Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0017638 (glioma)
 30,880 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

With the aim of finding characteristics pointing to the primary site, computed tomography examination from 9 patients with primary brain malignant lymphoma (non-Hodgkin's lymphoma originating in the central nervous system, NHL-CNS) (5 single, 4 multiple lesions) were analyzed. The tumors were usually situated in the basal ganglia, corpus callosum, or cerebellum and were always in contact with either the ependyma of the ventricles or the subarachnoid space. Tumors with widespread infiltration of white matter surrounding the ventricles were characteristic of NHL-CNS. Microscopic examination of 3 autopsy cases revealed infiltration of the subependymal layer of the lateral ventricles and the third and fourth ventricles by lymphoma cells. The entire extent of the choroid plexus was invaded by tumor cells. There were multiple foci of similar cells invading the periventricular white matter. The subarachnoid space was filled with lymphoma cells. In many areas the Virchow-Robin spaces and pial-glial membranes were disrupted, and invasion of the underlying gray matter by tumor cells was seen. The ultrastructure of the blood vessels of NHL-CNS was compared with those in glial, nonglial, and metastatic brain tumors. The essential feature in NHL-CNS was fenestrated vessels. They resembled the blood vessels found in nonglial and metastatic brain tumors, but were distinctly different from those seen in glial tumors with nonfenestrated vessels. Although the following scheme in proposed with reservations, it could account for the sites of origin of NHL-CNS: lymphocytes located in the choroid plexus stroma or the subarachnoid space are activated, caused to proliferate, and finally become neoplastic.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Sites of origin of primary intracerebral malignant lymphoma. 275 72

Twenty two patients with meningeal neoplasia were treated with biweekly combination intraventricular chemotherapy using methotrexate, cytosine arabinoside, and thiotepa. Patients with the following malignancies were included: breast cancer, ten patients; lung cancer, seven; non-Hodgkin's lymphoma, two; malignant melanoma, one; transitional cell carcinoma of the bladder, one; and malignant glioma, one. Eight of 22 patients (36%) had a Karnofsky performance status of less than 50%. Eleven of 22 patients received radiotherapy to symptomatic areas, and seven received systemic chemotherapy in addition to combination intraventricular therapy. Patients were evaluated for both toxicity and response to therapy. Myelosuppression was the major toxic condition and occurred in 17 of 22 patients (77%). Ten patients (45%) had a nadir WBC count of less than 1000/microL or a platelet count of less than 25,000/microL. No patient achieved a complete response (CR), although nine patients (41%) had partial responses (PRs) lasting 4 to 24 + weeks. Median survival for the entire group was 10 weeks (range, 6 to 24+ weeks). In this small group of patients, simultaneous triple-drug intraventricular chemotherapy caused unacceptable myelosuppression without increasing the response rate, response duration, or survival when compared with single-agent methotrexate and radiotherapy.
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PMID:Combination intraventricular chemotherapy for meningeal neoplasia. 307 22

The alpha-interferons have been explored in a wide variety of clinical applications in cancer. Significant activity has been demonstrated in AIDS-related Kaposi's sarcoma, ovarian carcinoma, bladder carcinoma, malignant glioma, non-Hodgkin's lymphoma, chronic granulocytic leukemia, the carcinoid syndrome and hairy cell leukemia. Although these leads are promising, the research has only just begun.
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PMID:Alpha interferon: a look to the future. 329 35

The familial occurrence of gliomas, in the absence of well-defined neurological tumor syndromes such as the neurofibromatoses, is uncommon. We present a family of ten children in which the four eldest suffered from gliomas. Three of these siblings had histologically verified glioblastoma multiforme, and one patient also had an intestinal non-Hodgkin's lymphoma, but there were no stigmata or family history of a neurological tumor syndrome. Cytogenetic studies of the proband revealed a normal karyotype. Molecular genetic analysis of the proband's glioblastoma revealed two mutations in the p53 tumor suppressor gene, but these were not present in the germline DNA, mutations were not detected in the MTS1 gene in the tumors or in the germline DNA. These findings suggest that a genetic factor may be responsible for the clustering of glial tumors in this family, but it is unlikely that the genetic alteration is mutation of the p53 gene. The data are discussed in light of the literature on familial brain tumors.
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PMID:Glioblastoma multiforme in four siblings: a cytogenetic and molecular genetic study. 759 55

Animal models of leptomeningeal metastasis (LM) should give insight into pathophysiological mechanisms and allow to evaluate new treatments including their neurotoxicity. Syngeneic models use tumor cells of mouse, rat, rabbit or guinea pig origin. Allogeneic models usually rely on human tumor cells injected into nude mice or rats. A review of the literature revealed 2 (4) different glioma, 3 medulloblastoma, 3 (3) carcinoma, 3 (1) melanoma, 1 rhabdomyosarcoma, 2 (8) leukemia and 2 (2) non-Hodgkin's lymphoma allogeneic (syngeneic) models of LM. These models have been used to study the evolution of LM and to evaluate systemic or intrathecal chemotherapy, intrathecal immunotherapy (interleukin-2, interferon-beta, uncoupled, toxin- or radionuclide-conjugated antibodies), and recently gene therapeutic approaches. On the whole, pathophysiological, therapeutic and neurotoxic findings have been well transferable to the clinical situation. Therefore, it seems rational to preclinically test new treatments in an appropriate animal model of LM before using them in patients.
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PMID:Animal models of leptomeningeal metastasis. 969 72

The PTEN gene is involved in 10q23 deletions in several types of cancer, including glioma, melanoma, endometrial and prostate carcinomas. The PTEN gene product is a dual-specificity phosphatase with putative tumor suppressor function. Deletions and rearrangements of 10q22-25 have been reported in approximately 5%-10% of non-Hodgkin's lymphomas (NHLs), raising the possibility of PTEN involvement in these tumors. In order to address this question, we analyzed a panel of NHLs (n = 74) representative of the main histologic subtypes for mutations and homozygous deletions of PTEN. We report somatic coding/splice site mutations in 20% (2 of 10) of Burkitt's lymphoma cell lines and in 3% (2 of 64) of primary NHL cases analyzed. No homozygous deletions were found in these tumors. Interestingly, this study showed that cytogenetically characterized NHL cases (n = 6) with 10q22-q25 abnormalities displayed neither biallelic deletions nor mutations of PTEN. These results suggest that a tumor suppressor gene distinct from PTEN may be involved in 10q deletions in this subgroup of NHL cases.
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PMID:Analysis of PTEN mutations and deletions in B-cell non-Hodgkin's lymphomas. 1009 30

Data from the annual survey on transplant activity 1997, collected from 457 transplant teams in 31 European countries by the European Group for Blood and Marrow Transplantation (EBMT) were used to describe current status and to assess relative and absolute changes in indication, donor type and stem cell source compared to 1991. A total of 16950 patients were reported to have a first blood or marrow transplant in 1997, a total of 18 923 procedures, including re- and double transplants were performed. Of the 16950 first transplants, 4751 (28%) were allogeneic, 12199 (72%) autologous transplants. Of the autologous transplants, 829 (7%) were bone marrow derived, 11370 (93%) from peripheral blood stem cells or combined bone marrow and peripheral blood stem cell transplants. Of the allogeneic transplants, 3311 (70%) were bone marrow, 1440 (30%) were peripheral blood stem cell transplants. In 1991, the respective figures were 2175 allogeneic (44%) and 2786 (56%) autologous transplants, more than 90% of the autologous, all allogeneic transplants bone marrow derived. Main indications in 1997 were leukemias with 5253 transplants (31%), 70% allogeneic; lymphomas with 6773 transplants (40%), 94% autologous; solid tumors with 4154 transplants (24%), 99% autologous; non-malignant disorders with 770 transplants (5 %), 85 % allogeneic. There was an absolute increase of 11971 transplants since 1991. An increase was observed in all disease categories. Marked differences were found, when the relative increase index (RII) for specific disease categories over time was analyzed. In allogeneic transplants, relatively more transplants were performed in 1997 for acute myeloid leukemia beyond 1st complete remission (RII 1.28), myelodysplastic syndromes (RII 1.58), chronic lymphocytic leukemia (RII 1.33) and non-Hodgkin's lymphoma (RII 1.58). For autologous transplant indications, a high relative increase index was observed in myelodysplastic syndromes (RII 3.77), in multiple myeloma (RII 2.12) and carcinoma of the breast (RII 6.37) with a relative decrease in leukemias (RII 0.39) and certain solid tumors such as glioma (RII 0.27) and neuroblastoma (RII 0.46). These data present the current status of blood and marrow transplantation in Europe. They show the change from bone marrow to blood as stem cell source and highlight shifts in indication. They provide a basis for patient counselling and health care planning.
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PMID:Blood and marrow transplantation activity in Europe 1997. European Group for Blood and Marrow Transplantation (EBMT). 1045 92

Extended schedules of oral etoposide have been evaluated in many types of advanced cancer. In addition to their use in the common solid tumours, extended schedules have been employed in Kaposi's sarcoma (both AIDS-related and endemic types), medulloblastoma, glioma, and hepatocellular carcinoma. Single agent activity was demonstrated in all of these tumour subtypes. For patients with carcinoma of unknown primary site, we have recently incorporated a 10-day oral etoposide schedule into a combination regimen that also includes paclitaxel and carboplatin. With this regimen we achieved a 47% response rate in a group of 53 evaluable patients, with a median survival of 13.4 months. Patients with adenocarcinoma and poorly differentiated carcinoma of unknown primary site had comparable response rates and survival. According to a large number of clinical trials and pharmacokinetic data, a daily oral etoposide dose of 50 mg/m2 consistently produces serum concentrations >1 mg/L for several hours each day. Lower doses fail to consistently produce this serum concentration, which is considered necessary for optimum tumoricidal activity. Optimal dose duration is 10 to 14 days, particularly when combination regimens are being employed. Oral etoposide has an established role as a single agent in patients with low grade non-Hodgkin's lymphoma, Kaposi's sarcoma, and testicular cancer (if residual carcinoma is resected after first-line treatment). The optimal use of extended-schedule etoposide in combination regimens is not defined but is being evaluated in a number of etoposide-sensitive malignancies.
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PMID:Extended-schedule oral etoposide in selected neoplasms and overview of administration and scheduling issues. 1071 42

Among non-neoplastic lesions of the central nervous system, demyelinating pseudotumors of the group of acute disseminated encephalomyelitis (ADEM) most frequently occasion neurosurgical intervention for purposes of definitive diagnosis and thus enter the domain of the surgical pathologist. Typically, ADEM presents with multifocal, bilateral lesions in an asymmetrical distribution. Especially monolocular manifestations may be diagnostically challenging. Due to the acuteness of clinical symptoms and the expansive, space-occupying character of the lesions a diffuse glioma, a metastatic disease, a primary cerebral Non-Hodgkin's lymphoma, brain abscess, a parasitosis or an ischemic brain tissue necrosis may be suspected. This impression is supported by uptake of contrast-medium most pronounced at the periphery of the lesion and the subcortical location. The histomorphologic feature of relative axonal preservation in areas with acute myelin breakdown and lymphocytic infiltrates make the diagnosis of an acute primary demyelinating disease probable. A diagnosis of glioma may be prompted by the florid, cytologically atypical astrogliosis especially in intraoperative request. Based on a series of 14 cases of radiologically and bioptically documented cases of ADEM typical examples will be demonstrated and discussed.
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PMID:[Neuropathological and neuroradiological aspects of acute disseminated encephalomyelitis (ADEM)]. 1114 18

Therapeutic options for the treatment of malignant brain tumors have been limited, in part, because of the presence of the blood-brain barrier. For this reason, the Sixth Annual Meeting of the Blood-Brain Barrier Disruption Consortium, the focus of which was the "Importance of Dose Intensity in Neuro-Oncology Clinical Trials," was convened in April 2000, at Government Camp, Mount Hood, Oregon. This meeting, which was supported by the National Cancer Institute, the National Institute of Neurological Disorders and Stroke, and the National Institute of Deafness and Other Communication Disorders, brought together clinicians and basic scientists from across the U.S. to discuss the role of dose intensity and enhanced chemotherapy delivery in the treatment of malignant brain tumors and to design multicenter clinical trials. Optimizing chemotherapy delivery to the CNS is crucial, particularly in view of recent progress identifying certain brain tumors as chemosensitive. The discovery that specific constellations of genetic alterations can predict which tumors are chemoresponsive, and can therefore more accurately predict prognosis, has important implications for delivery of intensive, effective chemotherapy regimens with acceptable toxicities. This report summarizes the discussions, future directions, and key questions regarding dose-intensive treatment of primary CNS lymphoma, CNS relapse of systemic non-Hodgkin's lymphoma, anaplastic oligodendroglioma, high-grade glioma, and metastatic cancer of the brain. The promising role of cytoenhancers and chemoprotectants as part of dose-intensive regimens for chemosensitive brain tumors and development of improved gene therapies for malignant gliomas are discussed.
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PMID:Importance of dose intensity in neuro-oncology clinical trials: summary report of the Sixth Annual Meeting of the Blood-Brain Barrier Disruption Consortium. 1130 17


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