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Biomedical subjects

T Mapstone

Publications and source records attributed to T Mapstone.

9 recordsLinked to original sources
PubMed2001

Pediatric supratentorial intraventricular tumors.

A variety of mass lesions can arise within or in proximity to the ventricular system in children. These lesions are relatively uncommon, and they present a unique diagnostic and surgical challenge. The differential diagnosis is determined by tumor location in the ventricular system, clinical presentation, age of the patient, and the imaging characteristics of the lesion. In this report the authors provide an introduction to and an overview of the most common pediatric supratentorial intraventricular tumors. The typical radiographic features of each tumor and location preference within the ventricular system are reviewed. Management and treatment considerations are discussed. Examination of tissue samples to obtain diagnosis is usually required for accurate treatment planning, and resection without adjuvant therapies is often curative. The critical management decision frequently involves determining which lesions are appropriate for surgical therapy. Careful preoperative neuroimaging is extremely useful in planning surgery. Knowledge of the typical imaging characteristics of these tumors can help to determine the diagnosis with relative certainty when a tissue sample has not been obtained, because a small subset of these lesions can be managed expectantly.

Cerebral Ventricle Neoplasms↗
PubMed1994

A search for gli expression in tumors of the central nervous system.

The gli gene was originally isolated from DNA amplified in double minutes in a glioblastoma (D259MG). Using a sensitive RNA-RNA hybridization, we tested a series of central nervous system tumors for expression of the gli gene. These included 8 glioblastoma cell lines, plus cell cultures of 5 glioblastomas, 4 anaplastic astrocytomas, 3 different ependymal tumors, a malignant meningioma, and a medulloblastoma. Two normal glial cell cultures were also examined. There was no gli expression in any of these specimens. In glioblastoma D259MG, approximately 130 molecules of gli mRNA per cell were present and the half-life of the mRNA was approximately 5 h. By reverse transcription and PCR, gli mRNA was observed in 4 cell lines and in normal human glial cells, but the level was estimated to be less than one five hundredth of that in the D259MG cell line. The results suggest that gli expression in central nervous system tumors is a rare event and mostly likely associated with amplification of the gene.

Central Nervous System Neoplasms↗
PubMed1994

The identification of four protein kinase C isoforms in human glioblastoma cell lines: PKC alpha, gamma, epsilon, and zeta.

Levels of protein kinase C (PKC) isoforms in eight human glioblastoma cell lines and two normal human glial cell cultures were determined. Earlier studies identified PKC-alpha and PKC-gamma in these cell lines but PKC-beta was not present. In this study, PKC-epsilon and PKC-zeta are demonstrated immunologically in these cell lines and also in two normal human glial cell cultures. Protein kinase C-delta was not present. When levels of the four isoforms in the tumor cells were compared to levels in the normal cells, no increase was observed in PKC-alpha or PKC-gamma, but PKC-epsilon was elevated three to 30 times in six of the eight tumors, and PKC-zeta was elevated approximately two times in all of the tumors. Incubation of cell line A172 with phorbol ester for 6 hours resulted in a 48-fold maximum increase in the nuclear PKC-epsilon and a sevenfold increase in the plasma membrane fraction with no change in the cytoplasmic fraction. A similar incubation for 4 hours produced a 0.5- to onefold increase of PKC-zeta in cytoplasmic, nuclear, and plasma membrane fractions. Other researchers have shown that overexpression of PKC-epsilon in fibroblasts results in tumorigenesis, and that blocking PKC-zeta function inhibits deoxyribonucleic acid synthesis. These data suggest that alteration in the expression of PKC-epsilon and PKC-zeta could be a factor in the conversion of normal glial cells to glioblastomas.

Cell Line↗
PubMed1991

Expression of platelet-derived growth factors, transforming growth factors, and the ros gene in a variety of primary human brain tumors.

Ribonucleic acid was isolated from a wide spectrum of central nervous system tumors to examine the expression of platelet-derived growth factors (PDGF) A and B, tumor growth factors (TGF-beta) 1 and 2, and ros messenger ribonucleic acid. Eight glioblastoma cell lines were examined as well as cell cultures from 22 tumor explants. The explants included 6 glioblastomas, 4 anaplastic astrocytomas, 5 astrocytomas, 3 ependymal tumors, 2 meningiomas, 1 medulloblastoma. and 1 ganglioglioma. For comparison, 2 nontumor glial cell cultures were included. The PDGF B-chain was expressed in 5 of 8 glioblastoma cell lines, 2 of 6 glioblastomas, and in 3 of 4 anaplastic astrocytoma explants. There was no PDGF B expression in 4 astrocytomas, 3 ependymomas of varying malignancy, in the remainder of the tumors, or in the nontumor glial cells. The PDGF A-chain was expressed in all of the tumors, with the exception of the malignant ependymoma and in both nontumor glial cell cultures. TGF-beta 1 was expressed in all of the tumors and in nontumor glial cells. The expression of TGF-beta 2 was expressed in many of the benign and malignant tumors and also in both nontumor glial cell cultures. The ros messenger ribonucleic acid was expressed in 1 of 5 glioblastoma cell lines and in 2 of 6 glioblastoma cell explants, but in none of the other tumors or in the nontumor glial cells.(ABSTRACT TRUNCATED AT 250 WORDS)

Brain Neoplasms↗
PubMed1987

Vertebral hemangiomas: MR imaging.

Vertebral hemangiomas, unlike most bone lesions, show increased signal on T1- and T2-weighted magnetic resonance (MR) images. To define the basis for these signal characteristics, a retrospective review was done of the MR imaging findings in ten vertebral hemangiomas (eight patients), and these were correlated with the findings from plain radiographic, computed tomographic (CT), and histopathologic studies. MR images showed mottled increased signal in T1- and T2-weighted images from the osseous portions of the tumors. In three patients, the extraosseous components failed to show increased signal on T1-weighted images. Chemical shift images and histologic studies demonstrated that adipose tissue caused the increased signal on T1-weighted images. The extraosseous components of the tumor contained little, if any, adipose tissue, which explained the lack of high-intensity signal on T1-weighted images. These signal changes appear to make a specific constellation of findings for the diagnosis of vertebral hemangioma with MR imaging.

Adult↗