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2243
Is Primitive Neuroectodermal Tumor of the Kidney a
Distinct Entity?
Carlos Rodriguez-Galindo,
Neyssa M. Marina, M.D.1,4
Barry D. Fletcher, M.D.2,4,5
David M. Parham, M.D.3,6
Sara M. Bodner, M.D.3,6
William H. Meyer, M.D.1,4
1
BACKGROUND. Primitive neuroectodermal tumors (PNETs) constitute a family of
M.D.
neoplasms of presumed neuroectodermal origin, most often presenting as bone
or soft tissue masses in the trunk or axial skeleton in adolescents and young adults.
As a soft tissue neoplasm, PNET arising in the kidney has not been well described,
with only three cases previously reported.
METHODS. Four patients with PNET of the kidney were diagnosed and treated at
1
Department of Hematology-Oncology, St.
Jude Children’s Research Hospital, Memphis,
Tennessee.
2
Department of Diagnostic Imaging, St. Jude
Children’s Research Hospital, Memphis, Tennessee.
3
Department of Pathology, St. Jude Children’s
Research Hospital, Memphis, Tennessee.
4
Department of Pediatrics, University of Tennessee
School of Medicine, Memphis, Tennessee.
5
Department of Radiology, University of Tennessee
School of Medicine, Memphis, Tennessee.
6
Department of Pathology, University of Tennessee
School of Medicine, Memphis, Tennessee.
Supported in part by Grants P30 CA-23099 and
P30 CA-21765 from the National Cancer Institute, by the American Lebanese Syrian Associated Charities (ALSAC), and by Grant 93/5431
from the Fondo de Investigaciones Sanitarias of
the Spanish National Institute of Health.
The authors thank Sharon Naron for editorial
assistance.
Dr. Marina’s current address: Department of Pediatrics, Stanford University Medical Center,
Stanford University School of Medicine, Stanford, California.
Dr. Parham’s current address: Department of
Pediatric Pathology, Arkansas Children’s Hospital, Little Rock, Arkansas.
Address for reprints: William H. Meyer, M.D.,
Dept. of Hematology-Oncology. St. Jude Children’s Research Hospital, 332 N. Lauderdale,
Memphis, TN 38105-2794.
Received October 18, 1996; revision received
February 6, 1997; accepted February 6, 1997.
St. Jude Children’s Research Hospital. The authors reviewed the clinical, radiologic,
and pathologic features and outcomes of these cases and of those previously described.
RESULTS. The authors’ patients were age 4–20 years. They presented with unilateral
renal masses and metastatic disease in the lymph nodes (three patients), lungs
(three patients), bone (two patients), liver (one patient), and bone marrow (one
patient). Treatment included surgery, radiotherapy, and multiagent chemotherapy.
Three of the patients died of progressive disease within 14 months of diagnosis.
Features and outcomes were similar to those of the three previously reported cases.
CONCLUSIONS. PNET of the kidney appears to be a distinct entity. Although rare,
it must be included in the differential diagnosis of renal tumors in children and
young adults. Patients usually present with advanced disease and show poor response to combined-modality therapy. Cancer 1997;79:2243–50.
q 1997 American Cancer Society.
KEYWORDS: primitive neuroectodermal tumor (PNET), peripheral neuroepithelioma,
renal neoplasms, malignant rhabdoid tumor, intrarenal neuroblastoma, Wilms’ tumor.
F
irst described by Stout in 1918,1 the concept of primitive neuroectodermal tumor (PNET) has evolved to include a group of small
round cell malignancies of ubiquitous location and presumed neuroectodermal origin. They are defined by expression of the same protooncogene2 and the presence of a balanced t(11; 22)(q24; q12) chromosomal translocation or a (21; 22) rearrangement that results in the
fusion of the gene EWS with the FLI1 or ERG gene, respectively.3 PNET
manifests a continuum of neurogenic differentiation, with Ewing’s
sarcoma representing the least differentiated and peripheral neuroepithelioma the most differentiated forms.4 In general, PNET is a very
aggressive neoplasm, with 25 – 50% of patients presenting with metastatic disease, and a 5-year disease free survival rate of 45 – 55%.5 – 7
Renal location of PNET is extremely rare, with only three previously
reported cases8 – 10 and a small series from the National Wilms Tumor
Study (NWTS) published only in abstract form.11
Between March 1962 and August 1996, four cases of PNET of the
kidney were diagnosed and treated at St. Jude Children’s Research
Hospital (SJCRH). The authors describe the clinical characteristics,
pathologic features, clinical course, response to treatment, and out-
q 1997 American Cancer Society
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CANCER June 1, 1997 / Volume 79 / Number 11
come of these patients and review the cases previously
described. Their results suggest that this tumor is a
distinct entity with a very aggressive behavior and poor
response to therapy that must be included in the differential diagnosis of renal neoplasms in children and
young adults.
Case Reports
A review of the records of all children with PNET diagnosed and treated between March 1962 and August
1996 at SJCRH identified four patients with a primary
renal tumor. A previous histologic review of patients
with renal tumors diagnosed and treated between
March 1962 and December 1984 revealed no cases
of PNET.12 The clinical course, imaging studies, and
histologic sections of the patients’ tumors were reviewed. Two patients had been diagnosed and previously treated at other institutions before referral to
SJCRH. In all cases, histologic sections were prepared
from formalin fixed, paraffin embedded tissue and
stained with hematoxylin and eosin and periodic acidSchiff stains. Immunohistochemical testing used the
standard avidin-biotin complex procedure with specific monoclonal antibodies. Electron microscopy
studies were performed in selected cases. The diagnosis was confirmed in all four cases by two of the authors (D.M.P. and S.M.B.) using previously described
histopathologic criteria.4,6 Clinical characteristics,
pathologic features, treatment, and outcome (including the data from previously reported cases) are summarized in Table 1.
Case 1
An 18-year-old white male was examined at his local
hospital in October 1991 after an 8-month history of
abdominal pain. Computed tomography (CT) scan of
the abdomen revealed a mass nearly replacing the left
kidney, with small areas of calcification and mild retroperitoneal lymph node enlargement. The patient underwent a left nephrectomy. On pathologic examination, the tumor measured 12.5 cm X 9.5 cm X 6.5 cm,
was spongy and soft, distorted the renal parenchyma,
and penetrated the renal capsule without extension to
the renal vein or ureter. Microscopically, it was a
highly cellular neoplasm that infiltrated the renal parenchyma and was comprised of sheets of small,
round-to-oval cells with round nuclei and pale pink
cytoplasm. There were foci of Homer Wright rosette
formation (Fig. 1A) and extensive areas of hemorrhage
and necrosis.
Immunohistochemical stains were positive for
neuron specific enolase (NSE), S-100, and vimentin
and negative for CD56, actin, and cytokeratin. These
findings were consistent with a primitive neural tumor, favoring the diagnosis of neuroblastoma. The pa-
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tient was subsequently referred to SJCRH. At the time,
catecholamine urine excretion was normal. CT scan
of the chest revealed multiple, noncalcified bilateral
pulmonary nodules consistent with metastases. 99mTcmethylene diphosphonate (MDP) skeletal scintigraphy
showed a small focus of increased activity involving
the left seventh rib. Review of pathology at SJCRH did
not allow a distinction between neuroblastoma and
peripheral neuroepithelioma and a thoracotomy was
performed to obtain more tissue for further tumor
evaluation. Immunohistochemical stains on the second sample were positive for NSE, CD99 (HBA-71) (cytoplasmic surface membrane staining) (Fig. 1B), and
beta-2-microglobulin, and negative for CD56, synaptophysin, and chromogranin. Cytogenetic studies revealed a t(11; 22)(q24; q12) chromosomal translocation, confirming the diagnosis of PNET.
The patient received 3 induction chemotherapy
courses with ifosfamide, carboplatin, and etoposide
(ICE), followed by radiation therapy to the left hemiabdomen (3600 centigrays [cGy]) and both lungs (1650
cGy), along with weekly doses of vincristine and biweekly administration of actinomycin D. After reevaluation showed resolution of the lung metastases, the
patient was treated with four courses each of cyclophosphamide/doxorubicin and ifosfamide/etoposide
in rotation. Twelve months after diagnosis (4 months
after completing therapy), he developed new bilateral
pleuropulmonary metastases without evidence of local
recurrence. He was treated with topotecan in a Phase
I study but had no response, and died of tumor progression 14 months after diagnosis. An autopsy was
not performed.
Case 2
In June 1992, a 20-year-old white male was examined at
his local hospital with a 4-month history of abdominal
pain, a right-sided abdominal mass, and massive hematuria. CT scan of the abdomen (Fig. 2A) showed an inhomogeneous, partially calcified 12 cm X 10 cm X 16 cm
mass arising from the right kidney, and retrocaval lymph
node enlargement. CT scan of the chest showed a solitary left upper lobe pulmonary nodule. 99mTc-MDP skeletal scintigraphy (Fig. 2B) showed abnormally increased
activity in the right kidney mass with no skeletal abnormalities. After a right nephrectomy and a diagnosis of
Stage IV Wilms’ tumor of blastemic type, the patient was
referred to SJCRH. A repeat CT scan of the chest showed
bilateral pulmonary metastases. Review of the tumor tissue showed monomorphic sheets of cells with round to
oval nuclei and abundant eosinophilic cytoplasm, with
some areas showing distinct Homer Wright rosettes. Immunohistochemical stains were positive for CD99 (cytoplasmic surface membrane) and NSE, which confirmed
the diagnosis of metastatic peripheral neuroepithelioma.
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TABLE 1
Clinical and Pathologic Features of PNET of the Kidney
Patient
Age
(yrs)
Gender
Race
Symptoms
1
18
M
C
Abd. pain
2
20
M
C
3
4
F
4
14
58
Metastases at
diagnosis
Pathology
Treatment
Outcome
RPLN, lung,
bone
LM: Homer Wright rosettes
IH: NSE /, S-100 /, Vim /, CD99 /,
b2 mcg /, CD56 0, Act 0, Ker 0
t(11;22)(q24;q12)
DOD, 14 mos
Abd. pain, hematuria
RPLN, lung
LM: Homer Wright rosettes
IH: CD99 /, NSE/
C
Abd. pain, fever
RPLN, liver
M
C
Bone pain, weight
loss
Lung, bone,
bone
marrow
22
F
C
Abd. pain
No
69
61
M
C
RPLN
710
24
M
C
Abd. pain, weight
loss
Abd. pain, weight
loss, hematuria
IH: S-100/, CD99/, NSE/, Ker/, Act0,
Vim0, Chromogr0
EM: Microtubules, neurosecretory granules
LM: Homer Wright rosettes
IH: CD99/, NSE/, Vim/, Synapto/, S1000, NFP0, Chromogr0, Ker0, Act0,
PCR: EWS/FLI-1, EWS/ERG0
EM: microtubules, neurosecretory granules
LM: pseudorosettes
IH: NSE/, S-100/, Synapto0 Chromogr0,
NFP0
EM: neurosecretory granules
IH: NSE/, Chromogr/, Ker0, Vim0,
Synapto0
LM: Homer Wright rosettes
IH: CD99/, NSE/, S-1000 NFP0,
Chromogr0, Ker0, Synapto0
Sx: resection
Chx: [IFO, CBP, VP-16] X 3
[CYC, ADR] X 4 [IFO,
VP-16] X 4
Rtx: 3600 cGy abdomen
1650 cGy lungs
Sx: resection
Chx: [VCR, ADR, ActD] X 1
[IFO, VP-16] X 4
Sx: Biopsy
Chx: [IFO, CBP, VP-16] X 1
Rtx: 1400 cGy
On treatment
RPLN, lung
DOD, 4 mos
DOD, 1 mos
Sx: resection
ChX: CYC, VCR, ADR
Rtx: NS
DOD, 10 mos
Sx: resection
Chx: VCR, ADR, CYC, ActD
Sx: resection
DOD, 6 mos
Dead after surgery
PNET: primitive neuroectodermal tumor; M; male; F: female; C: caucasian; Abd: abdominal; RPLN: retroperitoneal lymph nodes; LM: light microscopy; IH: immunohistochemistry; EM: electron microscopy; PCR:
polymerase chain reaction; Sx: surgery; Chx: chemotherapy; Rtx: radiotherapy; cGy: centigrays; DOD: dead of disease; NS: not specified; VCR: vincristine; ActD: actinomycin D; CYC: cyclophosphamide; VP-16:
etoposide; ADR: doxorubicin; IFO: ifosfamide; CBP: carboplatin; NSE; neuron specific enolase; Vim: vimentin, b2 mcg: b2 microglobulin; Act: actin; ker: keratin; Chromogr: chromogranin; Synapto: synaptophysin;
NFP: neurofilament.
The patient received four courses of ifosfamide/etoposide. However, his metastatic lung disease progressed,
and he developed bone marrow disease and died 4
months after diagnosis. An autopsy was not performed.
Case 3
A 4-year-old white female was referred to SJCRH in
March 1993 with a 2-week history of a palpable right
flank mass and low grade fever. Physical examination
revealed a large mass extending 9 cm below the right
costal margin. Laboratory evaluation included a lactate
dehydrogenase (LDH) level of 1689 U/dL and a ferritin
level of 154 mg/dL. CT scan of the abdomen showed a
8.4 cm X 7.5 cm X 7 cm mass in the lower pole of the
right kidney, with extensive retroperitoneal lymph node
enlargement and multiple low attenuation lesions in
both hepatic lobes. Both CT scan and ultrasonography
showed tumor extension into the right renal vein. CT
scan of the chest and 99mTc-MDP skeletal scintigraphy
were normal. A core needle biopsy revealed extensive
areas of tumor necrosis and cells arranged in sheets and
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clumps. Nuclei were ovoid, and contained prominent
eosinophilic nucleoli. Cells contained amphophilic to
slightly eosinophilic cytoplasm with occasional acidophilic paranuclear inclusion bodies. A diagnosis of malignant rhabdoid tumor (MRT) was initially considered.
Immunohistochemical stains were positive for cytokeratin, NSE, S-100, and CD99 (cytoplasmic surface membrane), and negative for actin, vimentin, and chromogranin. Electron microscopy showed microtubules,
neurosecretory granules, and intermediate filaments in
some cells and cytoplasmic processes in many cells.
These findings were consistent with PNET. The patient
received an initial course of ICE but developed progressive disease. She had no response to radiotherapy (1400
cGy) and died of multiorgan failure 3 weeks after diagnosis. Postmortem studies showed a chemo/radiotherapeutic effect, with marked rhabdoid features in the residual tumor, and metastatic lesions.
Case 4
A 14-year-old white male was referred to SJCRH in
August 1996 with a 2-month history of generalized
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CANCER June 1, 1997 / Volume 79 / Number 11
FIGURE 1.
Case 1. (A) Microscopic view of renal primitive neuroectodermal tumor
(PNET). Numerous rosettes
were visible (H & E, original
magnification 150). (B) CD99
immunostain of renal PNET.
There was strong membranous positivity. Stromal cells
were negative (avidin–biotincomplex technique, original
magnification 1500).
bone pain, decreased appetite, and a 15-kg weight loss.
Physical examination disclosed a firm mass, palpable
6 cm below the right costal margin. Laboratory evaluation was significant for an LDH level of 1186 U/dL,
ferritin level of 1266 ng/mL, and NSE level of 87 ng/
mL. Urine catecholamine levels were within normal
limits. A CT scan of the abdomen demonstrated a large
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heterogeneous mass arising from the upper pole of
the right kidney, measuring 16 cm X 15 cm X 13 cm
and containing a small focus of calcification. A 99mTcMDP skeletal scintigram showed multiple skeletal foci
of abnormally increased activity and uptake of radiopharmaceutical within the tumor. A CT scan of the
brain confirmed a left frontal skull metastasis with as-
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2247
FIGURE 2. Case 2. (A) Contrast-enhanced computed tomography (CT) scan
of the abdomen showed a large mass replacing most of the right kidney. The
unusual geometric areas of increased attenuation (also present on CT sections
obtained before contrast injection) indicate calcification. (B) Skeletal equilibrium phase of 99mTc-methylene diphosphonate scintigram (posterior view)
showing abnormal activity in the tumor (arrow) arising from the superior pole
of the right kidney.
sociated epidural soft tissue mass, without evidence
of parenchymal involvement. A bone marrow aspirate
showed a bone marrow replaced by a metastatic small
round cell tumor with extensive cohesive nests of tumor cells. A core needle biopsy showed sheets of small
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hyperchromatic cells with indistinct cell margins and
pale, fibrillar, amphophilic cytoplasm. Some areas
showed Homer Wright rosettes. Immunohistochemistries were positive for CD99 (cytoplasmic surface
membrane), NSE, vimentin, and synaptophysin, and
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CANCER June 1, 1997 / Volume 79 / Number 11
negative for S-100, chromogranin, keratin, actin, desmin, and neurofilament. Although these findings were
consistent with a diagnosis of PNET, the polymerase
chain reaction did not show the presence of either
the EWS/FLI-1 or the EWS/ERG chimeric transcripts.
Electron microscopy was thus performed, and showed
neurosecretory granules and microtubules. At last follow-up, the patient was undergoing treatment with
intensified chemotherapy with vincristine, ifosfamide,
cylophosphamide, doxorubicin, and etoposide, and
was scheduled to receive consolidation treatment with
autologous bone marrow transplantation.
DISCUSSION
Renal PNET appears to be a unique clinical entity that
behaves more aggressively than PNET arising at other
sites. The current series suggests that patients with
renal PNET are usually children and adolescents who
commonly have metastatic disease at presentation
and a poor response to therapy. All patients in the
current series received multimodal treatment shown
to be effective for PNETs at other locations (radical
surgery, radiation therapy, and chemotherapy including alkylating agents).5 – 7 However, three patients died
of progressive disease within 1 year of diagnosis. A
similar outcome is reported for the previously described cases.8 – 11 In the brief NWTS report, only 3 of
17 patients with Stages II to IV disease survived, 2
of whom had Stage IV disease and were treated with
myeloablative chemoradiotherapy followed by autologous bone marrow rescue.11 The absence of clinical
response to an alkylator-based regimen in these patients may reflect a different biologic behavior with
inherent drug resistance.
The four cases of renal PNET in the current study
were confirmed by positive cytoplasmic surface membrane staining for CD99 and by the presence of the
t(11; 22)(q24; q12) translocation in one of the two cases
tested. In the patient in Case 4, although the histologic
features were clearly consistent with the diagnosis of
PNET, polymerase chain reaction did not reveal the
presence of either the EWS/FLI-1 or the EWS/ERG fusion transcripts. It is possible that this patient represents the 5% of patients with PNET in whom these
hybrid transcripts are not detected,3 and who have
other atypical cytogenetic abnormalities.13
The diagnosis of renal PNET must thus be considered in patients with renal neoplasms, particularly
those with advanced disease at presentation. It is especially important to distinguish PNET of the kidney
from Wilms’ tumor, because therapeutic approaches
and results of therapy are quite different in these two
entities. The findings of the current study revealed
imaging findings that may aid in the diagnosis. Although all renal neoplasms can metastasize to the
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lungs, there were several features in the patients in
the current study that were atypical for Wilms’ tumor,
such as the presence of calcifications in three of the
tumors, the tumor uptake of the bone-seeking radiopharmaceutical that was apparent in two cases (Fig.
2B), and the bone metastases suggested by the skeletal
scintigram in Cases 1 and 4.14 The presence of calcification and bone involvement were more consistent
with neuroblastoma or, in younger patients, clear cell
sarcoma of the kidney.
In one of the current study cases and in one reported case,9 a diagnosis of Wilms’ tumor of blastemic
type was made initially. The distinction between
Wilms’ tumor of blastemic type and PNET may be
difficult because Wilms’ tumor with blastemic elements may occasionally test positive for CD99,15 and
renal tubules may also test positive.16 The diagnosis
of renal PNET must be especially considered in cases
of adult Wilms’ tumor because the latter is most common in young adults, an age group in whom PNET is
also common, and these patients appear to have more
advanced disease at diagnosis.17,18
Several reports have documented the occurrence
of renal neuroblastoma, which also appears to be characterized by extensive disease and unusually aggressive behavior.19 – 24 Interestingly, PNET may be histologically indistinguishable from classic neuroblastoma, and also has been termed peripheral
neuroblastoma.25 Neuroblastoma-like features may
occur in PNETs26 and some patients may present with
a moderate increase in catecholamine excretion, serum ferritin, and plasma NSE.5 However, current immunohistochemistries, including CD99, can usually
confirm the diagnosis of PNET.27 Because CD99 has
only been available in recent years, it is possible that
some of the previously reported cases of adult intrarenal neuroblastoma may in fact be PNET of the kidney.
These cases presented in young adults, with normal
or only mildly elevated urinary catecholamine levels
and very aggressive disease behavior.22 – 24 The behavior of renal PNET will be better defined as more cases
are unequivocally identified via selective immunohistochemical staining of the cytoplasmic surface membrane with CD99 and/or the presence of the defining
cytogenetic abnormalities.
In one of the patients in the current study, a diagnosis of MRT was initially considered. The histologic
distinction between PNET and MRT can sometimes
be difficult, due to the high phenotypic diversity of
the latter,28 and the presence of different cytogenetic
abnormalities may be the only definitive factor.29 – 31
Weeks et al., in a histopathologic review of 56 renal
neoplasms mimicking MRT, reported 8 cases that appeared to be PNET of the kidney and all had prominent
filamentous cytoplasmic inclusions, the hallmark of
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MRT.32 These inclusions have been described in several tumors of neuroectodermal origin. In a review of
42 cases diagnosed as extrarenal MRT, Parham et al.
found 4 tumors of neuroectodermal origin.33 Interestingly, the clinical course of PNET of the kidney is similar to that of MRT, characterized by a poor response
to therapy and a mortality rate of 80%. However, MRT
usually occurs during the first 2 years of life.28 There
also is some suggestion that MRT may be of neuroectodermal origin,29,30 and it has been associated with
brain tumors of neuroectodermal origin.28,34 This hypothesis is reinforced by the presence of a 22q11.2
breakpoint in close proximity to the EWS and NF2
genes.31 Therefore, it is possible that the two tumors
share the same primitive cell of origin, which may
explain the similar clinical behavior. Further molecular study of these two tumors is essential to elucidate
their relationship.
The authors believe that PNET of the kidney constitutes a clinical entity different from typical PNET.
It is characterized by very aggressive clinical behavior,
which in some ways is similar to MRT. PNET must be
included in the differential diagnosis of renal neoplasms and must be differentiated from intrarenal
neuroblastoma, MRT, and Wilms’ tumor. Cytogenetic
studies and immunohistochemistry for CD99 should
be performed in any patient in whom PNET is considered.
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