Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0017636 (glioblastoma)
 18,345 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Fenestrae were found in freeze-fractured cisternae of the Golgi apparatus and endoplasmic reticulum of glioblastoma, oligodendroglioma, ependymoma, medulloblastoma, medulloepithelioma, meningioma, cerebellar sarcoma, hemangioblastoma, and chromophobe adenoma. They were about 200--400 A in diameter and often diffusely distributed or concentrated in groups in Golgi cisternae, while they were around 300--600 A in size and scattered in distribution in cisternae of endoplasmic reticulum. They appeared as conical protrusions or circular broken-off necks of face A and as circular holes on face B in tangential fractures, and as several constrictions of cisternae in cross fractures.
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PMID:Fenestrae in golgi and endoplasmic reticulum cisternae of human brain tumours. 16 55

A number of cases of multiple primary intracranial neoplasms have been reported, including tumors of neuroepithelial and mesenchymal origin. The presence of meniogioma has been reported in association with glioblastoma, oligodendroglioma, astrocytoma, and eosinophilic adenoma. This case represents a unique example of adjacent chromophobe adenoma and meningioma. The usefulness of computed tomography in the diagnosis of concomitant lesions with different density attenuations is discussed.
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PMID:Case report. Tandem lesions: chromophobe adenoma and meningioma. 61 35

The familial occurrence of brain tumors are exceedingly rare except in cases with phacomatosis. We encountered pituitary adenomas in two sisters of a family, so far presenting no evidence of multiple endocrine adenomatosis (MEA). Case 1, K. O. a 26-year-old woman was admitted to our Hospital on September 10, 1970 with visual acuity and field disturbance, irregular menstruation and acromegaly. Neurological examination: Her visual acuity was Vd 0.6 and Vs 0.3, visual field was bitemporal hemianopsia, and ther was papilledema bilaterally. She had left exophthalmos and left abducens palsy. Roentgenogram of the skull, brain scanning, cerebral angiogram, pneumoencephalogram suggested the presence of a pituitary tumor. On Sep. 17, 1970, through a left frontotemporal craniotomy the tumor was removed subtotally. The pathological diagnosis was pituitary adenoma (chromophobe). Case 2, M. T. a 31-year-old woman, sister of case 1, was admitted to the Hospital on September 19, 1973, with mild headache, left visual field disturbance and amenorrhea. She had a child, and a past history of pulmonary tbc. Neurological examination: Her visual acuity was Vd 1.2 and Vs 0.03, and visual field of the right eye was temporal lower quandrant anopsia. There was optic nerve atrophy in the left eye. Plain X-ray craniogram, brain scanning, cerebral angiogram and pheumoencephalogram suggested the presence of a pituitary tumor. On Sep. 28, 1973, a right frontal craniotomy was performed. The tumor tissue with capsule was removed subtotally. The pathological diagnosis was pituitary adenoma (mixed type). In the literatures about familial brain tumors with histological diagnosis, glioma and glioblastoma are common, meningioma is relatively rare. Pituitary adenoma with no evidence of MEA is exceedingly rare. The two sisters presented in this paper, have no evidence of hyperparathyroidism, pancreas adenoma and peptic ulcer. So, we consider, at present, these cases should not be field in MEA.
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PMID:[Familial occurrence of pituitary adenoma (author's transl)]. 94 79

Between 1975 and 1989, 58 patients, 32 females and 26 males, mean age 50 years, with intracranial giant aneurysms with a diameter more than 2.5 cm were treated at our clinic. 48% of the patients presented with subarachnoidal hemorrhage. The most of the other 30 patients presented with cranial nerve dysfunctions. The most common site of the aneurysm was the internal carotid artery (25 cases, 43%), followed by the anterior cerebral artery (14%), and the vertebro-basilar region (11 cases, 19%). In 14 patients direct surgery was not performed because of the poor general condition of the patient, the high risks, or non-consent. In seven patients (12%) the aneurysm had been misdiagnosed as meningeoma, pituitary-adenoma, craniopharyngeoma or glioblastoma. 47% of all patients were discharged as "independent" and 19% died. Patients without SAH had better chance of survival: 7% of patients without SAH died and 29% of patients with hemorrhage. 50% of patients without hemorrhage were discharged as "independent" but only 18% of patients with SAH. Because of the high incidence of hemorrhage and the better prognosis for patients without hemorrhage, we recommend routine surgical treatment of patients with giant aneurysms.
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PMID:Management and prognosis of intracranial giant aneurysms. A report on 58 cases. 163 31

An autopsy case of glioblastoma multiforms of the pons with a colon cancer, a rectal carcinoid, a renal adenoma and three gastric leiomyomas in a 81-year-old-woman is reported with a statistical analysis on multiple primary cancers associated with primary brain tumors as reported in the Japan autopsy annuals. Out of 329, 705 autopsy cases from 1975 to 1984 in the Japan autopsy registry, double cancers and triple cancers that included a primary brain tumor amounted to 123 cases (0.037%) and 12 cases (0.0036%), respectively. Other sites for primary cancers were the thyroid (23%), the stomach (15%), the lungs (12%), and the colon (10%) in that order of frequency.
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PMID:[An autopsy case of triple primary cancers consisting of glioblastoma multiforme of the pons, colon cancer and rectal carcinoid--a statistical analysis of cases of brain tumor combined with other primary cancers in Japan autopsy annuals]. 282 42

We studied two autopsy cases of primary pituitary carcinoma. Case-1. A 45 year old female was admitted on Oct. 4 1978, with a complaint of right homonymous hemianopsia. And diagnosis was pituitary adenoma. Partial removal of pituitary tumor was performed on Oct. 23 1978. She died on Dec. 5 1978 due to bleeding of gastrointestinal tract. Autopsy disclosed a pituitary carcinoma invading the left hypothalamus, mamillary body, optic and V cranial nerves, and mid brain as well as sphenoid bone. No extracranial metastasis was noted. Case-2. A 44 year old female with a history of acromegaly for 6 years was admitted with a complaint of headache on May 8 1976. She was diagnosed as having pituitary adenoma. The subtotal removal of pituitary tumor was performed on May 21 1976 and followed by 4500 rad irradiation. At this time, pathological diagnosis was eosinophilic adenoma. Seven years later, she complained of progressive right hearing disturbance, dysarthria and ataxic gait 1983. The second subtotal removal of pituitary tumor was performed with a diagnosis of recurrence of pituitary adenoma on Oct. 7 1983. After the operation, she complicated sepsis and died on Jan. 14 1984. An autopsy disclosed a pituitary carcinoma from residual pituitary gland, continuously extending to the subarachnoid space of the pons, and invading right cerebello-pontine angle and cerebellum. The histological examination revealed pituitary carcinoma with high pleomorphism and glioblastoma multiform-like feature were within the tumor.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Two autopsy cases of primary pituitary carcinoma]. 341 67

Analysis of the CT findings in 35 cases of tumoral hemorrhage (taken from 973 intracranial tumors) revealed three distinct patterns of bleeding: (a) hematoma, (b) central hemorrhage, and (c) hemorrhagic infarction. The location, multiplicity of lesions, and contrast enhancement are important in the diagnosis, and the clinical history and arteriography may also be helpful. The largest single group in this series consisted of 12 metastatic lesions: the others included glioblastoma (7), chromophobe adenoma (4), Grade I astrocytoma (3), medulloblastoma (3), central neuroblastoma (2), histiocytic lymphoma (2), and ependymoma (1). The relatively low mortality rate (21/35) despite marked neurological deterioration is attributed to prompt CT demonstration of hemorrhage followed by aggressive therapy (surgical evacuation, total resection, radiotherapy, and/or steroids or mannitol).
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PMID:Computed tomography of acute intratumoral hemorrhage. 736 26

Increasing numbers of patients within the Mohave Valley region of the United States are reporting symptoms attributable to atypical neurological illness. Many of these patients have experienced an acute-onset gastrointestinal illness during the spring and summer of 1996. Stealth viral cultures performed on the blood of 40 of these patients have been uniformly positive, yielding unequivocal transmissible cytopathic effect (CPE) in both human- and monkey-derived cell lines. One patient has died from a stealth-CPE-positive glioblastoma, while another patient has developed a plemorphic adenoma of the parotid. Viral cultures and epidemiological data support human-to-human, and probable human-to-dog, transmission of the Mohave stealth virus infection.
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PMID:Stealth virus epidemic in the Mohave Valley. I. Initial report of virus isolation. 920 Jan 90

Recent advancement of molecular biology disclose responsible genes of FAP(familial adenomatous polyposis) and HNPCC(hereditary non polyposis colorectal cancer). Gardner Syndrome is now categorized as subtype of FAP. Turcot Syndrome is now known as a heterogeneous disease. Turcot Syndrome caused by APC gene develops medulloblastoma and Turcot Syndrome caused by mismatch repair gene develops glioblastoma. Because of the discovery of APC gene, the presymptomatic diagnosis of asymptomatic gene carriers are now available and preventive surgery can be planned. FAP patients with mutated APC gene between codon 1250 and 1464 shows severe phenotype. It is known that FAP patient whose APC gene mutation locates at codon 1309 develops cancer 10 years earlier in comparison to the rest of the cases. Consequently risky rectal mucosa should be removed in this group of patients. As for HNPCC, presymptomatic diagnosis is still not possible because the penetrance rate has not been estimated yet and some additional responsible genes are expected to be discovered. Replication error, mutator phenotype of mismatch repair gene is useful indicator to predict second primary cancers. When the patient in a HNPCC family develops adenoma with microsatellite mistability, preventive colectomy might be one of the surgical option with the informed consent of the patient.
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PMID:[Molecular biological background of FAP and HNPCC, and treatment strategies of both diseases depend upon genetic information]. 969 69

Germline mutations in the tumor-suppressor gene PTEN (MMAC1, TEP1) are found in Cowden syndrome, which predisposes to hamartomas, breast cancer, trichilemmomas, and thyroid tumors of follicular epithelium. PTEN has also been found to be somatically deleted, mutated, and/or silenced in various sporadically occurring cancers such as glioblastoma, breast cancer, kidney cancer, malignant melanoma, and endometrial cancer. Loss or reduction of PTEN protein expression as well as inappropriate subcellular compartmentalization is seen in non-medullary thyroid cancers. However, although allelic loss of the PTEN locus in 10q23.3 is frequently seen, this is not coupled with mutations in the PTEN gene. To approach further the frequency and mechanism behind PTEN silencing, we screened a panel of 87 sporadic thyroid tumors for PTEN mRNA expression, including 14 anaplastic carcinomas, 37 follicular carcinomas, 21 atypical adenomas, and 15 ordinary adenomas. Complete loss of PTEN mRNA expression was evident in six of the tumors, including four anaplastic carcinomas, one widely invasive carcinoma, and one ordinary adenoma. The transcriptional silencing of PTEN was significantly associated with the anaplastic subtype, suggesting that PTEN is involved in the carcinogenesis of highly malignant or late-stage thyroid cancers, whereas this particular mechanism appears to be of minor importance in differentiated follicular thyroid tumors. No association was observed between the expression, loss of heterozygosity, and mutation status in the 33 cases in which these parameters were compared. This indicates that PTEN silencing is a result of a wide variety of epigenetic and/or structural silencing mechanisms rather than a consequence of structural biallelic inactivation of the classical type. Furthermore, the high rate of alterations in the 10q23 region might indicate the presence of an as-yet unknown tumor-suppressor gene with an important role in the development of thyroid tumors.
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PMID:Silencing of the PTEN tumor-suppressor gene in anaplastic thyroid cancer. 1220 92


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