Epidemiology of primary central nervous system neoplasms. I. Mortality from primary central nervous system neoplasms in Minnesota.
Explore the source record for details and available documents.
SEARCH · PubMed Health
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.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
The incidence rates of primary nervous system neoplasms in 5 districts (large administrative units) of Western Poland with a relatively homogeneous health care system but some contrasts in economic activity, as well as in 224 communes (smallest administrative units) located within these 5 districts, with a total population of 3,097,000 were estimated on the appointed day (31.12.79). Testing the hypothesis, assuming a homogeneous distribution of nervous system neoplasms over the region under investigation, that the incidence rates were distributed as a Poisson variable has revealed a focal distribution of these tumours; in 15 communes the frequency was higher than 9.0 and deviated from the remainder in the 5% right tail of the distribution. The main conclusion from the presented results was that tumours of the nervous system, of which 90% were intracranially located, may occur in clusters or foci, and this could prove to be of clinical as well as statistical import.
Classic histopathologic study revealed a series of highly treasured criteria for diagnosing central and peripheral nervous system neoplasms. The advent of immunohistochemistry galvanized further improvements in the accuracy of diagnostic neurooncologic pathology, and moreover, enriched our understanding of tumor histogenesis. Now with the tremendous technical advances in immunodetection and the commercial availability of high-quality monoclonal and polyclonal antibodies, the potential for first-rate diagnostic assessment is available to practically every laboratory, regardless of how small or remotely located. Intensive immunohistochemical analysis of nervous system neoplasms has taught us that neuroectodermal cells have a limited repertoire of highly redundant antigenic phenotypes and that neoplastic cells usually mimic their non-neoplastic immature or fully differentiated counterparts. These observations led to the concept that a panel of antibodies ought to be used to identify the "immuno-gestalt" of tumors, because it is often difficult if not impossible to subcategorize the tumors on the basis of a single immunohistochemical determination. The ensuing tour through the immunodiagnostic neurooncology summarizes approximately 10 years of original work in this field. I have attempted to provide consensus opinions, and whereever appropriate, highlight dissenting arguments. The salient immunohistochemical features of most nervous system tumors also are summarized in tabular form to facilitate diagnostic considerations at your own institutions.
The diagnosis and assignment of grade in neoplasms of the central nervous system (CNS), for the most part, are morphologically based and predicated on the interpretation of descriptions of what the phenotypic findings are for a particular tumor type. Not surprisingly, the application of various grading systems in CNS neoplasia has been limited somewhat by interobserver variability. Since assignment of grade and tumor type is the basis upon which therapeutic intervention is grounded, investigators have been searching for ancillary means by which morphologically based systems can be improved. Utilization of cell proliferation markers in the evaluation of tumors can be potentially useful in this endeavor. This review focuses on issues surrounding the utilization of MIB-1 or Ki-67 antibody in the evaluation of CNS neoplasms.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Current data indicate that mortality for primary malignant nervous system neoplasms (NSNs) provides a fairly accurate index of incidence. Average annual age- and sex-specific death rates among whites for primary malignant NSNs in the 48 contiguous United States from 1940 through 1975 showed a marked cohort effect among the elderly of either sex. For white men aged 60 through 64 years, mortality increased steadily from 5.3 per 100,000 per year for those born in 1880 to 16.1 per 100,000 per year for the 1910 cohort. No definite cohort effect was seen in the young. The increase in mortality could be due to better diagnosis and more complete case ascertainment for deaths due to primary malignant NSNs, but further studies are required to distinguish a real from an artifactual increase in mortality.
The authors report of 3 observations of the familiar incidence of the central nervous system neoplasms. In the first case it was brain astrocytoma in 2 brothers, in the second case is was man with the meningioma of falx cerebri and his sister with capillary hemangioma of the cerebellum, in the third case it was a woman with astrocytoma of the left temporal lobe and her brother with medulloblastoma. The authors are of the opinion that it was only coincidence in all three cases.
This study evaluated the relationship between central nervous system neoplasms (CNSN) and exposure to epichlorohydrin (ECH) among 11 CNSN cases and 44 controls who were members of a cohort of chemical workers. Information on area of employment and potential exposure to ECH was obtained from plant personnel and medical records and from interviews with long-term employees. An elevated odds ratio (OR) for CNSN was observed for subjects who worked in the epoxy resin process line (OR = infinity, 95% confidence interval [CI] = 1.2-infinity), and in the production of anthraquinone intermediate dyes (OR = infinity, 95% CI = 1.7-infinity) and azo dyes (OR = 3.6, 95% CI = 0.6-41). Routine potential exposure to ECH was associated with CNSN (OR = 4.2, 95% CI = 0.7-26). Dose-response relationships were found with duration and with cumulative routine potential exposure to ECH (p = .11 and .08, respectively). Acute exposure to ECH requiring treatment at the plant infirmary also was associated with subsequent CNSN (OR = infinity, 95% CI = 1.5-infinity).
To determine whether nervous system neoplasms are associated with primary malignancies elsewhere, we studied the frequency of multiple primary tumous in patients in whom at least one of the primary tumors was within the nervous system. The patients were Conneticut residents with tumors diagnosed between 1935 and 1964. Of 135 patients, 130 had two primary tumors, four had three primary tumors, and one had four primary tumors. Only with multiple primary tumors involving the brain and breast did the number of observed cases significantly exceed the number of expected cases; eight patients who had a meningioma associated with a breast cancer accounted for this excess. Patients with breast cancer presenting with signs or symptoms of an intracranial neoplasm should be carefully evaluated, for the intracranial lesion may be a potentially curable meningioma.
Explore the source record for details and available documents.
Expression of the vascular permeability factor/vascular endothelial growth factor (VEGPF) gene was investigated in human central nervous system (CNS) neoplasms and normal brain. Adsorption of capillary permeability activity from human glioblastoma multiforme (GBM) cell conditioned medium and GBM cyst fluids by anti-VEGPF antibodies demonstrated that VEGPF is secreted by GBM cells and is present in sufficient quantities in vivo to induce vascular permeability. Cloning and sequencing of polymerase chain reaction-amplified GBM and normal brain cDNA demonstrated three forms of the VEGPF coding region (567, 495, and 363 nucleotides), corresponding to mature polypeptides of 189, 165, and 121 amino acids, respectively. VEGPF mRNA levels in CNS tumors vs. normal brain were investigated by the RNase protection assay. Significant elevation of VEGPF gene expression was observed in 81% (22/27) of the highly vascular and edema-associated CNS neoplasms (6/8 GBM, 8/8 capillary hemangioblastomas, 6/7 meningiomas, and 2/4 cerebral metastases). In contrast, only 13% (2/15) of those CNS tumors that are not commonly associated with significant neovascularity or cerebral edema (2/10 pituitary adenomas and 0/5 nonastrocytic gliomas) had significantly increased levels of VEGPF mRNA. The relative abundance of the forms of VEGPF mRNA was consistent in tumor and normal brain: VEGPF495 > VEGPF363 > VEGPF567. In situ hybridization confirmed the presence of VEGPF mRNA in tumor cells and its increased abundance in capillary hemangioblastomas. Our results suggest a significant role for VEGPF in the development of CNS tumor neovascularity and peritumoral edema.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
A 22-year-old man with previous radiation treatment for childhood astrocytoma underwent resection of a right parietooccipital lesion. Histopathology revealed a malignant neoplasm with areas of astrocytic and primitive neuroectodermal components. To resolve the relationship and cellular origin, representative tissue was microdissected from several targets, obtaining a balanced mixture of each element. Nonneoplastic brain parenchyma was separately microdissected to determine polymorphic marker informativeness and to serve as an internal negative control. Despite the relatively small quantity of tissue removed for each microdissection target, sufficient material was available for reliable, balanced, polymerase chain reaction-format genotyping encompassing a panel of tumor suppressor genes and genetic loci associated with these forms of neoplasia. The findings revealed distinct discordant genotypic profiles for each of the neoplastic components. The efficacy of the approach used for molecular analysis of this complex neoplasm and the implication of the genotypic findings are discussed.
The "ideal" classification of pediatric brain tumors will depend on a full characterization of pathologic variables and their influence on prognosis. Currently available information about these variables remains incomplete, even for traditional histologic and cytologic features, and certainly for those studied by the newer methods that will continue to appear. In light of the multiplicity and specialized nature of some of the techniques that are or will become available, it is suggested that specific pediatric central nervous system neoplasms be targeted for study by groups of pathologists according to a protocol that delegates specific studies to specific individuals. In light of the large number of cases required, as well as the need to control for effects of different treatments, such studies are most readily done within the framework of large cooperative clinical trials. Such organizations provide the mechanism to test the biologic significance of pathologic findings that can then be used in the ideal classification.
Explore the source record for details and available documents.