Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0027651 (tumor)
 685,946 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Choroid plexus carcinoma(CPC) is a rare intracranial neoplasm that usually arises in the supra-tentorial region of infants. We report an adult case of CPC that arose in the foramen Luschka. A 61-year-old woman presented with a 10-year history of dysarthria. CT showed an iso- to slightly high density mass in the left foramen Luschka. The tumor appeared as a low- to iso-intensity area in T1-weighted MR images, and as an iso- to high-intensity area in T2-weighted images. The tumor showed homogeneous enhancement with the administration of contrast medium. Imaging findings were non-specific and the differential diagnosis was difficult.
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PMID:[Choroid plexus carcinoma of the foramen Luschka: a case report]. 1293 52

Three patients, two women aged 72 and 45 years, and a man aged 80 years, presented with transient neurological deficits due to a brain tumour, a glioblastoma multiforme and two meningiomas respectively. A fourth patient, an 84-year-old man, had a transient ischaemic attack (TIA) with a meningioma as an incidental finding. The first woman had normal CT findings, but MRI revealed the neoplasm. Symptoms included motor loss, sensory disturbances, dysphasia and dysarthria, lasting from 30 seconds up to 10 minutes. The first two patients had surgery; the first one later died when the tumour recurred. The other two patients still exhibit a spontaneous recovery. Of all patients with a clinical presentation of a TIA, 0.4-1% harbour a brain tumour. Clinical symptoms do not distinguish 'transient tumour attacks' from TIAs with a primarily vascular origin. Transient tumour attacks are mainly seen with meningiomas, and to a lesser extent with high-grade gliomas. Changes in intracranial pressure leading to focal ischaemia may explain the occurrence of this phenomenon. A part from intracerebral tumours, non-vascular entities mimicking TIAs can also be seen with demyelinating processes, metabolic disturbances, epilepsy or migraine. Brain imaging is always required in patients with transient neurological deficits. A CT scan may provide false-negative results and in case of doubt, MRI is the preferred diagnostic tool.
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PMID:[Not every TIA is primarily vascular]. 1500 60

In the present study, a rare autopsy case of primary squamous cell carcinoma of the brain is described. The patient was a 49-year-old man who showed brainstem symptoms and signs. These included oculomotor, abducens and facial palsies, dysphagia, dysarthria, and long tract signs such as quadriplegia with Babinski's signs during the 3-year and 6-month course of his illness. Neuropathologically, poorly differentiated squamous cell carcinoma was seen in the pons, medulla oblongata, part of the midbrain and spinal cord, the base of the cerebellum, the hypothalamus, the optic chiasm, and the left parahippocampal gyrus. The base of the pons and medulla oblongata were extensively destroyed by tumor cells. The relevant literature regarding primary squamous cell carcinomas of the brain was reviewed, and the characteristic features of this rare condition were discussed.
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PMID:Primary squamous cell carcinoma of the brain. A rare autopsy case. 1457 Feb 92

Paraneoplastic syndrome (PNS) with two distinct neurological features was reported in a 50-year-old man who presented initially with vertigo, ataxia, dysarthria, tremor, confusion, urinary retention and hypotension. Pulmonary X-ray findings, class IIIb sputum cytology, and positive anti-Hu antibody established the diagnosis of PNS associated with small-cell lung cancer (SCLC). Two cycles of combined chemotherapy resulted in shrinkage of the lung tumor together with complete recovery of neurological symptoms and disappearance of anti-Hu antibody. Relapse of SCLC 4 months later with re-appearance of anti-Hu antibody required additional chemotherapy and irradiation. Eight months later, when multiple liver metastasis of SCLC was noticed, muscular weakness with positive waxing phenomenon compatible with Lambert-Eaton myasthenic syndrome (LEMS) developed. Postmortem examinations revealed residual SCLC in the primary lung, and massive liver metastasis with generalized lymph node involvement, but no tumors in the CNS. In the cerebellum, there was a slight loss of Purkinje cells with torpedo formation but without apparent lymphocytic infiltration. The present PNS was unique in that the relapse of SCLC was accompanied by the appearance of anti-Hu antibody, and that initial signs of brainstem-cerebellar symptoms, encephalopathy and autonomic failure were replaced by LEMS coinciding with the tumor recurrence.
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PMID:Anti-Hu paraneoplastic syndrome presenting with brainstem-cerebellar symptoms and Lambert-Eaton myasthenic syndrome. 1457 Feb 93

We report a case of paraneoplastic cerebellar degeneration (PCD) associated with adenocarcinoma of the esophagus and anti-Yo antibodies in a male patient. The patient presented with progressive ataxia, dysarthria, and significant weight loss. Extensive work-up suggested paraneoplastic neurologic syndrome. A wide search for a cancer was undertaken and a small mass was identified in the distal esophagus on upper endoscopy. Biopsies of this lesion revealed well-differentiated invasive adenocarcinoma of the esophagus. The endoscopic ultrasound staged the tumor as T3N1M0. Despite trials of multiple therapeutic modalities, the patient's cerebellar dysfunction progressed. This is only the second report of PCD caused by esophageal adenocarcinoma and the fourth report of anti-Yo antibodies occurring in a male patient.
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PMID:Anti-Yo antibody-mediated paraneoplastic cerebellar degeneration in a man with esophageal adenocarcinoma. 1460 Jun 54

Paraneoplastic neurologic syndromes are disorders of the nervous system function caused by cancer but not due to metastatic disease, vascular or metabolic deficits, infections, nutritive deficiency, nor side effects of antineoplastic drugs or irradiation. Immunologic factors probably play the crucial role in the pathogenesis of paraneoplastic neurologic syndromes, but nonimmunologic mechanisms that include metabolic abnormalities and competition for substrate are also involved. Paraneoplastic cerebellar degeneration most commonly occurs in the setting of gynecologic cancers, but it accompanies the small-cell lung cancer too. Other tumors are infrequently associated with cerebellar degeneration. Several paraneoplastic antibodies have been identified in patients with paraneoplastic cerebellar degeneration. Their association with particular cancers may help identify an occult lesion. Anti-Yo antibodies are directed against Purkinje cell antigens and occur in patients with cerebellar degeneration who have breast cancer or gynecologic tumors. A target antigen of anti-Yo antibody is CDR2 protein that is normally expressed only in the brain and testis. Patients with paraneoplastic cerebellar degeneration present with dizziness, nausea and vomiting followed by gait instability, diplopia, gait and appendicular ataxia, dysarthria and dysphagia. Therapeutic options include tumor excision, chemotherapy and/or irradiation, and adjuvant therapy with glucocorticoids, immunoglobulins and plasmapheresis. The role of plasmapheresis in the treatment of paraneoplastic cerebellar degeneration is still uncertain. Reports of its efficacy are anecdotal. We present patient with paraneoplastic cerebellar degeneration with positive anti-Yo antibodies and tumor of the ovaries whose neurologic status significantly improved after four daily plasmaphereses, which was accompanied by a fourfold decrease in the anti-Yo antibodies titer. Further investigations are needed to define a protocol for plasmapheresis in the treatment of patients with paraneoplastic syndromes.
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PMID:[Importance of plasmapheresis in the treatment of paraneoplastic cerebellar degeneration]. 1512 96

The purpose of this case report is to record the unusual combination of occipital neuralgia and hypoglossal nerve palsy causing dysarthria, dysphagia, and unilateral weakness of tongue protrusion, with no other neurological findings. The cause was a discrete tumor in the clivus and the right occipital condyle. Following surgical resection of the tumor, dysarthria and dysphagia persisted. These improved with therapy by a speech therapist, but deviation of the tongue persisted on protrusion. No similar case reports were found in the literature. In addition, the tumor was an unusual one, a chondromyxoid fibroma (CMF); these tumors uncommonly involve the skull base.
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PMID:Occipital neuralgia and twelfth nerve palsy from a chondromyxoid fibroma. 1521 23

A 61-year-old man had been treated for malignant fibrous histiocytoma with the pulmonary and the lymph node metastasis in the department of orthopedics in our hospital. He was admitted to our department because of an acute onset of conscious disturbance and non-fluent aphasia. Diffusion-weighted imaging (DWI) showed high signal intensity areas in the bilateral cerebella, thalami and posterior lobes. T2WI did not show any mass effects. Enhanced CT did not reveal any enhanced lesion. He was diagnosed as having cerebral embolism, and his conscious disturbance was improved after medication. Eight weeks later, he presented dysphagia, dysarthria, and ataxia in his extremities. DWI showed multiple lesions of low signal intensity located at the identical place where had showed high signal intensity in the initial DWI. T2WI showed high signal intensity area with mass effect. It was indicated that cerebral metastasis might grow after tumorgenic embolism. This is a rare case that tumor emboluses were developed to the metastatic brain tumors.
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PMID:[A case of malignant fibrous histiocytoma with metastatic brain tumors after tumorgenic embolism]. 1538 7

The clinical efficacy of gefitinib, a tyrosine kinase inhibitor of epidermal growth factor receptor (EGFR), on brain metastases (BMs) from non-small-cell lung cancer (NSCLC) was evaluated. Fifteen patients with recurrent NSCLC with metastasis to the brain were treated with gefitinib. The objective tumor response rate (60%; 9 of 15 patients) for BM was the same as for primary tumors. The median time to response of BM was 26 days. In 8 of 9 patients who exhibited partial response in the thoracic lesion, BM showed dramatic regression, including 1 complete response. One patient with stable primary tumor also exhibited partial response in BM with this monotherapy. Brain metastasis-related neurologic symptoms such as hemiparesis, dysarthria, dysphagia, and vertigo improved or disappeared with the objective response of BM as confirmed by magnetic resonance imaging. Central nervous system toxicities were not observed during the treatment. Four of the 9 BM responders are still under treatment with neither adverse events nor disease progression. Two discontinued the treatment because of severe hepatic toxicity and 3 died because of acquired resistance in pulmonary lesions, even though partial response was observed in the BMs. Finally, median duration of response of BM was 8.7 months and median overall survival was 8.3 months (range, 1.8 to > 15.7 months). Molecular targeted therapy against EGFR could be an option for the treatment of BM from NSCLC refractory to conventional chemotherapy plus radiation therapy because it has demonstrated a distinct therapeutic potential against BM compared with primary lung tumor and extracranial metastases.
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PMID:Gefitinib in patients with brain metastases from non-small-cell lung cancer: review of 15 clinical cases. 1547 98

Opsoclonus myoclonus with ataxia (OMA) is a rare neurological disorder. The syndrome is characterized by involuntary, conjugate, multidirectional eye movements accompanied by involuntary movements of limb or face, and sometimes ataxia, dysarthria, irritability, dementia, altered level of consciousness and even death. OMA is associated with various etiologies including infectious, toxic, drug-related, vascular and paraneoplastic conditions. Paraneoplastic opsoclonus myoclonus with ataxia (POMA) is more common in patients over 40 years of age and is usually associated with lung (especially small cell), breast and ovarian cancer but has also been reported with many other cancers. The syndrome is thought to be mediated by autoantibodies directed against onconeural antigens that are expressed by the tumor as well as by neurons. Studies from several laboratories were able to demonstrate a role for the cellular response in the pathogenesis of POMA. The results for treatment of this syndrome have been disappointing, although aggressive multimodality immunosuppressive treatments have been used. This is a case study of a patient with POMA who clearly demonstrates the difficulties in the diagnosis and treatment of this syndrome.
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PMID:[Opsoclonus myoclonus with ataxia]. 1584 53


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