PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “Peripheral Nervous System Neoplasms”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

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

At least 289 records · Page 16Linked to original sources
PubMed1989

Exposure of newborn mice to adenosine causes neural crest dysplasia and tumor formation.

In the first part of this paper, we show that intraperitoneal injection of adenosine into newborn mice causes multiple neural crest tumors, neural crest hyperplasia, and heterotopic melanin pigmentation. In the second part, we review published data to propose (1) that microtubule proteins, phosphorylated through the action of calmodulin-dependent kinase and cyclic adenosine monophosphate and the adenosine A2 receptor of neural crest cells, may participate in neurotransmission and (2) that at least some neural crest tumors may be associated with disorders of neurotransmission in embryonic neural crest cells.

Adenosine↗
PubMed1996

Study of post-natal effect of chemopreventive agents on ethylnitrosourea-induced transplacental carcinogenesis in rats. III. Inhibitory action of indomethacin, voltaren, theophylline and epsilon-aminocaproic acid.

The influence of the arachidonic acid metabolism inhibitors, indomethacin and voltaren; an inhibitor of phosphodiesterase activity, theophylline and the protease inhibitor epsilonaminocaproic acid (EACA) on N-ethyl-N-nitrosourea (ENU)-induced transplacental carcinogenesis was studied in rats. ENU was given to pregnant rats as a single i.v. exposure at a dose of 75 mg/kg body weight on the 21st day after conception. Indomethacin and voltaren (20 p.p.m. in drinking water), theophylline (0.01% in diet) and EACA (1000 p.p.m. in drinking water) were given to the offspring throughout their post-natal life until all survivors were killed at 12 months. In the ENU-only control groups, 100% of the offspring developed tumors of brain, spinal cord, peripheral nervous system or kidneys, with a total average number of 3.1 tumors per rat. The most marked inhibitory effect was exerted by theophylline, which significantly decreased the incidence and multiplicity of total tumors, and at all main sites selectively (brain, spinal cord, peripheral nerves and kidneys). It also prolonged average survival time of the offspring. Indomethacin and voltaren significantly decreased total tumor incidence and multiplicity and brain tumor incidence and multiplicity. Indomethacin also decreased kidney tumor multiplicity and voltaren diminished spinal cord tumor multiplicity. EACA decreased multiplicities of total, brain, peripheral nerve and kidney tumors, and diminished the incidence of brain tumors. These chemopreventive agents decreased tumor incidences 20-33% and tumor multiplicities 1.4-2.7 times, compared with the ENU-only controls.

Aminocaproic Acid↗
PubMed2003

Structural genomic abnormalities of chromosomes 9 and 18 in myxopapillary ependymomas.

Myxopapillary ependymomas (MPEs) are low-grade neuroepithelial tumors typically occurring in the conus-cauda equina-filum terminale region. Limited molecular and cytogenetic analysis of MPEs has not demonstrated consistent abnormalities. In an attempt to clarify the chromosomal status of these tumors and identify commonly aberrant regions in the genome we have combined 3 molecular/cyto/genetic methods to study 17 MPEs. Comparative genomic hybridization of 7/17 tumors identified concurrent gain on chromosomes 9 and 18 as the most frequent finding. The majority of the 17 tumors were also studied using microsatellite analysis with marker spanning the whole chromosomes 9 and 18 and interphase-FISH with centromeric probes for both chromosomes. Our combined results were consistent with concurrent gain in both chromosomes 9 and 18 in 11/17 cases, gain of either chromosome 9 or 18 and imbalance in the other chromosome in 3/17 tumors and allelic imbalances of chromosomes 9 or 18 in 3/17 and 1/17 tumors, respectively. Other abnormalities observed included gain of chromosomes 3, 4, 7, 8, 11, 13, 17q, 20, and X and loss of chromosomes 10 and 22. Our findings represent some steps towards understanding the molecular mechanisms involved in the development of MPE.

Adolescent↗
PubMed1988

Gamma-enolase and glial fibrillary acidic protein in nervous system tumors. An immunohistochemical study using specific monoclonal antibodies.

A large series of central and peripheral nervous system tumors was studied for the presence of glial fibrillary acidic protein (GFAP) and gamma-enolase (neuron-specific enolase, NSE), using specific monoclonal antibodies (mAbs). Occurrence in and specificity of GFAP to glial and mixed tumors was confirmed and depended on the malignancy grade and features such as meningeal invasion. Using a well-characterized mAb, gamma-enolase was demonstrated in neuronal, as well as in a whole range of non-neuronal tumors. This lack of specificity of gamma-enolase prohibits its use as an exclusive neuronal marker. Nevertheless quantization or comparison with other types of enolases could still prove to be useful in well-defined situations. The advantages inherent to mAbs and a highly sensitive detection system turn GFAP stainings into a specific and readily reproducible technique.

Antibodies, Monoclonal↗
PubMed1977

Massive neuraxial spread of aural rhabdomyosarcoma.

An embryonal rhabdomyosarcoma that initially was seen as a polyp in the external auditory canal underwent uncontrollable direct extension along the facial nerve through the internal auditory meatus, with encasement of the base of the brain and entire spinal cord despite radical surgery, supervoltage irradiation, and multidrug chemotherapy. This degree of massive neuraxial spread without systemic metastases appears to be unique.

Brain↗
PubMed1992

Cutaneous T-cell lymphoma presenting with diffuse lymphomatous infiltration of the peripheral nerves: response to combination chemotherapy.

A patient with nonepidermotropic cutaneous T-cell lymphoma presented with severe diffuse peripheral neuropathy that was the result of lymphomatous infiltration of the peripheral nervous system. There was no other evidence of systemic disease. The diagnosis was delayed because of the unusual presentation. A peripheral nerve biopsy was instrumental in establishing the etiology of the neuropathy. The patient achieved complete clinical remission with combination chemotherapy.

Antineoplastic Combined Chemotherapy Protocols↗