Nervous system neoplasms.
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Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Brain tumor development and their recurrence are accompanied by an increase in IgG levels in liquor as well as in the number of circulating immunocomplexes and by the presence of blockage factors in liquor. The data presented in the paper, on the whole, illustrate the development of autoimmune reactions, which happen to be mechanisms involved in the pathogenesis of brain tumor growth and recurrence. Surgical removal of tumor is followed by a reduction in the rates of IgG synthesis.
Sixty human nervous system neoplasms were examined by immunohistochemistry using a monoclonal antibody against neurofilament triplet proteins. Only those of neuronal origin had tumor cells with intracytoplasmic, immunoreactive neurofilament triplet proteins. However, not all such neoplasms contained labeled tumor cells. Benign or differentiated neuronal tumors more often contained labeled cells than malignant, less differentiated neoplasms of the neuron series. We conclude that anti-neurofilament monoclonal antibodies are useful reagents for the evaluation of human neoplasms.
Metastatic neoplasms to the central nervous system are often encountered in the practice of surgical neuropathology. It is not uncommon for patients with systemic malignancies to present to medical attention because of symptoms from a brain metastasis and for the tissue samples procured from these lesions to represent the first tissue available to study a malignancy from an unknown primary. In general surgical pathology, the evaluation of a metastatic neoplasm of unknown primary is a very complicated process, requiring knowledge of numerous different tumor types, reagents, and staining patterns. The past few years, however, have seen a remarkable refinement in the immunohistochemical tools at our disposal that now empower neuropathologists to take an active role in defining the relatively limited subset of neoplasms that commonly metastasize to the central nervous system. This information can direct imaging studies to find the primary tumor in a patient with an unknown primary, clarify the likely primary site of origin in patients who have small tumors in multiple sites without an obvious primary lesion, or establish lesions as late metastases of remote malignancies. Furthermore, specific treatments can begin and additional invasive procedures may be prevented if the neuropathologic evaluation of metastatic neoplasms provides information beyond the traditional diagnosis of "metastatic neoplasm." In this review, differential cytokeratins, adjuvant markers, and organ-specific antibodies are described and the immunohistochemical signatures of metastatic neoplasms that are commonly seen by neuropathologists are discussed.
Leptomeningeal dissemination of primary CNS tumors varies widely by histologic subtype. In certain tumors including medulloblastoma, ependymoma, germ cell tumors, and primary CNS lymphoma, seeding of the cerebrospinal fluid space is a critical factor in determining stage, prognosis and appropriate therapy. Other tumor types, such as glioma, may have radiographic evidence of leptomeningeal metastases without clear impact on prognosis or therapy.
The Norwegian Cancer registry includes reports on 8,933 cases of primary central nervous system neoplasms diagnosed in the period 1955-1984. Before submitting this data set to epidemiological analysis, errors were searched out and subsequently corrected, and a quality control was performed. First, seven categories of neoplasm records likely to be faulty were defined. In this way 109 cases (1.2% of the total) were identified for extensive study. Minor or major errors were found and corrected in 86 cases. The main source of error was misinterpretation of data by cancer registry staff (67 out of 109 cases). The second approach was to evaluate the quality of the corrected data set by a random draw of 300 cases. Errors concerning total incidence rates and rates for main groups of gliomas, meningiomas and neurilemmomas represented 0.3% of the total, and altogether 9.3% of errors of varying severity were revealed. The series is discussed with regard to prerequisites for serving as reliable data on CNS neoplasm epidemiology. The results indicate that the data from the Norwegian Cancer Registry is sufficiently valid for a thorough study of CNS neoplasms.
Magnetic resonance evaluation of central nervous system neoplasms has improved tremendously since the introduction of gadolinium-based contrast agents. The optimal application of these agents in clinical imaging, however, has not been well established. The article discusses the recent application of these agents to a number of intracranial neoplasms, including metastases, gliomas, pituitary adenomas, and acoustic neurinomas/cerebellopontine angle tumors.
Studies of multiple primary neoplasms and their relation to the nervous system should consider two important principles: 1) neoplasms of the nervous system have certain unusual features that distinguish them from tumors occurring elsewhere in the body; and 2) there is good evidence that the various histologic types of nervous system tumors should be regarded as separate diseases. The association of nervous system neoplasms and tumors of other sites may occur in patients with phacomatoses or particular genetic syndromes. In addition, certain nervous system neoplasms may be multicentric in origin. Retinoblastoma and osteosarcoma occur together in the same patient more often than expected by chance, as do meningioma and breast cancer. These relationships are important in that they serve to identify the high risk patient, may provide etiologic clues, may point to the presence of genetic syndromes, and may highlight sites in which subsequent tumors are most likely to develop.
Primary melanocytic neoplasms of the central nervous system (CNS) consist of a spectrum ranging from well-differentiated melanocytoma to its overtly malignant counterpart, melanoma. Diagnostically difficult intermediate lesions lie between these extremes. Clinicopathologic features of 33 cases were studied to define histologic appearances, diagnostic criteria, and the clinical behavior of lesions along this spectrum. Seventeen cases were well-differentiated, solitary leptomeningeal tumors classified as melanocytomas. They contained variably pigmented melanocytic cells arranged in tight nests, sheets, or fascicles. Mitotic rates ranged from zero to one per 10 high-power fields (HPFs), with most having zero per 10 HPFs. All tumors were immunoreactive for HMB-45 and S-100 protein and negative for epithelial membrane antigen. MIB-1 staining was low (<1-2%). Nuclei were regular, often with small, eosinophilic nucleoli. These lesions arose predominantly in the spinal canal (65%) in patients ranging in age from 17 to 73 years. None recurred after surgical resection. In contrast to these benign lesions, there were 13 cases with histologic and cytologic features consistent with those of malignant melanoma. These cases contained larger, cytologically atypical, pigmented tumor cells growing in loose nests or sheets, often with CNS invasion or necrosis. Some contained bizarre, pleomorphic nuclei; others were densely cellular and mitotically active, but less pleomorphic. Mitotic rates (mean, 5.7 per 10 HPFs) and MIB-1 labeling indices (mean, 8.1%) were higher than those of melanocytomas. Melanomas occurred at spinal (38%), posterior fossa (38%), and supratentorial (23%) levels in patients ranging in age from 15 to 71 years. After resection, 8 of 13 lesions recurred, with four being fatal (mean survival, 14 months). Of five totally resected melanomas, four did not recur (mean follow-up, 26 months). Three intermediate-grade melanocytic tumors could not be classified as melanocytoma or melanoma. All showed sheetlike growth patterns, microscopic CNS invasion, and occasional mitoses. MIB-1 staining ranged from 1% to 4%. One tumor recurred after 17 months; one patient was lost to follow-up after 5 months; and the third died after surgery. Although melanocytic tumors represent a spectrum of lesions, certain histopathologic features are helpful in predicting biologic behavior.
The gastrointestinal autonomic nerve tumors (GAN tumor) are uncommon stromal tumors of the intestinal tract and retroperitoneum. The distinction of GAN tumors from other gastrointestinal stromal tumors is based on electron microscopic findings. However further study of additional cases is needed to fully characterize both their gross and microscopic features and to further characterize the natural history of such tumors. In the present study we report two cases of GAN tumor that arose from the stomach and small intestinal with different prognostic evolution in two patients of 73 and 65 years old. They were both treated by surgery, but only one case was successful. In addition patient 1 aged 73, died 11 months after surgical treatment with liver metastases on CT. scan. Patient 2, is clinically well five years after surgical treatment.
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There is concern about possible association between PUVA treatment and an increased risk of noncutaneous cancer. An alteration in the risk of cancer among persons with psoriasis has also been postulated. To test this hypothesis, for nearly two decades we have prospectively followed 1380 patients who first began PUVA treatment for psoriasis in 1975-1976. We compare the risk of noncutaneous cancer in our cohort with that expected based on general population incidence rates. The overall risk of noncutaneous cancer was nearly identical to that expected in general population. For three separate sites, we noted significant increases: thyroid cancer (RR = 3.57, 95% CI = 1.16-8.34), breast cancer (RR = 1.81, 95% CI = 1.19-2.64), and central nervous system neoplasms (RR = 2.80, 95% CI = 1.13-5.57). Since 1987, however, the risk of central nervous system neoplasms has not been elevated (RR = 0.00, 95% CI = 0.00-3.35) and the relative risk of breast cancer was lower than in the prior decade and not statistically significant. There was no association between higher levels of exposure to PUVA and the risk of any of these cancers. We did not detect any significant increase in the risk of lymphoma or leukemia. Our study does not support the hypothesis that long-term PUVA treatment increases the risk of noncutaneous cancer.