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PubMed1998

Intraabdominal desmoplastic small round cell tumor with EWS/ERG fusion transcript.

This report describes an intraabdominal small cell tumor in a 37-year-old woman, with clinical, topographic, and morphologic features highly suggestive of the desmoplastic small round cell tumor. Immunohistochemical analysis revealed a polyphenotypic profile consistent with this tumor--positivity for keratin, epithelial membrane antigen, neuron-specific enolase, vimentin, and desmin--but, in addition, a strong membranous immunoreactivity for CD99 (MIC2 protein). Reverse transcription polymerase chain reaction revealed a EWS/ERG fusion transcript characteristic of the Ewing's sarcoma/peripheral primitive neuroectodermal tumor group of tumors, rather than the EWS/WT1 chimeric transcript typical of the desmoplastic small round cell tumor. This is the third report of a hybrid tumor with features of the desmoplastic small round cell tumor and Ewing's sarcoma/peripheral primitive neuroectodermal tumor, and the first one with the EWS/ERG fusion gene. Our case shows the existence of some overlap between these two groups of tumors, which are considered to be histogenetically different, and the need for further studies of molecular characterization of small cell tumors, especially in those with atypical morphologic or immunohistochemical features.

Abdominal Neoplasms↗
PubMed2006

Temozolomide in resistant or relapsed pediatric solid tumors.

PURPOSE: We report the off-label study aimed at investigating the use of temozolomide (TMZ) as single agent in relapsed or resistant pediatric solid tumors. The drug was administered at the dose of 215 mg/m2/day x 5 days or 180 mg/m2/day x 5 days in patients with prior craniospinal irradiation (CSI) or autologous bone marrow transplantation (ABMT). PATIENTS AND METHODS: Fifty two patients, median age 127.6 months, with resistant or relapsed solid tumors were enrolled. Tumor types were: neuroblastoma (NB; n = 17), medulloblastoma (MB; 8), brain stem glioma (BSG; 8), extraosseous Ewing's sarcoma/peripheral neuroectodermal tumor (EOES; 4), Ewing's sarcoma (ES; 4), anaplastic astrocytoma (AA; 3), rhabdomyosarcoma (RMS; 2), ependymoma (EP; 2), cerebral primitive neuroectodermal tumor (cPNET; 2), hepatocarcinoma (HC; 1), and osteosarcoma (OS; 1). All patients were pre-treated. Two outpatient courses were administered, with a median of 4.8 courses/pt. RESULTS: Objective response-rate (CR + PR + MR) in our series was 13.4% (1.9% CR, 3.8% PR, and 7.7% MR), SD occurred in 38.4% of patients and 48% had PD. The median survival was 7.8 months (range 1-37) and median time to progression was 3.4 months (range 1-20); these data were significantly correlated with histology and previous nitrosureas administration in multivariate analysis. Haematological toxicity grade 3-4 (mainly thrombocytopenia) was observed in 21.4% of administered courses, nausea was reported in 3.1% and respiratory distress in 0.7%. CONCLUSION: Oral TMZ was well tolerated in children with resistant or relapsed solid tumors and showed activity in NB and CNS tumours refractory to standard chemotherapy.

Adolescent↗
PubMed2004

Novel PMS2 pseudogenes can conceal recessive mutations causing a distinctive childhood cancer syndrome.

We investigated a family with an autosomal recessive syndrome of cafe-au-lait patches and childhood malignancy, notably supratentorial primitive neuroectodermal tumor. There was no cancer predisposition in heterozygotes; nor was there bowel cancer in any individual. However, autozygosity mapping indicated linkage to a region of 7p22 surrounding the PMS2 mismatch-repair gene. Sequencing of genomic PCR products initially failed to identify a PMS2 mutation. Genome searches then revealed a previously unrecognized PMS2 pseudogene, corresponding to exons 9-15, within a 100-kb inverted duplication situated 600 kb centromeric from PMS2 itself. This information allowed a redesigned sequence analysis, identifying a homozygous mutation (R802X) in PMS2 exon 14. Furthermore, in the family with Turcot syndrome, in which the first inherited PMS2 mutation (R134X) was described, a further truncating mutation was identified on the other allele, in exon 13. Further whole-genome analysis shows that the complexity of PMS2 pseudogenes is greater than appreciated and may have hindered previous mutation studies. Several previously reported PMS2 polymorphisms are, in fact, pseudogene sequence variants. Although PMS2 mutations may be rare in colorectal cancer, they appear, for the most part, to behave as recessive traits. For technical reasons, their involvement in childhood cancer, particularly in primitive neuroectodermal tumor, may have been underestimated.

Adenosine Triphosphatases↗
PubMed1993

A saturation threshold for taxol cytotoxicity in human glial and neuroblastoma cells.

The cytotoxic effects of taxol at concentrations of 0.001-1.0 microgram/ml were determined in two human glioblastoma multiforme, two neuroblastoma and two primitive neuroectodermal tumor cell lines. The neuroectodermal cell lines were established from previously treated patients, while the glioblastomas were from untreated patients. At exposure durations of 1, 4 and 24 h there was an inverse taxol concentration-survival relationship for all six cell lines as measured by the MTT method. Significant differences in sensitivity to taxol among these cell lines were observed; the most resistant cell line SK-N-FI is characterized by very high levels of MDR1 expression and the most sensitive SK-N-AS by very low levels. An additional level of complexity concerns a saturation threshold for taxol-induced cytotoxic effects which when reached precludes additional effects of prolonged or additional exposure. Tumors of the brain and peripheral nervous system appear to be sensitive to taxol. However, dosage necessary to maximize cytocidal effects in tumors requires knowledge of at least the range of each tumors constitutive sensitivity to taxol and a way to optimize drug delivery.

Brain Neoplasms↗
PubMed1997

Expression of c-met proto-oncogene product (c-MET) in benign and malignant bone tumors.

The expression of c-met proto-oncogene product (c-MET) has been reported to be related to invasive growth or tumor stage in some tumors, but little is known concerning the significance of c-MET expression in bone tumors. With use of formalin-fixed, paraffin-embedded tissue specimens and polyclonal antibody for c-MET, we studied the expression of c-MET in 122 cases of malignant bone tumors (43 osteosarcomas, 24 chondrosarcomas, 21 malignant fibrous histiocytomas of bone, 16 Ewing's sarcoma versus primitive neuroectodermal tumors, 18 chordomas), 65 cases of benign tumors and tumor-like lesions (including 8 giant cell tumors of bone, 8 chondroblastomas, 12 enchondromas, 7 osteochondromas, 10 fibrous dysplasias), 7 cases of articular cartilaginous tissue, and 10 cases of fetal vertebral tissue consisting of foci of enchondral ossification and notochordal tissue. In malignant tumors, c-MET expression was most frequently detected in chordoma (94.4%), followed by chondrosarcoma (54.2%) and osteosarcoma (23.3%). Among the osteosarcoma specimens, c-MET expression was frequently detected in the chondroblastic subtype (66.7%), but the incidence was low in the cases with other subtypes of osteosarcoma. We found no significant correlation between the c-MET expression and the histologic grade of malignancy in either osteosarcoma or chondrosarcoma. c-MET expression was either rarely observed or completely negative in malignant fibrous histiocytomas of bone (4.8%) and primitive neuroectodermal tumors (0%). In benign tumors and tumor-like lesions, c-MET expression was frequently detected in cartilaginous tumors, such as chondroblastoma (62.5%), enchondroma (66.7%), and osteochondroma (71.4%), but no expression was observed in giant cell tumors of bone or any other benign tumors or tumor-like lesions. In normal tissue, c-MET expression was frequently detected in the articular cartilage (100%) and notochord (70.0%) specimens examined. We conclude that c-MET expression as frequent as that observed in the notochordal tissue, chordomas, articular cartilage, and cartilaginous tumors is related to the development of both normal tissue and chondroid tumors.

Adolescent↗
PubMed2003

Epithelial differentiation in medulloblastoma: comparison with other embryonal tumors of neuroectodermal origin.

Three cases of medulloblastoma characterized by epithelial differentiation are described in patients 6-months-, 1-month- and 8-years-old. Histologically, tumors from the two infant patients showed a perivascular arrangement without apparent radiated cytoplasmic processes from the vessels. Tumor cells displayed round and/or pleomorphic vesicular nuclei and a more abundant eosinophilic cytoplasm than that found in classic medulloblastoma. Neither Homer-Wright rosettes nor ependymal or ependymoblastic rosettes were noted in these tumors. The tumor in the 8-year-old patient exhibited a classic medulloblastoma component intermingled with abundant eosinophilic cytoplasm forming a tubular structure. Immunohistochemically, tumor cells in all cases were positive for cytokeratin, synaptophysin, and vimentin. In the third case involving the 8-year-old patient, epithelial tumor cells were positive for cytokeratin, whereas classic medulloblastoma components were negative for cytokeratin. Positive staining for melanoma-specific antigen was seen only in the third case, where strong reactivity of tumor cells formed a tubulus. However, the classic medulloblastoma component was negative for melanoma-specific antigen. Ultrastructurally, basal laminae were observed around tumor cells in the 6-month-old patient. These morphological and immunohistochemical features suggest that medulloblastoma with epithelial differentiation is a rare but distinct variant of medulloblastoma, and that some of these tumors should show differentiation in ocular pigment epithelium.

Antigens, Neoplasm↗
PubMed2000

Ewing sarcoma of the rib: results of an intergroup study with analysis of outcome by timing of resection.

OBJECTIVE: We sought to establish the outcome and optimal therapeutic sequence for patients with nonmetastatic Ewing sarcoma/primitive neuroectodermal tumor of the chest wall. METHODS: Patients 30 years of age or younger with nonmetastatic Ewing sarcoma/primitive neuroectodermal tumor of the bone were randomly assigned to receive vincristine, doxorubicin, cyclophosphamide, and dactinomycin or those drugs alternating with ifosfamide and etoposide. Local control was obtained with an operation, radiotherapy, or both. RESULTS: Fifty-three (13.4%) of 393 patients had primary tumors of the chest wall (all rib). Event-free survival at 5 years was 57% for the chest wall compared with 61% for other sites (P >.2). Ifosfamide and etoposide improved outcome in the overall group (5-year event-free survival, 68% vs 54%; P =.002), and a similar trend occurred in chest wall lesions (5-year event-free survival, 64% vs 51%). Patients with chest wall lesions had more attempts at initial surgical resection (30%) than those with other primary tumor sites (8%, P <.01). The attempt at initial resection for chest wall lesions did not correlate with size. Initial resections at other sites were restricted to smaller tumors. Initial resection resulted in negative pathologic margins in 6 of 16 patients, whereas the delayed resection resulted in negative margins in 17 of 24 patients (P =.05). Although there was no difference in survival by timing of the operation in rib lesions, a higher percentage of patients with initial surgical resection received radiation than those with resection after initial chemotherapy (P =. 13). CONCLUSIONS: Although rib primary tumors are significantly larger than tumors found in other sites, their outcome is similar. We favor delayed resection whenever possible to minimize the number of patients requiring radiation therapy.

Adolescent↗
PubMed2000

Ganglioside patterns in neuroepithelial tumors of childhood.

To elucidate a relationship between neuronal anaplasia, tumor proliferation, and ganglioside contents, we quantified gangliosides by HPTLC in tumors of neuroepithelial tissues at different grade, i. e. peripheral primitive neuroectodermal tumor (PPNET, grade IV), ependymoma (EPEN, grade III), neuroblastoma (NB, grade IV), and dysembryoplastic neuroepithelial tumor (DNT, grade I). PPNET, the most undifferentiated tumor examined had lowest concentration of total lipid-bound sialic acid. GM3 was the major ganglioside in all undifferentiated tumors (46-72.7% of total lipid-bound sialic acid). GD3 was an another component in PPNET and EPEN (7.2-17.3%). Concentration of a complex gangliosides GM1 was decreased in all tumor tissues and those of GT1a, GD1b and GT1b were decreased in tumors of high grade. The results suggest that the composition of gangliosides could be of considerable value in refining the classification of neuroepithelial tumors in infancy and childhood.

Adolescent↗
PubMed2003

Immunophenotype of desmoplastic small round cell tumors as detected in cases with EWS-WT1 gene fusion product.

Desmoplastic small round cell tumor is a rare tumor typically involving peritoneum. Although the histogenesis of desmoplastic small round cell tumor has yet to be elucidated, immunophenotypical and morphological analysis shows a characteristic divergent phenotype overlapping with other round cell tumors such as Ewing's sarcoma/primitive neuroectodermal tumor, rhabdomyosarcoma, small cell mesothelioma, and carcinoma. Detection of the EWS-WT1 gene fusion is characteristic of desmoplastic small round cell tumor and has been used reliably in tumor diagnosis. In this study, we evaluated the immunophenotype of 23 desmoplastic small round cell tumor cases with the EWS-WT1 gene fusion product identified by reverse transcription-polymerase chain reaction. Paraffin sections were stained with antibodies against calretinin, WT1 (C19), desmin, myoglobin, MyoD, Myf5, myogenin, placental alkaline phosphatase, cytokeratins, MIC2, HER2/neu and c-kit using standard immunohistochemical methods. Immunoreactivity was evaluated semiquantitively by light microscopy. Desmoplastic small round cell tumors showed reactivity with calretinin in 4/21, desmin in 21/23, myoglobin in 5/17, placental alkaline phosphatase in 17/21, HER2/neu in 7/18 (3+ in 1 and 1+ in 6), c-kit in 2/14, MIC2 in 13/23, WT1 in 16/23, CAM5.2 in 21/23, and AE1/3 in 16/23 cases. The most sensitive myogenic and epithelial markers are desmin and CAM 5.2. Although nuclear reactivity of the early myogenic regulatory factors (MyoD, myogenin, Myf5) was not detected, myoglobin immunoreactivity was present in 29% of desmoplastic small round cell tumors. HER2/neu overexpression (3+) and c-kit expression are uncommon in desmoplastic small round cell tumors. A panel of myogenic and epithelial markers should be used to detect the divergent phenotype in desmoplastic small round cell tumors, a key feature in the differential diagnosis. Detection of EWS-WT1 fusion becomes critical for the diagnosis when the characteristic divergent phenotype cannot be detected immunohistochemically.

Antigens, Neoplasm↗
PubMed1992

Midline brain tumors in MSV-SV 40-transgenic mice originate from the pineal organ.

Adult transgenic mice expressing the large T-antigen of the Simian virus 40 (SV 40) under the control of the Moloney murine sarcoma virus (MSV) enhancer and the SV 40 promoter develop inheritable uniform midline brain neoplasms showing features of primitive neuroectodermal tumors. The origin and histogenesis of these tumors were investigated in the present study. The brain and pineal organ of fetal and young transgenic mice less than 3 months old displayed normal macroscopic and microscopic features. In 3.5-month-old animals, the pineal organ was considerably enlarged due to hyperplasia, finally leading to tumor formation. Immunocytochemical demonstration of large T-antigen showed that this oncoprotein was already expressed in the nuclei of certain cells in the pineal organ of fetuses (16 and 18 days old) and newborn animals, but was absent from all other parts of the brain. The immunocytochemical demonstration of S-antigen (arrestin), a highly characteristic marker for pinealocytes, was used for further characterization of the large T-antigen-immunoreactive cells. The fetal pineal organ did not contain immunoreactive S-antigen. This first occurred in certain pinealocytes of newborn mice. Double immunostaining revealed that in newborn and older transgenic mice the immunoreactive large T-antigen was exclusively found in nuclei of cells containing S-antigen immunoreaction in their cytoplasm. Thus, transformed pinealocytes appear as stem cells of the experimental tumors. The results of this study suggest that primitive neuroectodermal tumors and the normal tissue from which they originate share certain molecular and immunocytochemical features.

Animals↗
PubMed1992

The gene for leukocyte antigen-related tyrosine phosphatase (LAR) is localized to human chromosome 1p32, a region frequently deleted in tumors of neuroectodermal origin.

In situ hybridization was employed to localize a cDNA probe from the human protein tyrosine phosphatase gene LAR to human metaphase chromosomes. LAR, a putative tumor suppressor gene, has been localized to 1p32, a chromosomal region that is frequently found deleted in human neuroblastoma and pheochromocytoma.

Adrenal Gland Neoplasms↗
PubMed1997

Molecular detection of GAGE expression in peripheral blood and bone marrow: utility as a tumor marker for neuroblastoma.

The GAGE family of tumor-associated antigens is present in a wide spectrum of human tumors but is highly restricted among normal tissues except to the testis. By reverse transcription-PCR, GAGE expression was detected in 55 of 67 neuroblastomas (NBs; 8 of 12 stage 1, 13 of 13 stage 2, 9 of 12 stage 3, 7 of 12 stage 4S, and 18 of 18 stage 4), 5 of 5 Ewing's and peripheral neuroectodermal tumors, and 11 of 11 tumor cell lines (9 NBs, 1 peripheral neuroectodermal tumor, and 1 melanoma). In contrast, 5 of 6 normal tissues (normal testis was positive), 18 of 18 NB-negative bone marrow (BM; 9 normal, 6 non-NB remission, and 3 stage-2 NB), and 9 of 10 NB-negative peripheral blood (PB; 9 normal and 1 stage 2B) were undetectable. In 18 patients with widespread NB under treatment, GAGE expression in paired samples of BM and PB was 89% concordant. Both correlated strongly with disease measured by conventional methods, including marrow histology or immunocytology, bone scan, meta-iodo-benzylguanidine scan, computed tomography/magnetic resonance imaging, and urine vanilly-mandelic acid/homovanillic acid. When serial samples from 14 patients with stage 4 NB were studied, BM from 7 of 7 patients at diagnosis and 14 of 14 patients (25 samples) on treatment were positive for GAGE. Thirteen patients were in continual remission off therapy, and their GAGE expression (12 BM and 9 PB) was undetectable at follow-up. When compared to molecular detection of tyrosine hydroxylase mRNA, GAGE may offer added sensitivity in detecting NB in both BM and PB. The GAGE family of antigens may be potential tumor markers of minimal residual disease.

Antigens, Neoplasm↗
PubMed1998

Askin tumors in children: a report of four cases.

Primary malignant tumors of the chest are rare in the pediatric age group. Askin tumor belongs to the peripheral primitive neuroectodermal tumor family, and typically involves the periosteum, soft tissue and extrapulmonary tissue of the thoracic wall. We report our ten years experience with four cases of this rare tumor.

Child↗
PubMed2000

CD31 immunoreactivity in small round cell tumors.

CD31 has been shown to be a sensitive and specific marker for endothelial differentiation among epithelioid and spindled-pleomorphic human neoplasms. However, the role of this marker in the evaluation of small round cell tumors has not been evaluated. Formalin-fixed, paraffin-embedded tissue sections from 276 small round cell tumors, including 85 Ewing's sarcoma/primitive neuroectodermal tumors (ES/PNET), 52 rhabdomyosarcomas, 10 extraabdominal polyphenotypic small cell tumors, six desmoplastic small cell tumors, 11 neuroblastomas, 23 Wilms' tumors, 20 retinoblastomas, 13 esthesioneuroblastomas, and 56 small cell malignant lymphomas were stained with CD31 (JC/70A, 1:40), using a modified avidinbiotin-peroxidase complex technique, after citrate buffer microwave epitope retrieval. Among nonlymphoid small round cell tumors, four of 85 ES/PNET were at least focally reactive. No other lesion in this group was positive. In contrast, the majority of well-differentiated (11 of 17), intermediately differentiated (two of three), and lymphoblastic lymphomas (three of three) were positive. Small cleaved lymphomas (three of 13 follicular, one of 13 diffuse) were less often reactive, whereas small noncleaved lesions were negative. Although reactivity for CD31 in ES/PNET is uncommon, the presence of platelet/endothelial cell adhesion molecule in a small cell neoplasm should not in isolation be taken as evidence of hematopoietic origin. These results further define the utility of CD31 in the evaluation of human neoplasms.

Biomarkers, Tumor↗
PubMed1993

Cytogenetic analysis of 109 pediatric central nervous system tumors.

Reports of cytogenetic abnormalities in pediatric central nervous system (CNS) tumors are important for collection and comparison of large numbers of karyotypes of primary CNS neoplasms to produce statistically significant correlations. We report cytogenetic results of 119 samples of pediatric CNS tumors from 109 patients. Tumors included 33 low-grade astrocytomas, 18 high-grade astrocytomas, 14 gangliogliomas, 13 ependymomas, 17 primitive neuroectodermal tumors (PNET), three choroid plexus papillomas and carcinomas, and a miscellaneous group of 20 rare primary CNS tumors and metastases. In each group, cytogenetic results were correlated with histologic subtype and survival. The study indicated specific chromosome abnormalities in different groups of tumors. Low-grade astrocytomas showed mostly numeric abnormalities with gains of chromosome 7, high-grade astrocytomas showed differences from karyotypic changes observed in adults in lacking double minutes (dmin) and monosomy 10. The ependymoma group showed the largest proportion of abnormal karyotypes with frequent involvement of chromosome 6 and 16. Chromosome 6 was the single most common abnormal chromosome in this study, closely followed by chromosomes 1 and 11. Pediatric CNS neoplasms differ from adult tumors cytogenetically as well as histologically and biologically.

Adolescent↗
PubMedDate not supplied

Small round blue cell tumor of seminal vesicle in a young patient.

Seminal vesicle tumor is a rare disease with unclear origin. Generally, it is presented as a pelvic mass that can be detected by sonography and digital rectal exam. The authors report a 25-year-old patient with a pelvic mass which the magnetic resonance and surgical specimen reveal a seminal vesicle tumor. Immunohistochemical findings favored a primitive neuroectodermal tumor of the seminal vesicle. Herein, the treatment, histological and histochemical findings of this entity are discussed.

Adult↗
PubMed2005

Increased p53 immunopositivity in anaplastic medulloblastoma and supratentorial PNET is not caused by JC virus.

BACKGROUND: p53 mutations are relatively uncommon in medulloblastoma, but abnormalities in this cell cycle pathway have been associated with anaplasia and worse clinical outcomes. We correlated p53 protein expression with pathological subtype and clinical outcome in 75 embryonal brain tumors. The presence of JC virus, which results in p53 protein accumulation, was also examined. METHODS: p53 protein levels were evaluated semi-quantitatively in 64 medulloblastomas, 3 atypical teratoid rhabdoid tumors (ATRT), and 8 supratentorial primitive neuroectodermal tumors (sPNET) using immunohistochemistry. JC viral sequences were analyzed in DNA extracted from 33 frozen medulloblastoma and PNET samples using quantitative polymerase chain reaction. RESULTS: p53 expression was detected in 18% of non-anaplastic medulloblastomas, 45% of anaplastic medulloblastomas, 67% of ATRT, and 88% of sPNET. The increased p53 immunoreactivity in anaplastic medulloblastoma, ATRT, and sPNET was statistically significant. Log rank analysis of clinical outcome revealed significantly shorter survival in patients with p53 immunopositive embryonal tumors. No JC virus was identified in the embryonal brain tumor samples, while an endogenous human retrovirus (ERV-3) was readily detected. CONCLUSION: Immunoreactivity for p53 protein is more common in anaplastic medulloblastomas, ATRT and sPNET than in non-anaplastic tumors, and is associated with worse clinical outcomes. However, JC virus infection is not responsible for increased levels of p53 protein.

Adolescent↗
PubMed1996

Infrequent alterations of the p15, p16, CDK4 and cyclin D1 genes in non-astrocytic human brain tumors.

While several genetic alterations associated with the evolution of the astrocytomas have been identified, the molecular basis of non-astrocytic brain tumors has remained largely unknown. In this study, p15, p16, CDK4 and cyclin D1 genes were analyzed in 69 nonastrocytic human brain tumors, including 17 oligodendrogliomas, 16 medulloblastomas/primitive neuroectodermal tumors (PNETs), 14 ependymomas and 22 meningiomas. Southern blot analysis of DNA from frozen samples showed no homozygous deletions in p15 or p16 genes in any of these tumors. No mobility shift was found by PCR-single-strand conformation polymorphism (PCR-SSCP) analysis in exons 1 and 2 of the p15 gene and exons 1 and 2 of the p16 genes, except for one oligodendroglioma. Direct sequencing of DNA from this tumor showed a G --> A transition at nucleotide 436 (codon 140) in exon 2 of the p16 gene, which is a common polymorphism. Southern blot analyses revealed no amplification of CDK4 and cyclin D1 genes in any of the neoplasms analyzed. In contrast to astrocytic brain tumors, which show frequent loss of the p16 gene and amplification of the CDK4 gene, alteration of these genes appears to be rare in other neoplasms of the human nervous system.

Astrocytoma↗