an aberrant immunophenotype and whether the tumor actually represents a poorly dif- ferentiated neoplasm. Primary rhabdomyosarco- mas occur in the CNS, as do teratomas with rhab- domyosarcomatous, sarcomatous, germ cell, and malignant epithelial elements. Markers for germ

TABLE 4 Primary rhabdoid tumors of the CNS: immunocytochemical and cytogenetics characteristics

lmmunocytochemistry Virnentin Epithelial membrane antigen Cytokeratin S-100 protein Glial fibrillary acidic protein Neurofilament protein Neuron specific enolase Desmin Synaptophysin Myoglobin Germ cell tumor markers (AFP, HCG, PLAP) Smooth muscle actin Leukocyte common antigen Leu-7 CEA Antichymotrypsin

Cytogenetic features Cytogenetic abnormalities

Chromosome 22 (ql1.2) abnormality Chromosome 22 monosomy Chromosome 22 (ql1.2) partial deletion Translocation involving chromosome

22 t(l1;22) and t(18.22)(q21;pl1.2) Chromosome 22 de1(22)(q11)

that for Ewing's sarcoma family of tumors Breakpoint cluster region different from

100% 85% 75% 66% 48% 50% 48% 16% 10% 0% 0% 0% 0% 0% 0% 0%

Note. Compiled from references 3-19 and includes present 2 cases.

Note, Compiled from references 3-19 and includes present 2 cases.

Primary Rhabdoid Tumors of CNS

cell and hematopoietic neoplasms should be negative in CNS-MRTs.

Recent cytogenetic and molecular investigations [9,12, 17,19-231 of rhabdoid tumors have provided new insights into this unusual neoplasm. Cytoge- netic abnormalities have been seen repeatedly with chromosome 22 and these include translocations, monosomy, and deletions (Table 4). Although no characteristic or tumor-defining cytogenetic abnormalities have been defined, these findings provide some evidence for the derivation of such tumors. The breakpoint cluster region has been shown to be different from those identified with Ewing‘s sarcoma family of tumors [t(l1:22)(q24;q12) EWS/FLIl; t(2 1 ;22)(q22;q 12) EWS/ERG; t(7;22)(p22;q 12) EWS/ EVTI] [20-231. At the same time, rhabdoid tumors do not have chromosomal alterations associated with myogenic malignant tumors such as alveolar rhabdomyosarcoma [t(2; 13)(q35;q 14) PAX3/FKHR; t(l:13)(p36;q14) PAX7IFHKRI or embryonal rhabdomyosarcoma (extra copies of chromosomes 2, 8, 20). A single retroperitoneal MRT 1191 has been reported with a karyotype [t(l1;22)(p15.5;ql1.23), which has similar but different breakpoint from that characteristically seen in desmoplastic small round cell tumors [t(l1;22)(p13;q12) EWS/WTIl.

Further information regarding the derivation of MRTs has been provided by cell culture experi- ments [191. Rhabdoid tumor cells grown in culture may be induced to undergo neuroectodermal differentiation. In the presence of retinoic acid or TPA (tetradecnoylphorbol-13 acetate), neuroblastic features that may be identified include sprouting of neurites, neurosecretory granules, and immunore- activity for neuron specific enolase, neurofilament protein, and synaptophysin. Molecular analysis has detected RNA expression of c-myc protein and ab- sence of MYCN (n-myc) at the RNA or DNA level. The findings are similar to those of the Ewing’s sarcoma family of tumors. Especially interesting is the lack of myoDl expression and the failure to induce such expression in the presence of myogenic inducers in cell culture.

It appears that malignant rhabdoid tumors in the CNS are derived from primitive mesenchymal cells. However, the evidence from cytogenetic and molecular studies suggest that these tumors may represent a subset of peripheral primitive neuroectodermal tumors with the potential for neuroglial differentiation [18-231. This hypothesis is sup- ported by the expression of s-100 protein, GFAP, and NSE in some tumors and the induction of neural-crest marker proteins in cell lines from MRTs 13-8, 19-231. Alterations in chromosome 22 are found in a number of neural crest-derived neoplasms, including the Ewing’s sarcoma family of tumors, malignant melanoma of soft parts, desmoplastic small round cell tumor, malignant ectomes- enchymoma, acoustic schwannoma, meningioma, and neurofibroma [20-231. The most common cytogenetic finding in MRTs is monosomy of chro-

mosome 22, which has also been identified in acoustic neuromas, meningiomas, and neurofibro- mas [17, 19-23]. It also well known that the neuro- fibromatosis type 2 gene (NF2) has been mapped to the long arm of chromosome 22 and that it is a tumor suppressor gene 117, 18, 20, 221. With translocation of chromosome 22 or monosomy of chromosome 22, it is possible that a similar tumor suppressor gene may become inactive, or that a fusion product may become active. Either event could re- sult in proliferation and transformation of these cells into a neoplastic process. While this tumor is a relatively rare entity (especially those primarily involving the CNS), a considerable knowledge base has developed to support a neural-crest derivation.

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