Disease relevance of Neuroectodermal Tumors

• These data suggest that the endogenous opioid system is an integral component of brain tumors and that met-enkephalin may represent a useful malignancy marker in neuroectodermal tumors [1].
• The gene encoding the leukocyte common-antigen-related (LAR) PTP receptor maps to chromosome 1p32-33, a region in which loss of heterozygosity is associated with human pheochromocytoma and other neuroectodermal tumors [2].
• Taken together, the data suggest that ECK maps to 1p36.1, a region that is frequently deleted in neuroblastoma, melanoma, and other neuroectodermal tumors [3].
• Type 1 neurofibromatosis (NF1) is a common autosomal dominant disorder that results in neuroectodermal tumors [4].
• Olfactory neuroblastoma (ONB) is a rare neuroectodermal tumor whose clinical course is not effectively predicted by initial stage or grade; p53 tumor suppressor gene alterations have not been determined concerning the ONB pathobiology and recurrence [5].

High impact information on Neuroectodermal Tumors

• Aloe-emodin is a new type of anticancer agent with selective activity against neuroectodermal tumors [6].
• Differential spectrum of expression of neural cell adhesion molecule isoforms and L1 adhesion molecules on human neuroectodermal tumors [7].
• In recent years, we reported the isozyme shift of pyruvate kinase from the M- toward the K-type in human neuroectodermal tumors [8].
• Our observations suggest that N-myc expression is not limited to neuroectodermal tumors as was previously thought, but is a marker for several neoplasms that derive from primitive cell precursors [9].
• Its function in adults is as yet unknown, but significantly, CD155 is aberrantly expressed in neuroectodermal tumors [10].

Chemical compound and disease context of Neuroectodermal Tumors

• The induction of neuroectodermal tumors in BDIX rats by N-ethyl-N-nitrosourea (EtNU) is a model system for the analysis of transformation risk as a function of target cell properties [11].
• Therefore, this drug combination, inhibiting guanylate de novo and salvage pathways, may prove useful in the treatment of human neuroectodermal tumors [12].
• Synergistic action of tiazofurin with hypoxanthine and allopurinol in human neuroectodermal tumor cell lines [12].
• Valproic acid (VPA) has been shown to induce growth-arrest and differentiation of human neuroectodermal tumors similarly to several other fatty acids [13].
• Although the total creatine concentrations decreased according to the malignancy, the concentration of total creatine was relatively preserved in neuroectodermal tumors but was low in nonneuroectodermal tumors [14].

Anatomical context of Neuroectodermal Tumors

• Within this gene family, the leukocyte common antigen-related (LAR) gene is of particular interest with respect to the nervous system because it has sequence similarity to the neural cell adhesion molecule N-CAM and is located in a chromosomal region (1p32-33) frequently deleted in neuroectodermal tumors [15].
• The intermediate filament nestin is expressed in neural stem cells, neuroectodermal tumors and various adult tissues [16].
• Expression of p67 (Munc-18) in adult human brain and neuroectodermal tumors of human central nervous system [17].
• A possible relationship of pyrophosphate uptake in this tumor with uptake in other neuroectodermal tumors which are of neural crest origin is considered [18].

Gene context of Neuroectodermal Tumors

• The anti-apoptotic effect of BMP-2 and BMP-4 on this neuroectodermal cell line has potential clinical implications for neuroectodermal tumors [19].
• We have searched for the expression of CD24 in the developing and in the mature human brain as well as in a wide range of neuroectodermal tumors [20].
• Seventy-four canine neuroectodermal tumors were examined immunocytochemically for the presence of glial fibrillary acidic protein (GFAP) [21].
• Pretreatment samples from 24 children with neuroectodermal tumors (two ganglioneuromas, 22 neuroblastomas) and from 106 others with various tumors were submitted to the enzymatic determination of the serum neuron-specific enolase (NSE) [22].
• These data indicate autocrine stimulatory loops for PDGF and bFGF, which may be blocked, may have different relevance in neuroectodermal tumors in vitro, and may have conceivable future therapeutic implications [23].

Analytical, diagnostic and therapeutic context of Neuroectodermal Tumors

• Paraffin section p53 protein immunohistochemistry in neuroectodermal tumors [24].

References