Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0027819 (neuroblastoma)
 27,800 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The case histories of 273 patients with primary neoplasms of the central nervous system seen in The New York Hospital and Memorial Hospital during the years 1968 through 1973 were reviewed. Neoplastic cells were identified in cytologic preparations obtained from 76 patients. These include patients with meningioma, astrocytoma, glioblastoma multiforme, oligodendroglioma, ependymoma, medulloblastoma, neuroblastoma, retinoblastoma, pineoblastoma, and pituitary adenoma. It is concluded that there are certain suggestive cellular features of these neoplasms in cytologic preparations, but additional studies are needed to establish the cytomorphologic characteristics which may aid in the differential diagnosis of primary intracranial neoplasms from extracranial neoplasms which are metastatic to the central nervous system.
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PMID:Cytology of primary neoplasms of the central nervous system. 26 57

Consistent cytogenetic abnormalities have been described in many pediatric solid tumors, including Ewing's sarcoma, Wilms' tumor, and neuroblastoma. Similar analysis of pediatric central nervous system (CNS) tumors has been hampered by technical problems. We report chromosome results from 39 pediatric CNS tumors. Abnormalities of chromosome 17 were noted in 3 of 11 primitive neuroectodermal tumors (including i(17q) in 2 tumors), confirming data observed by other investigators. Cells from 2 of 11 primitive neuroectodermal tumors (PNET) exhibited loss or structural abnormalities involving chromosome 11. Loss or distal deletion of chromosome 7q was noted in cells from two PNETs. Because other investigators have shown loss of heterozygosity on 17p in about one-third of PNET, we propose that chromosome regions 7q and 11 are areas worthy of further study in pediatric PNET. Numerical abnormalities were noted in 6 of 21 astrocytomas. Hyperdiploidy was demonstrated in 1 of 4 pilocytic astrocytomas and pseudopolyploidy was demonstrated in 4 of 13 anaplastic astrocytomas. Structural chromosome abnormalities (translocations, deletions) were noted in 4 of 13 anaplastic astrocytomas. Complex structural anomalies were observed in one craniopharyngioma. A rhabdoid tumor of the brain exhibited multiple complex structural rearrangements but did not exhibit the monosomy 22 observed in some rhabdoid tumors. Hypodiploidy and loss of chromosome 22 were noted in a clinically aggressive meningioma, corroborating observations by other investigators.
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PMID:Cytogenetic analysis of 39 pediatric central nervous system tumors. 131 29

Infectivity of human T-lymphotropic virus type I (HTLV-I) to human nervous tissue cells was explored using co-cultivation with X-irradiated, HTLV-I-producing MT2 cells. Examined cells included normal cerebellar cells, brain tumor cells (astrocytoma, medulloblastoma, meningioma, hemangioblastoma, and schwannoma), and various cell lines (astrocytoma, ependymoma, oligodendroglioma, medulloblastoma, and neuroblastoma). Successful HTLV-I infection was confirmed immunohistochemically using monoclonal antibodies to HTLV-I p19, p24, and pX product. All cell lines and primary cultures from normal cerebellar tissues and brain tumors could be infected with HTLV-I. Double immunostaining showed that glial fibrillary acidic protein-, S-100 protein- or vimentin-positive cells were susceptible to infection. Neurofilament- or neuron-specific enolase-positive cells in medulloblastoma could also be infected. Reverse-transcriptase assay revealed the productive infection in U251-MG (astrocytoma) and KG-IC (oligodendroglioma) lines. Co-cultivated U251-MG cells formed syncytial polykaryons after serial passages, and polymerase chain reaction assay detected HTLV-I genome in U251-MG syncytial polykaryons and p19+ mononuclear cells. HTLV-I viral RNA was also detected in infected U251-MG cells by in situ hybridization. These data show that HTLV-I may have a wide spectrum of infectivity in human nervous tissues.
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PMID:Infectivity of human T-lymphotropic virus type I to human nervous tissue cells in vitro. 138 59

We developed a new approach for detecting the gene amplification of cancer DNAs with restriction landmark genomic scanning (RLGS). In cancer research, much effort has been made to find the amplified loci of cancer DNAs, because many lines of evidence indicate association between oncogene amplification and carcinogenesis. Conventionally, such gene amplification has been detected by using Southern hybridization with DNA probes. However, only the information of one locus can be obtained by one hybridization procedure, and analysis of many loci throughout the genome is too laborious and time consuming, even if only several candidate genes are investigated. On the other hand, the "in-gel renaturation method" was reported as another alternative for detection of amplified regions. However, even though this method is much improved, it is difficult to detect less than 7-fold amplification, which is often higher than the amplification of many cancer cases. To overcome these limitations and, in addition, to locate the amplified DNA two dimensionally, we applied RLGS for analysis of DNA amplification in cancer tissues, such as breast cancer (infiltrative tubuloadenocarcinoma), neuroblastoma, meningioma (endotheliomatous meningioma), and thyroid cancer (papillary adenocarcinoma). In some cases of breast cancer, several amplified spots located on the same amplicon were detected. In thyroid cancer, in which no amplification has yet been reported, low-grade amplification was also detected. In this report, we demonstrated that RLGS allows us to screen 2000-3000 restriction landmarks distributed on the genome simultaneously, and even low-grade amplification could be detected effectively. Thus, RLGS has proven to be a very useful method in detecting DNA amplification.
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PMID:New approach for detection of amplification in cancer DNA using restriction landmark genomic scanning. 161 37

A 56-year-old male was admitted with the complaints of nasal bleeding, gait disturbance, and disturbance of consciousness. Neurological examination revealed drowsiness, right hemiparesis, and choked discs. Computed tomography scan showed an enhanced mass at the frontal base, which extended to the left nasal and paranasal cavities. Angiography showed a tumor stain with a mass sign. The intracranial part of the tumor was removed completely and he was discharged ambulatorily. Two months after surgery, however, he was admitted again for the regrowth of the tumor. Ventriculoperitoneal shunting was placed and radiation therapy was given to the brain and nasal cavity. After 3000 rad irradiation the clinical condition suddenly became worse because of pneumocephalus. The cranial tumor disappeared after irradiation but he died of metastases and general prostration. Clinically this case was diagnosed as an olfactory groove meningioma at first, but immunohistochemical diagnosis was olfactory neuroblastoma.
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PMID:[Olfactory neuroblastoma complicated by postirradiation pneumocephalus. Case report]. 170 66

Constitutional chromosome abnormalities that may predispose a group of individuals to develop certain neoplasms have been reported for some human solid tumors. Deletions of 13q in retinoblastoma, 11p in Wilms' tumor, 1p in neuroblastoma, 3p in renal cell carcinoma, 5q in colorectal carcinoma and 22q in meningioma are examples of such anomalies. In breast carcinoma, a specific cytogenetic defect has not been conclusively identified. We have studied Phytohemagglutinin-stimulated lymphocytes of 76 breast cancer patients, 68 predisposed family members, 40 controls, and 30 additional controls with lung cancer to determine whether nonrandom chromosome defects are present. From each sample 100, G-or Q-banded metaphase spreads were studied for rearrangements. A marked clustering of alterations in the long arm of chromosome no. 1 (q11-22) was seen in breast cancer patients and in some predisposed family members. Alterations in 1q were present in 1% to 3% of metaphases, and included translocations to chromosomes 3, 6, 7, 9, 12, 15, 17, 18, 21 and the X; deletion of 1q, or pericentric inversion. Twelve out of 62 (19.3%) familial cases, 3 out of 14 (21.4%) sporadic cases, 9 out of 68 (13.2%) predisposed cases and 2 out of 40 (5%) control cases showed 1q alterations. None of the 30 lung cancer patients showed chromosome 1 anomaly in this region. This is consistent with the reports on primary breast tumor tissues, cell lines and pleural effusions where 1q defects have been reported. We conclude that chromosome 1q rearrangement might be one of the primary lesions specifically associated with the development of breast cancer.
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PMID:Chromosome anomalies in human breast cancer: evidence for specific involvement of 1q region in lymphocyte cultures. 188 38

We have used cell-culture techniques to investigate growth-factor production by human meningioma cells. Meningioma tissue was dispersed with collagenase and the cells grown to high density in tissue-culture flasks. The cultures were used to generate conditioned medium (MEN-CM), which was used to cultivate IMR32 cells (a human neuroblastoma line) and freshly dispersed primary meningioma cells. MEN-CM profoundly stimulated the in vitro growth of both IMR32 and meningioma cells. In addition, H3-thymidine uptake by cultured meningioma cells was increased in a dose-dependent manner by varying concentrations of MEN-CM. A neutralizing anti-body against platelet-derived growth factor (PDGF) completely abolished the stimulatory effects of MEN-CM, whereas an antibody against TGF-alpha was without effect. The mitogenic activity of MEN-CM, as assayed by promotion of H3-thymidine uptake by cultured meningioma cells, eluted from a Sephadex G-100 column in 3 peaks corresponding to molecular weights of greater than or equal to 150, 56 and 28 kDa. Our results show that proliferation of human meningiomas may be under autocrine control via secretion of PDGF-like molecules.
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PMID:Autocrine control of human meningioma proliferation: secretion of platelet-derived growth-factor-like molecules. 191 38

In this study, we have investigated the expression of the neural cell adhesion molecule (NCAM) in the human brain, primary brain tumours and neuroblastoma. Adult brain was found to express discrete isoforms of 180, 170, 140 and 120 kDa, which on neuraminidase treatment resolved into bands of 180, 170, 140, 120 and 95 kDa. Primary brain tumours such as Schwannoma and medulloblastoma expressed embryonic NCAM characterised by a high level of glycosylation, whereas other tumours, e.g. astrocytoma, meningioma, glioma and oligodendroglioma expressed adult NCAM. Post-neuraminidase treatment, differential expression of the 180, 170, 140, 120 and 95 kDa isoforms were noted in these various tumour types. On the other hand, neuroblastoma cell lines were found to express only embryonic NCAM, which after neuraminidase treatment resulted in differential presence of only 180, 140 and 120 kDa proteins.
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PMID:Expression of the cluster 1 antigen (neural cell adhesion molecule) in neuroectodermal tumours. 203 10

Using a database comprising 13,266 cytogenetically abnormal neoplasms, the geographic heterogeneity of neoplasia-associated chromosomal abnormalities was investigated by comparing the frequencies of characteristic aberrations in consecutive series of patients with the same diagnosis. Significant frequency differences between geographic areas were found for the aberrations +8, i(17q), +19, and an additional Ph1 chromosome in chronic myeloid leukemia (CML); -5, 5q-, and +8 in acute nonlymphocytic leukemia (ANLL); t(8;21) in ANLL-M2; t(15;17) in ANLL-M3; 5q- and -7 in myelodysplastic syndromes (MDS); t(9;22) and +21 in acute lymphocytic leukemia (ALL); t(14;18) in follicular lymphoma; -8 and -22/22q- in meningioma; and structural abnormalities of 12q in pleomorphic adenoma of the salivary glands (PAS). No geographic incidence variation was detected for -7 and +21 in ANLL; +8 in MDS; 6q- and +8 in ALL; +12 in chronic lymphocytic leukemia; 6q- in non-Hodgkin's lymphoma (NHL); t(8;14) in Burkitt's lymphoma; t(11;22) in Ewing's sarcoma; i(12p) in germ cell tumors; 1p- in neuroblastoma; structural abnormalities of 3q, 8q, and 9p in PAS; or 3p- in renal cell carcinoma. Intraregional frequency similarities between cytogenetically identical abnormalities in related tumor types were also analyzed. No significant correlations were found regarding the incidence of 5q- in ANLL and MDS, 6q- in ALL and NHL, -7 in ANLL and MDS, +8 in ANLL and CML, +8 in ANLL and MDS, +8 in ALL and ANLL, or +21 in ALL and ANLL. The findings indicate that some geographic heterogeneity of tumor-associated aberrations exists both in hematologic neoplasms and in solid tumors.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Geographic heterogeneity of neoplasia-associated chromosome aberrations. 195 98

Two patients presented with primary meningiomas arising in the paranasal sinuses. Despite nonspecific symptoms, both patients had extensive local clinical disease. One patient had a lateral rhinotomy with total removal of tumor; he has remained well for 3 years. The second patient, who was not a surgical candidate because of her cerebrovascular disease, was identified retrospectively. Her tumor was not originally studied using current day morphologic methods. She was irradiated following a diagnosis of malignant tumor. The histologic features of nasal meningioma are similar to those of conventional intracranial lesions, including nuclear pseudoinclusions. Although the unusual location may suggest carcinoma, melanoma, or olfactory neuroblastoma, adjunctive use of electron microscopy and immunohistochemistry can be combined to arrive at the correct diagnosis.
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PMID:Meningioma of the paranasal sinuses. A report of two cases. 229 84


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