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At least 19 recordsLinked to original sources
PubMed1996

Neuroectodermal cyst may be a rare differential diagnosis of fetal sacrococcygeal teratoma: first case report of a prenatally observed neuroectodermal cyst.

In spite of the fact that most anomalies can be accurately diagnosed prenatally, one may be confronted with an extremely rare fetal abnormality that has never been described before. We report a case of a neuroectodermal cyst arising from the posterior neuropore. After 21 weeks of gestation a fetal anechoic intra- and extra-abdominal tumor was detected. The mass grew to 75 x 41 x 33 mm at 35 weeks. Initially it was believed to be a sacrococcygeal teratoma. Serial scans and Doppler ultrasound examinations were performed, which demonstrated fetal well-being. Color Doppler imaging failed to demonstrate increased tumoral perfusion. After elective Cesarean section, the tumor was excised. The postoperative course was complicated by recurrent infections of the urinary tract due to neurological damage to the bladder. There was also impaired function of the anal sphincter. The histological finding of a monolayer of neuroepithelial cells and melanocytes led to the diagnosis of a neuroectodermal cyst.

Adult↗
PubMedDate not supplied

Primary cerebral neuroectodermal tumors: neuroblastoma, differentiated neuroblastoma, and composite neuroectodermal tumor.

Seven cases of primary cerebral neuroectodermal tumors with predominant neuroblastic features were studied ultrastructurally and five were evaluated immunohistochemically. The fine structural features were indicative of neuroblastic differentiation by the presence of elongated cytoplasmic processes, electron-dense neurosecretory granules, and neurotubules. Five of the seven cases had the morphologic findings of classic cerebral neuroblastoma, and the sixth case, originally diagnosed as an oligodendroglioma, had the features of a differentiated neuroblastoma. Desmoplastic and/or stromal foci were intermingled with neuronal-ganglionic cells and neuroblasts in the seventh case. In addition to strong immunoreactivity for S-100 protein and glial fibrillary acidic protein in the desmoplastic areas, the spindle cells had fibroblastic and Schwannian features by electron microscopy in the latter case. The neuroblastic cells and fibrillary network were immunoreactive for neuron-specific enolase and neurofilament in the five study cases. It is concluded that cerebral neuroectodermal tumors may express an range of phenotypic features from the exclusive neuroblastic stage to a neuronal and stromogenic phase analogous to the classic neuroblastoma of the sympathetic nervous system.

Adult↗
PubMed1997

Ewing's sarcoma and primitive neuroectodermal tumor in adults: are they different from Ewing's sarcoma and primitive neuroectodermal tumor in children?

PURPOSE: To determine whether age at diagnosis influences the behavior of Ewing's sarcoma and primitive neuroectodermal tumor (PNET). PATIENTS AND METHODS: We reviewed the clinical features, treatment, and outcome of 59 consecutive patients with Ewing's sarcoma and PNET treated on the Adult Sarcoma Unit at our institution from 1980 to 1995. RESULTS: The 37 male and 22 female patients had a median age of 24 years. Lower limb was the most common primary tumor site. Fifteen patients had nonmetastatic tumor less than 100-mL volume, 27 had nonmetastatic disease greater than 100-mL volume, and 17 had evidence of metastatic disease at presentation. The origin of the primary tumor was soft tissue in 28 cases, bone in 30, and uncertain in one. The Kaplan-Meier estimate of 5-year overall survival (OS) in all patients was 38% and of progression-free survival (PFS), 27%. When patients with metastatic disease at presentation were excluded, these figures increased to 52% and 34%, respectively. Bulk of disease at presentation and response to primary treatment were statistically highly significant predictors of both PFS and OS. Age and tissue of origin of the tumor did not influence outcome. CONCLUSION: The behavior of Ewing's sarcoma and PNET in adults is no different from its behavior in children. We feel the way forward in the treatment of adults with Ewing's sarcoma and PNET is for them to be included in the current multicenter trials of multidisciplinary treatment directed at children.

Adolescent↗
PubMed1991

MIC2 is a specific marker for Ewing's sarcoma and peripheral primitive neuroectodermal tumors. Evidence for a common histogenesis of Ewing's sarcoma and peripheral primitive neuroectodermal tumors from MIC2 expression and specific chromosome aberration.

This study reports on the specific expression of the MIC2 gene, a pseudoautosomal gene located on the short arms of the X and Y chromosomes, on Ewing's sarcoma (ES) and peripheral primitive neuroectodermal tumor (pPNET) cells. The gene product, a cell membrane protein, is recognized by the newly established monoclonal antibody (MoAb) HBA-71 and the previously described MoAb 12E7 and RFB-1. Furthermore, the reaction pattern of the MIC2 antibodies, especially HBA-71, with normal tissues and a great number of benign and malignant tumors (70 different tumors, 199 tumor samples), as well as the correlation between the specific chromosomal aberrations, i.e., the t(11;22) and the del(22) and the expression of this antigen, are demonstrated. Both ES and pPNET cells express the MIC2 gene in very high amounts, which represents a highly selective and almost unique feature of these cells, making an assignment of these tumors in one entity even more likely. The MIC2 antibodies are of great value for clinical and research purposes.

12E7 Antigen↗
PubMed1989

Molecular markers of primitive neuroectodermal tumors and other pediatric central nervous system tumors. Monoclonal antibodies to neuronal and glial antigens distinguish subsets of primitive neuroectodermal tumors.

Seventy-one tumors of the central nervous system in children were studied immunohistologically. Thirty-seven were classified histologically as PNETs, of which 35 were located in the cerebellum (medulloblastomas), one in the cerebrum, and one in the spinal cord. The 34 non-PNETs included five ependymomas, seven gangliogliomas, 15 astrocytomas, and seven tumors of other histology. We used monoclonal antibodies specific for neurofilament (NF) triplet proteins, for microtubule associated protein 2 and tau protein and for glial fibrillary acidic protein (GFAP) and myelin basic protein. In addition, a monoclonal antibody to epithelial membrane antigen was applied. The presence or absence of these antigens defined four major groups of PNETs: 1) PNETs not otherwise specified (10 cases), 2) PNETs with neuronal differentiation (eight cases), 3) PNETs with astrocytic differentiation (six cases), and 4) PNETs with both neuronal and astrocytic differentiation (12 cases). One case showed ependymal differentiation. The pattern of expression of NF isoforms in PNETs was reminiscent of that seen during normal mammalian development, such that phosphorylated NF-H was only present in combination with NF-M and NF-L. Among the other central nervous system tumors, all astrocytomas and gangliogliomas were positive for GFAP, and the gangliogliomas also expressed all NF isoforms. Three atypical teratoid tumors and two rhabdoid tumors showed strong positivity for epithelial membrane antigen and also for GFAP. We conclude that the differentiation antigens described here serve to distinguish PNETs from other pediatric central nervous system tumors and to identify subsets of PNETs. Accordingly, PNETs represent a heterogeneous group of pediatric brain tumors capable of neuronal and glial differentiation.

Adolescent↗
PubMed1995

Peripheral primitive neuroectodermal tumors of the head and neck.

OBJECTIVE: Primitive neuroectodermal tumor is a malignant small round cell tumor of neuroectodermal origin. The occurrence of these tumors in the head and neck is rare. Our objective is to document the frequency of presentation, methods of diagnosis, and forms of treatment used to combat primitive neuroectodermal tumors in the head and neck. DESIGN: Retrospective chart review. RESULTS: The most common location for primitive neuroectodermal tumors in our series was the thoracopulmonary region (46%); the next most common location was the head and neck (42%). Metastatic disease was present in 31% of patients at the time of diagnosis. Cytogenic analysis was found to be helpful in confirming the diagnosis of primitive neuroectodermal tumor. Therapy for primitive neuroectodermal tumors included surgery, chemotherapy, and radiation therapy. Survival statistics were poor, with 65% of the patients alive at 2 years' follow-up. CONCLUSIONS: Primitive neuroectodermal tumor is an aggressive malignant small round cell tumor that may present in the head and neck. Long-term survival for patients with primitive neuroectodermal tumor is still poor; however, the use of improved chemotherapeutic agents combined with aggressive surgical control of primary disease and, in some cases, radiation therapy should lead to improved long-term survival.

Adolescent↗
PubMed1994

Comparison of Ewing's sarcoma of bone and peripheral neuroepithelioma. An immunocytochemical and ultrastructural analysis of two primitive neuroectodermal neoplasms.

Ewing's sarcoma of bone (ESB) and peripheral neuroepithelioma (PN) are frequently considered to be different tumors. Some researchers have suggested that PN is morphologically a neuroectodermal Ewing's sarcoma. We sought to determine the extent of neuroectodermal features in conventional ESB on direct patient material (25 cases) and to compare these tumors with a similar group of readily diagnosed PNs (10 cases). Light microscopic, ultrastructural, and immunophenotypic parameters were assessed and compared for both groups. The avidin-biotin complex method was used. All tumors were antigenically intact since all stained for vimentin or at least one marker. Neuroectodermal antigens (neuron-specific enolase, Leu-7 [HNK-1], neurofilament 200 kd, and S100) were found in nine of 10 cases of PN and in 17 of 25 cases of ESB. In ESB, an atypical light microscopic appearance correlated with the presence of neuroectodermal features in most cases, but neuroectodermal phenotype was more frequent (68%) than morphological evidence of neuroectodermal differentiation (36%). These data support the concept that ESB and PN are both peripheral primitive neuroectodermal neoplasms, differing only in extent of neuroectodermal phenotype and morphological differentiation.

Adolescent↗
PubMed2006

Sp5l is a mediator of Fgf signals in anteroposterior patterning of the neuroectoderm in zebrafish embryo.

The neuroectoderm is patterned along the anterior-posterior axis in vertebrate embryos. Fgf signals are required to induce the posterior neuroectodermal fates, but they repress the anterior fate. Sp5l/Spr2, an Sp1-like transcription factor family member, has been shown to be required for development of mesoderm and posterior neuroectoderm. We demonstrate here that repression of the anterior neuroectodermal markers fez and otx1 by fgf17b or fgf3 coincides with induction of sp5l in the anterior neuroectoderm, and that this repression is efficiently rescued by simultaneous sp5l knockdown. On the other hand, sp5l knockdown is able to inhibit inductive activity of ectopic Fgf signals on the expression of the posterior neuroectodermal markers gbx2, hoxb1b, and krox20. Furthermore, effect of overexpression of a dominant negative Fgf receptor on anteroposterior patterning of the neuroectoderm is rescued by sp5l overexpression. Taken together, these data suggest that sp5l mediates the functions of Fgf signals in anteroposterior patterning of the neuroectoderm during zebrafish embryogenesis.

Animals↗
PubMed2006

Comparative analysis of neuroectodermal differentiation capacity of human bone marrow stromal cells using various conversion protocols.

Human adult bone marrow-derived mesodermal stromal cells (hMSCs) are able to differentiate into multiple mesodermal tissues, including bone and cartilage. There is evidence that these cells are able to break germ layer commitment and differentiate into cells expressing neuroectodermal properties. There is still debate about whether this results from cell fusion, aberrant marker gene expression or real neuroectodermal differentiation. Here we extend our work on neuroectodermal conversion of adult hMSCs in vitro by evaluating various epigenetic conversion protocols using quantitative RT-PCR and immunocytochemistry. Undifferentiated hMSCs expressed high levels of fibronectin as well as several neuroectodermal genes commonly used to characterize neural cell types, such as nestin, beta-tubulin III, and GFAP, suggesting that hMSCs retain the ability to differentiate into neuroectodermal cell types. Protocols using a direct differentiation of hMSCs into a neural phenotype failed to induce significant changes in morphology and/or expression of markers of early and mature glial/neuronal cells types. In contrast, a multistep protocol with conversion of hMSCs into a neural stem cell-like population and subsequent terminal differentiation in mature glia and neurons generated relevant morphological changes as well as significant increase of expression levels of marker genes for early and late neural cell types, such as nestin, neurogenin2, MBP, and MAP2ab, accompanied by a loss of their mesenchymal properties. Our data provide an impetus for differentiating hMSCs in vitro into mature neuroectodermal cells. Neuroectodermally converted hMSCs may therefore ultimately help in treating acute and chronic neurodegenerative diseases. Analysis of marker gene expression for characterization of neural cells derived from MSCs has to take into account that several early and late neuroectodermal genes are already expressed in undifferentiated MSCs.

Adolescent↗
PubMed2005

CNS midline cells contribute to maintenance of the initial dorsoventral patterning of the Drosophila ventral neuroectoderm.

Dorsoventral patterning of the Drosophila ventral neuroectoderm is established by the expression of three evolutionarily conserved homeodomain genes: ventral nervous system defective (vnd), intermediate neuroblasts defective (ind), and muscle segment homeobox (msh) in the medial, intermediate, and lateral columns of the ventral neuroectoderm, respectively. It was not clear whether extrinsic factor(s) from the CNS midline cells influence the initial dorsoventral patterning by controlling the expression of the dorsoventral patterning genes. We show here that the CNS midline cells, specified by single-minded (sim), are essential for maintaining expression of the dorsoventral patterning genes. Ectopic expression of sim in the ventral neuroectoderm during the blastoderm stage repressed expression of the three homeodomain genes in the ventral neuroectoderm. This indicates that the identity of the CNS midline cells is established by a series of repressions of the three homeodomain genes in the ventral neuroectoderm. Ectopic expression of sim in the ventral neuroectoderm during initial neurogenesis induced ectopic ind expression in the medial column in addition to that in the intermediate column via EGFR signaling between the ventral neuroectoderm and midline cells. In contrast, it repressed the expression of vnd and msh in the medial and lateral columns, respectively. Our findings demonstrate that the CNS midline cells provide extrinsic positional information via EGFR signaling that maintains the initial subdivision of the ventral neuroectoderm into three dorsoventral columns during initial neurogenesis.

Animals↗
PubMed2001

Stage-specific inductive signals in the Drosophila neuroectoderm control the temporal sequence of neuroblast specification.

One of the initial steps of neurogenesis in the Drosophila embryo is the delamination of a stereotype set of neural progenitor cells (neuroblasts) from the neuroectoderm. The time window of neuroblast segregation has been divided into five successive waves (S1-S5) in which subsets of neuroblasts with specific identities are formed. To test when identity specification of the various neuroblasts takes place and whether extrinsic signals are involved, we have performed heterochronic transplantation experiments. Single neuroectodermal cells from stage 10 donor embryos (after S2) were transplanted into the neuroectoderm of host embryos at stage 7 (before S1) and vice versa. The fate of these cells was uncovered by their lineages at stage 16/17. Transplanted cells adjusted their fate to the new temporal situation. Late neuroectodermal cells were able to take over the fate of early (S1/S2) neuroblasts. The early neuroectodermal cells preferentially generated late (S4/S5) neuroblasts, despite their reduced time of exposure to the neuroectoderm. Furthermore, neuroblast fates are independent from divisions of neuroectodermal progenitor cells. We conclude from these experiments that neuroblast specification occurs sequentially under the control of non-cell-autonomous and stage-specific inductive signals that act in the neuroectoderm.

Animals↗
PubMedDate not supplied

Melanotic neuroectodermal tumor of infancy: a molecular genetic study.

Melanotic neuroectodermal tumor of infancy is a rare but well-recognized entity in pediatric pathology. However, the relationship of this tumor to other pediatric small cell tumors with neuroectodermal features (such as neuroblastoma, Ewing sarcoma/peripheral primitive neuroectodermal tumor, and desmoplastic small round cell tumor) is undetermined. Molecular genetic studies of melanotic neuroectodermal tumor of infancy have not been reported. We studied three typical cases of melanotic neuroectodermal tumor of infancy in an attempt to link this tumor to other small cell tumors with well-characterized molecular genetic changes. Tests performed included: detection of MYCN gene amplification and deletion of 1p (all 3 cases), and presence of the t(11;22)(q24;q12) and the t(11;22)(p13;q12) translocations (2 of 3 cases). None of these tests yielded positive results. Thus, there is no genetic basis at present to link melanotic neuroectodermal tumor of infancy to neuroblastoma, Ewing sarcoma/peripheral primitive neuroectodermal tumor, or desmoplastic small round cell tumor.

Female↗
PubMed2001

Germ cell tumor associated primitive neuroectodermal tumors.

PURPOSE: This retrospective review was done to assess the prognosis and response in patients presenting with primitive neuroectodermal tumor admixed with germ cell tumor. MATERIALS AND METHODS: Of the 40 patients treated at our institution from 1984 to 1999, 15 had initial stage I and 25 had initial metastatic disease. Median followup after the diagnosis was 25 months (range 4 to 142). RESULTS: Of the 40 patients 15 presented with clinical stage I disease, including 9 treated with retroperitoneal lymph node dissection and 6 who elected surveillance. Seven of the 9 patients had normal lymph nodes and all continuously had no evidence of disease. Two of the 9 patients had lymph nodes involved with teratoma with or without primitive neuroectodermal tumor. Retroperitoneal relapse in 5 of the 6 patients on surveillance was treated with cisplatin based chemotherapy followed by post-chemotherapy retroperitoneal lymph node dissection. Residual primitive neuroectodermal tumor was noted in 4 of the 5 patients and only 3 of 6 are currently without disease at a median followup of 17 months (range 15 to 69). A total of 25 patients presented with metastatic disease, of whom 23 underwent cisplatin based chemotherapy. Only 3 patients achieved complete remission with chemotherapy alone and 2 of the 3 subsequently relapsed. Of the remaining 20 patients 16 underwent post-chemotherapy retroperitoneal lymph node dissection, including 11 with primitive neuroectodermal tumor in the resected specimen. Two of these 11 patients have continuously had no evidence of disease, while an additional 3 currently have no evidence of disease after further therapy. Teratoma was present in the resected specimen in 5 of 16 patients, of whom 2 have continuously had no evidence of disease, while an additional 2 currently have no evidence of disease after further surgical resection. Therefore, 11 of 25 patients who presented with metastatic disease currently have no evidence of disease at a median followup of 19 months (range 2 to 111). CONCLUSIONS: Primitive neuroectodermal tumor in the orchiectomy specimen has adverse prognostic significance. This condition in the retroperitoneum is potentially curable by retroperitoneal lymph node dissection but rarely eradicated by chemotherapy. Therefore, we recommend retroperitoneal lymph node dissection for all clinical stage I cases with primitive neuroectodermal tumor in the orchiectomy specimen. Patients who present with metastatic primitive neuroectodermal tumor should be treated aggressively with surgical resection as an integral part of the therapeutic strategy.

Adolescent↗
PubMed2000

The CNS midline cells coordinate proper cell cycle progression and identity determination of the Drosophila ventral neuroectoderm.

The CNS midline cells, specified by the single-minded (sim) gene, are required for the proper patterning of the ventral CNS and epidermis, which are derived from the Drosophila ventral neuroectoderm. Defects in the sim mutant are characterized by the loss of the gene expression, which is required for the proper formation of the ventral neurons and epidermis, and by a decrease in the spacing of longitudinal and commissural axon tracks. Molecular and cellular mechanisms for these defects were analyzed to elucidate the precise role of the CNS midline cells in proper patterning of the ventral neuroectoderm during embryonic neurogenesis. These analyses showed that the ventral neuroectoderm in the sim mutant fails to carry out its proper formation and characteristic cell division cycle. This resulted in the loss of the dividing neuroectodermal cells that are located ventral to the CNS midline. The CNS midline cells are also required for the cell cycle-independent expression of the neural and epidermal markers. This indicates that the CNS midline cells are essential for the establishment and maintenance of the ventral epidermal and neuronal cell lineage by cell-cell interaction. On the other hand, the CNS midline cells do not cause extensive cell death in the ventral neuroectoderm. This study indicates that the CNS midline cells play important roles in the coordination of the proper cell cycle progression and the correct identity determination of the adjacent ventral neuroectoderm along the dorsoventral axis.

Animals↗
PubMed2006

Evolutionary constraint on Otx2 neuroectoderm enhancers-deep conservation from skate to mouse and unique divergence in teleost.

Otx2 is a paired type homeobox gene that plays essential roles in each step and site of head development in vertebrates. In the mouse, Otx2 expression in the anterior neuroectoderm is regulated primarily by two distinct enhancers: anterior neuroectoderm (AN) and forebrain/midbrain (FM) enhancers at 92 kb and 75 kb 5'of the Otx2 locus, respectively. The AN enhancer has activity in the entire anterior neuroectoderm at headfold and early somite stages, whereas the FM enhancer is subsequently active in the future caudal forebrain and midbrain ectoderm. In tetrapods, both AN and FM enhancers are conserved, whereas the AN region is missing in teleosts, despite overt Otx2 expression in the anterior neuroectoderm. Here, we show that zebrafish and fugu FM regions drive expression not only in the forebrain and midbrain but also in the anterior neuroectoderm at headfold stage. The analysis of coelacanth and skate genomic Otx2 orthologues suggests that the utilization of the two enhancers, AN and FM, is an ancestral condition. In contrast, the AN enhancer has been specifically lost in the teleost lineage with a compensatory establishment of AN activity within the FM enhancer. Furthermore, the AN activity in the fish FM enhancer was established by recruiting upstream factors different from those that direct the tetrapod AN enhancer, yet zebrafish FM enhancer is active in both mouse and zebrafish anterior neuroectoderm at the headfold stage.

Animals↗
PubMed1991

Neuroectoderm in Drosophila embryos is dependent on the mesoderm for positioning but not for formation.

By studying neuroectoderm formation in the absence of mesoderm and mesectoderm in mutants of the zygotic genes snail and twist, we have found that the number of neuroblasts is not reduced in these mutants, suggesting that mesoderm and mesectoderm are not essential for the initiation of neural development. The position of the neuroectoderm, however, is ventrally shifted: Neuroectoderm takes over the presumptive peripheral mesoderm domain in single mutants, whereas the entire presumptive mesoderm domain in double mutants takes on the neuroectodermal fate. The shifted neuroectoderm still requires the proneural genes and the neurogenic genes. This shift is unlikely to be due to any shift in the nuclear localization gradient of the maternally supplied dorsal protein. A model for cell fate determination of the neuroectoderm, mesectoderm, and mesoderm will be discussed.

Animals↗
PubMed1992

Expression of Pax-3- and neuroectoderm-inducing activities during differentiation of P19 embryonal carcinoma cells.

A P19 embryonal carcinoma stem cell line carrying an insertion of the E. coli LacZ gene in an endogenous copy of the Pax-3 gene was identified. Expression of the Pax-3/LacZ fusion gene in neuroectodermal and mesodermal lineages following induction of differentiation by chemical treatments (retinoic acid and dimethylsulfoxide) was characterized using this line and is consistent with the previous localization of Pax-3 expression in the embryo to mitotically active cells of the dorsal neuroectoderm and the adjacent segmented dermomyotome. Pax-3/LacZ marked stem cells were also utilized as target cells in mixing experiments with unmarked P19 cells that had been differentiated by pretreatment with chemical inducers. Induction of beta-galactosidase and neuroectodermal markers in the target cells demonstrates that: (1) some differentiated P19 cell derivatives transiently express endogenous Pax-3- and neuroectoderm-inducing activities, (2) undifferentiated target stem cells respond to these activities even in the presence of leukemia inhibitory factor and (3) the endogenous activities can be distinguished from, and are more potent than, retinoic acid treatment in inducing neuroectoderm. These observations demonstrate that P19 embryonal carcinoma cells provide a useful in vitro system for analysis of the cellular interactions responsible for neuroectoderm induction in mammals.

Animals↗