Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Neuroectodermal Tumors, Primitive, Peripheral”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,477 records · Page 82Linked to original sources
PubMed1995

Expression of myogenic regulatory proteins (myogenin and MyoD1) in small blue round cell tumors of childhood.

The distinction of rhabdomyosarcoma (RMS) from other small blue round cell tumors of childhood, such as Ewing's sarcoma/peripheral primitive neuroectodermal tumor (pPNET) and neuroblastoma, continues to present a diagnostic challenge to pathologists. The recent recognition of the master role of myogenic regulatory proteins in skeletal muscle commitment and differentiation, and the availability of monoclonal antibodies to two of them (myogenin and MyoD1), has prompted us to test their diagnostic utility in routinely processed, formalin-fixed, and deparaffinized tissue. Preliminary studies had demonstrated that, with the use of heat-induced epitope retrieval techniques, expression of myogenin and MyoD1 could be documented specifically in nuclei of fetal skeletal muscle by the respective antibodies. We performed a retrospective immunohistochemical analysis on 72 cases of small blue round cell tumors, including 33 RMSs, 1 metastatic myogenous Wilms' tumor, 26 Ewing's sarcomas/pPNETs, and 12 neuroblastomas. Nuclear expression of myogenin and MyoD1 were both found in 30/33 non-overlapping cases of RMS, with no significant differences in the sensitivity with respect to histological subtypes, and in 1/1 case of myogenous Wilms' tumor. None of the neuroblastomas or Ewing's sarcomas/pPNETs demonstrated positive nuclear staining with either antibody. However, most of the neuroblastomas, and occasional Ewing's sarcomas/pPNETs, showed variable fibrillary, cytoplasmic immunoreactivity with antibody to MyoD1. We conclude that, with the use of microwave-based epitope retrieval, antibodies to myogenin and MyoD1 are both useful markers for the identification of RMS among other small blue round cell tumors of childhood, but antibodies to myogenin have technical advantages over those to MyoD1, as the latter may cross-react with an unknown cytoplasmic antigen in non-muscle cells and tumors.

Child↗
PubMed1993

Immunohistochemical evaluation of dystrophin expression in small round cell tumors of childhood.

Dystrophin, the protein product of the Duchenne muscular dystrophy locus, is a major component of the subsarcolemmal cytoskeleton in skeletal muscle cells and is a relatively muscle specific protein. We evaluated, retrospectively, the expression of dystrophin in 23 small round cell tumors of childhood including: 9 rhabdomyosarcomas, 4 neuroblastomas, 1 ganglioneuroblastoma, 2 small noncleaved cell lymphomas, 1 lymphoblastic lymphoma, 2 medulloblastomas, 2 primitive neuroectodermal tumors, 1 Wilms' tumor, and 1 undifferentiated sarcoma. Frozen sections were stained by the avidin biotin immunoperoxidase technique using a commercially available monoclonal antibody NCL-DYS1 (Novocastra) that recognizes the mid-rod domain (between amino acids 1181 and 1388) of human dystrophin. Positive controls were represented by frozen sections of normal skeletal muscle. Negative controls consisted of substituting the dystrophin antibody for normal rabbit serum. Eight of nine rhabdomyosarcomas revealed positivity whereas, none of the other tumors stained for dystrophin. This study provides evidence that monoclonal antibodies to dystrophin may be a potential useful addition to the panel of muscle markers used to diagnose small round cell tumors of childhood.

Adult↗
PubMed1994

Expression of stem cell factor and c-kit in human neuroblastoma. The Children's Cancer Group.

During development, mice with mutations of stem cell factor (SCF) or its receptor c-kit exhibit defects in melanogenesis, as well as hematopoiesis and gonadogenesis. Because melanocytes derive from neural crest cells, the role of SCF and c-kit was investigated in the neural crest-derived childhood tumor neuroblastoma. Using reverse transcription-polymerase chain reaction analysis, simultaneous expression of steady-state mRNA for the SCF ligand and its receptor c-kit was found in 14 of 14 (100%) human neuroblastoma cell lines and clones and in 8 of 18 (45%) human neuroblastoma tumor samples. Functional blockade of c-kit receptors in the cell lines SK-N-BE(2) and SH-SY5Y using the mouse monoclonal anti-c-kit antibody SR-1 resulted in a significant decrease in cellular growth rate when measured by either 3H-thymidine incorporation or clonogenicity. In addition, higher levels of c-kit mRNA expression were associated with parental neuroblastoma cell lines and subclones with a neuronal (N) differentiation phenotype, whereas lower levels of c-kit mRNA were associated with neuroblastoma cell line subclones having a schwannian/glial/melanocytic pattern of differentiation. However, the differentiation phenotype of neuroblastoma cell lines was not directly altered when c-kit expression was blocked using the SR-1 antibody. In summary, these data indicate that c-kit receptor expression may play a significant role in the growth regulation of the two neuroblastoma cell lines examined and suggest that c-kit may also play a similar role in neuroblastoma growth regulation in vivo. Simultaneous expression of SCF and c-kit mRNA in both neuroblastoma cell lines and tumors implies that c-kit may act as part of an autocrine growth loop in conjunction with endogenous production of SCF in this disease.

Animals↗
PubMed1995

Low CD4 lymphocyte count in a patient with P. carinii pneumonia after autologous bone marrow transplantation.

Authors report a case of P. carinii pneumonia in a child with 5% CD4 lymphocytes (absolute number 5/microliters) after autologous bone marrow transplantation followed by pulmonary irradiation. Serial evaluation of CD4 lymphocyte count or percentage or, at least, detection of significant and persistent lymphopenia could be useful for detecting a high risk of developing P. carinii pneumonia.

Antineoplastic Combined Chemotherapy Protocols↗
PubMed1993

Olfactory neuroblastoma: clinical and pathological aspects.

Twenty cases of olfactory neuroblastoma were available for clinical and histopathological evaluation. The usefulness of immunohistochemistry in the diagnosis of this tumour was investigated and was best achieved using a panel of monoclonal and polyclonal antibodies, notably neuron-specific enolase, PGP 9.5, S-100 protein, synaptophysin and chromogranin A. This study confirmed that immunohistochemistry is a useful adjunct in cases where conventional histology is equivocal.

Adolescent↗
PubMedDate not supplied

[Embryonal neuroepithelial tumors of the cerebral hemispheres].

33 embryonal neuroepithelial tumours of the cerebral hemispheres were examined light- and electron-microscopically, immunohistochemically. 4 types of tumours were distinguished: neuroblastoma, neuroepithelioma, ependymoblastoma and choroid carcinoma. Each type was characterised by its own pathohistological, immunohistochemical and ultrastructural features. Our results and literature data prove immunophenotypic and ultrastructural heterogeneity of embryonal neuroepithelial tumors of the cerebral hemispheres, in spite of some similarities in their pathohistological features.

Adolescent↗
PubMed1994

Down-regulation of c-myc oncogene during NGF-induced differentiation of neuroblastoma cell lines.

There may be a close relationship between myc oncogenes and carcinogenesis of human neuroblastoma. In previous studies, we were able to induce differentiation of certain neuroblastoma cell lines with NGF. In order to study gene regulation during differentiation, N-myc and c-myc cDNA probes were hybridized with RNA extracted from different cell lines before and after NGF treatment. It was found that cell lines which expressed N-myc did not express c-myc while those with c-myc did not express N-myc except for SHEP cell line which had neither c-myc nor N-myc expression. In NGF-induced differentiated neuroblastoma cells, c-myc oncogene was down-regulated in comparison with the control samples. The time course of c-myc down-regulation was concomitant with the appearance of morphological differentiation. In situ hybridization also showed remarkable reduction of c-myc oncogene expression in NGF-induced differentiated cells as compared with the untreated control cells. These results indicate that down-regulation of c-myc oncogene may be a key event during NGF-induced differentiation and over-expression of c-myc oncogene may, at least partially, be responsible for the genesis of neuroblastoma.

Cell Transformation, Neoplastic↗