Biomedical subjects
Publications and source records attributed to N de Tribolet.
A case of a spontaneous trigemino-pontine pneumocephalus in a 25-year-old man without any known risk factors is described. Other cases of spontaneous pneumocephalus in the literature are briefly reviewed.
A rare case of Turcot's syndrome is reported in a long-time survivor of glioblastoma multiforme. The patient was treated for his tumor in 1976 with macroscopically complete surgical resection and radiotherapy consisting of 60 Gy to the tumor bed and 40 Gy to the whole brain. Five years later, in 1981, he developed adenocarcinoma of the colon Dukes Stage B which was successfully treated at another hospital by surgery alone. In 1990, he presented with multiple colon polyps and adenocarcinoma Dukes Stage A. For more than 15 years, the patient has been afflicted with cystic and conglobate acne. Possible mechanisms and treatment with 13-cis retinoic acid are discussed.
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A case of intracranial extracerebral cavernous hemangioma of the middle fossa in a woman who suffered from a multiple sclerosis, is reported. Appearance of a lateral hemianopia suggested an other disease than multiple sclerosis to explain this symptom. Intracranial extracerebral cavernous hemangioma is a rare tumor reported more often in the middle fossa than in other sites. It usually produces symptoms by compression of nearby structure. Diagnosis is based on neuroradiological examination and we describe the MRI aspect. It is difficult to remove because of massive hemorrhage.
The first part of this work, published in 1988, included 25 patients who had computed tomographic (CT) scans without contrast enhancement and plain x-rays of the lumbar spine before, 1 week after, and 6 to 7 weeks after a successful operation for lumbar disc herniation. The present study extends the follow-up period to 3 years in 19 of the 25 original patients. Clinical examinations, lateral plain x-rays, and CT scans without contrast enhancement of the operated disc were repeated. The results indicate a decrease or even a disappearance of the hyperdense extradural material thought to represent fibrosis. An image suggestive of persistent disc herniation was still present in 5 of 8 patients with this finding on early postoperative CT scans. Persistent intradiscal gas was seen in nearly half of the patients. Total normalization of the posterior extraspinal structures was the rule. There was no correlation between CT appearance and residual complaints of the patients. CT scans without contrast enhancement may be sufficient to guide the surgeon in postoperative patients with massive signs and symptoms of recurrent root compression in whom a second operation is indicated on clinical grounds. In all other cases, myelography followed by CT scans is considered appropriate to investigate failed back surgery syndrome.
An unusual association of a meningioma and an arteriovenous malformation is reported. A 68-year-old man developed left homonymous hemianopsia, left hemiparesis, and gaze palsy. Magnetic resonance imaging showed a right occipital mass lesion containing multiple signal-void areas with tubular and honeycomb appearance, suggesting a marked vascular component. An angiogram showed abnormal vasculature in the mass supplied by the posterior cerebral artery and a dural arteriovenous malformation on the tentorium. Neuropathological examination after total removal of the mass revealed a meningothelial meningioma including major portions of an arteriovenous malformation that extended from the dura and leptomeninges, through the meningioma, and into the occipital lobe, where the tumor was located.
This study demonstrates interleukin 6 (IL-6) production and release by human glioblastomas. Twenty glioblastoma cell lines were tested for IL-6 bioactivity using an IL-6-dependent cell line (7TD1). All of the lines tested with one exception (LN-229) constitutively released IL-6. A significant induction of IL-6 production and secretion was observed when LN-229 cells were treated with interleukin 1 beta (IL-1 beta) or tumor necrosis factor alpha. Various amounts of IL-6 mRNA were found in five of six cell lines tested. IL-6 mRNA was detected in line LN-229 only when the cells were treated with IL-1 beta or tumor necrosis factor alpha, confirming the bioassay data. Glioblastoma cells also produce IL-6 in vivo. (a) IL-6 activity was detected in 11 of 13 cerebrospinal fluids and five of five tumor cyst fluids. (b) IL-6 mRNA was found in four of four tumors. (c) Immunohistochemical analysis showed IL-6 within the tumor cells in 15 of 20 glioblastoma sections. In conclusion, biologically active IL-6 is released by almost all glioblastomas both in vitro and in vivo. The elevated levels of serum acute phase proteins and immune complexes found in glioblastoma patients may be the result of this secretion.
Thoracic discal hernia is a rare condition which in most cases is associated with radiologic calcifications of the disc, the nature of which remains unclear. However, it is generally accepted that the calcifications consist of apatite. In our observation a calcified discal hernia caused progressive paraparesis. The fact that it occurred in a patient with diffuse chondrocalcinosis suggests that the discal calcification could be due to calcium pyrophosphate deposition.
In summary, many actual interactions between tumors in the CNS and the immune system have been demonstrated. The normal brain does not possess a lymphatic system and is partially hidden from the systemic immune system by the BBB, furthermore brain cells do not express MHC antigens which are necessary for the initiation of an immune response. In pathological conditions however, immunocompetent cells may find their way through transformed endothelial cells. Microglia and astrocytes may function as antigen presenting cells. Glioma cells when stimulated by cytokines such as IFN gamma can be induced to express MHC class I and class II antigens, thus making them more susceptible to an immune attack. In addition glioma cells are capable of secreting several cytokines including IL 1, IL 3 and IL 6 also involved in the generation of an immune response. Indeed, a functional analysis of lymphocytes infiltrating gliomas has revealed the accumulation at the tumor site of cytotoxic T lymphocytes as well as NK cells. However host-immune responses against gliomas seem to be weak in comparison to other cancers. Glioma cells are known to secrete TGF beta 2 and PGE 2 which may in part be responsible for this lack of immune response, thus shielding themselves from immune attack. In order to be recognized by the immune system the tumor cells must express TAA in addition to MHC antigens, and such TAA have been identified by MAbs. These MAbs can be used for "targeted" therapy when coupled to toxic agents or radionuclides. Preclinical studies have shown that, after intravenous or intracarotid injection, there is specific accumulation of the MAb in the tumor but in insufficient amounts for therapeutic use. The relatively small amount of MAb binding to the tumor in vivo can be due to several factors: not all the cells in a single tumor express a given tumor-associated antigens, the MAb may have a low affinity for the antigen, the BBB may hinder the passage of the MAb. Attempts have been made to overcome these drawbacks by opening the BBB for example. In addition MAbs can readily be used for the treatment of carcinomatous meningitis. There has been little success in the development of immunotherapy with IFN beta 1 and even less with adoptive immunotherapy using LAK cells plus IL 2. TIL as well as LAK cells can be expanded in vitro with IL2 and it is feasible to reinject these cells into the tumor site.(ABSTRACT TRUNCATED AT 400 WORDS)
It has been demonstrated that the epidermal growth factor receptor (EGFR) gene, the normal human counterpart of the viral erb-B oncogene is amplified and overexpressed in over 50% of human malignant gliomas (HMGs). In the present study, analysis of the immunohistological staining characteristics of 57 HMGs using an anti-EGFR monoclonal antibody (mab) showed positive staining in 65% of the tumours with large cellular and regional differences in staining pattern and intensity. Screening a smaller number of HMGs with molecular hybridization techniques revealed 10/21 glioblastomas (48%) amplified for the gene; of 11 glioblastomas studied by Northern blot hybridization, 7 tumours with gene amplification showed RNA overexpression, the remaining 4 without amplification did not. Regional differences in DNA levels were observed by Southern blot in 2 tumours: in one particular case, amplification and overexpression were found to be localized to one half of a single HMG, the other half showing neither EFGR gene amplification nor overexpression.
Glioblastoma cells constitutively produce various amounts of PGE2 (prostaglandin E2) in vitro. The amounts of PGE2 found in the conditioned medium of the glioblastoma cultures (less than 5 ng/ml) were not enough to inhibit the IL-2 (interleukin-2) activation of peripheral blood lymphocytes. However the amount of PGE2 produced by approximately 1 x 10(7) of the glioblastoma cells can be assumed to suppress the generation of IL-2-induced killing activity against glioblastoma cells.
The case of a middle-aged woman with a cavernous hemangioma of the right cavernous sinus who showed ipsilateral hemianopsia associated with contralateral blindness caused by left retrobulbar optic neuritis is presented. Total removal of the tumor was followed by recovery of the visual function of the right eye.
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A case of vagal schwannoma in the cerebellomedullary angle is reported. Preoperatively, the patient had paroxysmal episodes of postural hypotension with syncope. After total removal of the vagal tumor, her systemic blood pressure returned to normal.
Intercellular adhesion molecule-1 (ICAM-1) has recently been identified as one of the ligands for lymphocyte function-associated antigen-1 (LFA-1). Immunohistochemical staining of frozen tissue sections using the ICAM-1 antibody RR1/1 demonstrated significant levels of ICAM-1 expression on human glioblastoma cells and on intratumoural vascular endothelial cells. ICAM-1 was weakly expressed or absent from low grade gliomas and absent from normal and fetal brain. ICAM-1 expression was similar to that of MHC class II. HLA-DR antigens. Glioblastoma cell lines constitutively expressed ICAM-1 to a minimal or moderate extent. Surface antigen expression of ICAM-1 and ICAM-1-specific mRNA could be significantly increased by incubating glioblastoma cells with interleukin-1 beta (IL-1 beta), tumour necrosis factor-alpha (TNF-alpha), and interferon-gamma (IFN-gamma). IL-2, IL-4, IL-6 and transforming growth factor beta 2 (TGF-beta 2) had no significant effect on surface antigen expression. Significant enhancement of ICAM-1 expression was obtained using TNF-alpha and IL-1 beta at 1-10 U/ml and at 500 U/ml of IFN-gamma. Induction of ICAM-1 specific mRNA was observed 4 h after cytokine treatment and decreased by 24 h. Surface antigen expression of ICAM-1 increased for up to 48 h after treatment.
Human glioblastoma cells secrete factors, such as prostaglandin E (PGE) and transforming growth factor beta type 2, which are capable of suppressing several immune functions. The present study investigated the effect of PGE2 and agents known to increase intracellular cyclic adenosine monophosphate (cAMP) levels on 1) the induction of lymphokine-activated killer (LAK) cell activity from the peripheral blood lymphocytes (PBL) of both normal and glioma patients and on 2) the cytolytic activities of tumor-infiltrating lymphocytes (TIL's) isolated from malignant gliomas after expansion in vitro with interleukin-2 (IL-2). Cytolytic activity was measured against autologous and allogeneic tumor cells and the natural killer-resistant Daudi cell line. The results demonstrate that PGE2 and agents known to increase intracellular cAMP levels can significantly suppress the IL-2-dependent generation of cytolytic activity from the PBL of normal and glioma patients and from glioblastoma-derived TIL's. The inhibitory effects of these agents could not be reduced by higher concentrations of IL-2 or by cyclic guanosine monophosphate. Although the suppressive effect of PGE2 was most significant during the early stages of LAK cell generation, an inhibitory effect was still evident when PGE2 was added directly to the cytotoxicity assay. Secretion of PGE2 by glioblastoma cells in vivo may regulate both the generation of an immune response and the effectiveness of adoptively transferred immune cells.
Flow velocities (F.V.) in 65 patients admitted for subarachnoid hemorrhage (S.A.H.) were measured 4-7 times a week by Transcranial Doppler (T.C.D.). Patients were classified into 4 T.C.D. groups according to the highest mean flow velocity recorded in the M.C.A. during hospitalization: Group 1 (18 patients) with F.V. below 100 cm/s (normal), group 2 (19 patients) with F.V. between 100-150 cm/s (starting spasm), group 3 (23 patients) with F.V. between 150-200 cm/s (major spasm) and group 4 (5 patients) with F.V. over 200 cm/s (critical spasm). Based on clinical, radiological and ultrasound data as well as patient outcome (good results with no specific problems or with transient deficit, permanent deficit and pre- or postoperative death), the authors analyse the value of T.C.D. in the evaluation of vasospasms following S.A.H. The review involves 49 patients with surgically treated aneurysms (including two associated A.V.M.s), 9 patients who had suffered a S.A.H. of unknown origin and 7 patients who had died prior to surgery. T.C.D. is a non-invasive method of following post-S.A.H. spasms and the close correlation between the angiography and the T.C.D. makes pre-operative control angiographies unnecessary. A correlation between clinical status and T.C.D. was only observed in extreme cases where F.V. exceeded 200 cm/s or increased by 100 cm/s or more within 3 days (6 patients out of 65). M.C.A. spasm can, however, be underestimated by the T.C.D. approach in cases where there is an associated spasm of the infraclinoidal carotid artery. In these cases, classical Doppler evaluation of the cervical portion of the I.C.A. is indicated.(ABSTRACT TRUNCATED AT 250 WORDS)
Several established human glioma cell lines have been previously shown to express the common acute lymphoblastic leukemia antigen (cALLa, CD 10), an important marker in the diagnosis of human acute lymphocytic leukemia (ALL). The amino acid sequence of cALLa is identical to that of neutral endopeptidase (NEP,E.C.3.4.24.11), and cALLa expressed on leukemia and melanoma cell lines is enzymatically active NEP. In the present study, we investigated whether cALLa expressed on glioma cell lines is active NEP. We detected cALLa on 10 out of 13 glioma cell lines using 2 different anti-cALLa MAbs (A12-G4 and FAH99). NEP antigen, as detected by immunostaining with an anti-NEP MAb (135A3), was expressed on the same 10 lines. cALLa-positive, but not cALLa-negative cell lines displayed an endopeptidase activity. This activity could be blocked by phosphoramidon, a specific inhibitor of NEP. Furthermore, mRNAs hybridizing to an NEP-specific probe were present in cALLa-positive glioma cells but not in cALLa-negative cells. Taken together, the results provide strong evidence that cALLa-positive glioma cell lines express endopeptidase activity on the cell surface.