Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0027627 (metastases)
 103,950 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Expression of CD44 has been implicated in tumor growth and metastasis. Here we demonstrate CD44 expression in primary human brain tumors (n = 44) and brain metastases (n = 7) by RT-PCR and immunohistochemistry. Standard CD44 was found to be expressed by the majority of primary brain tumors and brain metastases. For the first time to our knowledge, CD44 expression is demonstrated for acoustic neurinomas and pituitary adenomas. Exon-specific analysis by RT-PCR and indirect immunofluorescence revealed expression of alternatively spliced CD44 isoforms in the group of brain metastases only. However, in one glioblastoma multiforme, expression of CD44v5 and CD44v6 was found immunohistochemically. This tumor took an unusual clinical course giving rise to multiple intrahepatic and lymph node metastases. Quantitatively different expression of standard CD44 in gliomas versus meningiomas is reported (p < 0.01).
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PMID:Combined detection of CD44 isoforms by exon-specific RT-PCR and immunohistochemistry in primary human brain tumors and brain metastases. 865 25

The expression levels of nm23-H1 have been reported to correlate with the metastatic potential of some tumours. We have treated a child with a rare case of astrocytoma with diffuse osteoblastic metastases. We therefore decided to examine the expression of the nm23 gene product in 24 gliomas in order to clarify the association of its expression with the clinical features of the disease. A polyclonal antibody against a GST/nm23-H1 fusion protein was raised in rabbits. Twenty-four specimens, including 5 recurrent gliomas and one extraneural metastasis, were obtained from 19 patients treated surgically between 1990 and 1993 in our hospital. Immunohistochemical staining was performed on paraffin sections using an avidin-biotinyl peroxidase complex method. Of the 24 astrocytic neoplasms, 3 (12.5%) specimens from one patient with diffuse bony metastases stained intensely with nm23-H1. Two specimens obtained from glioblastoma multiforme patients stained weakly. The other 19 specimens were negative for nm23-H1 expression. Little or no nm23 expression was observed in adjacent nontumourous cerebral tissues. The results suggest that high levels of nm23 expression might correlate with extraneural metastatic potential in astrocytic neoplasms.
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PMID:Immunohistochemical analysis of the nm23 gene product (NDP kinase) expression in astrocytic neoplasms. 873 95

Between May 1990, and June 1994, 79 patients with malignant tumors were treated radiosurgically using a Leksell gamma unit at Asan Medical Center. Of these patients, 57 were metastatic brain tumor, 12 were glioblastoma multiforme (GM), 4 were primitive neuroectodermal tumor, 3 were malignant germ cell tumor, 2 were recurrent lymphoma, and 1 was adenoid cystic carcinoma of the orbit. Among 57 patients with metastatic tumors, 28 patients harboring 60 tumors were followed clinically and radiographically. The median marginal dose for these tumors was 30 Gy and the median survival rate was 15 months. Twenty-one tumors disappeared and 32 tumors decreased in size during 2 to 6 months after radiosurgery on computed tomographic or magnetic resonance imaging scans. All 12 patients with GM were treated with conventional radiation (6,240 approximately 6,500 cGy) after surgical resection or biopsy prior to radiosurgery (13 approximately 15 Gy to margin). The results were varied. Radiosurgical treatment of two recurrent lymphomas and three recurrent mixed germ cell tumors after radiation and chemotherapy provided rapid clinical improvement with disappearance of the tumor. However, new lesions appeared in two lymphomas and one mixed germ cell tumor within 3 to 4 months. One patient with adenoid cystic carcinoma of the orbit, who was treated radiosurgically prior to resection, is alive without recurrence 31 months after the treatment. Gamma knife radiosurgery appears to be the best alternative method to surgical excision plus radiation therapy for single and multiple cerebral metastases. It also provides rapid palliation of symptoms due to recurrent malignant tumors. And it may have an adjuvant role in the treatment of some tumors delaying local recurrence, if given prior to resection. However, the preliminary results for the malignant gliomas were inconclusive.
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PMID:Gamma knife radiosurgery for malignant tumors. 875 65

Extracranial metastasis of cerebral glioblastoma is rarely seen. Craniotomy and diversionary shunt are widely accepted causes of dissemination. Prognosis is poor but new therapeutic modalities may improve the survival and lessen the patient's symptoms. It is also important to diagnose extracranial metastasis because of possible response to treatment and fine-needle aspiration cytology can then be helpful. Two cases of extracranial metastases of glioblastoma multiforme diagnosed by fine-needle aspiration cytology are reported and a review of the literature is presented.
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PMID:Extracranial metastasis of glioblastoma multiforme diagnosed by fine-needle aspiration: a report of two cases and a review of the literature. 940 15

Although survivals of infants with malignant brain tumors are worse than any other age group, one possible exception to this rule are the malignant gliomas. Eighteen children less than 3 years of age with malignant gliomas (glioblastoma multiforme, anaplastic astrocytoma and malignant glioma) were treated on the Pediatric Oncology Group regimen of prolonged postoperative chemotherapy and delayed irradiation, (1986-1990). Of 10 children evaluable for neuroradiologic response, 6 had partial responses (> 50% reduction) to two cycles of cyclophosphamide and vincristine. Progression free survivals at 1,3 and 5 years were 54.25% +/- 12, 43% +/- 16 and 43% +/- 23 respectively. Survivals at 5 years were 50% +/- 14. Four children were not irradiated after 24 months of chemotherapy due to parental refusal and none have developed recurrent disease. Neither degree of surgical resection, presence or absence of metastases, nor pathology influenced survival but this may reflect small sample size. This study suggests that some malignant gliomas in infants are chemotherapy sensitive and may be associated with a good prognosis. Why infants with these high-grade gliomas fare better than adults is not clear. It is likely that there is something intrinsically different about them that cannot be identified on routine pathologic examination.
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PMID:Treatment of infants with malignant gliomas: the Pediatric Oncology Group experience. 883 66

This retrospective immunohistochemical study compares the expression of five stress-response (heat-shock) proteins (srp's) [srp 90, srp 72, srp 27, alpha B-crystallin and ubiquitin], p53 protein and proliferating cell nuclear antigen (PCNA) in 118 primary brain tumors and 21 carcinoma metastases to the central nervous system. Serial sections of formalin-fixed, paraffin-embedded tissues were used. Most astrocytomas (9/13), ependymomas (5/5), glioblastoma multiforme (GBM) (11/12), schwannomas (19/21), meningiomas (22/23) and breast carcinoma metastases (Br-Mt) (9/10), and some medulloblastomas (5/15), primitive neuroectodermal tumors (PNETs) (5/11), pituitary adenomas (4/7) and lung carcinoma metastases (6/11), but none of 10 oligodendrogliomas had tumor cells that expressed one or more (up to five) srp's. The percentage of tumors with p53-positive cells was variable; the proportion was highest among srp-expressing GBMs (mean: 16.1%) and Br-Mts (mean: 15.3%). The mean PCNA-labeling index (LI) also varied, ranging from 1.2% in the group of pituitary adenomas to 24.5% in Br-Mts, with GBMs (20.4%) and medulloblastomas (18.4%) approaching the latter value. PCNA-LI was higher in the astrocytomas, GBMs, medulloblastomas and PNETs that expressed srp's than in those did not. A high proportion of p53-positive cells (31.3 to 59.0%) and the highest PCNA-LIs (41.0 to 49.0%) were seen in two GBMs and one Br-Mt that expressed all five srp's. We conclude that primary and metastatic tumors of the brain produce one or more stress-related proteins, and that a variable proportion of the tumor cells have immunohistochemically-detectable p53, the expression of which may depend, at least in part, on the growth potential of a given tumor.
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PMID:Brain tumor: immunohistochemical studies on the stress-response proteins, p53 protein and proliferating cell nuclear antigen. 886 93

Extraneural metastases from glioblastoma multiforme are rare. Spread to the extracranial head and neck may be evident on routine follow-up images of the original lesion. We present two cases, one with documented metastatic adenopathy in the head and neck from glioblastoma and the other with probable metastatic disease in a lymph node in which biopsy was not performed, and discuss probable mechanisms of extraneural extension of this tumor.
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PMID:Lymph node metastases from glioblastoma multiforme. 893 81

Astrocytic tumors are divided into two basic categories: circumscribed (grade I) or diffuse (grades II-IV). All diffuse astrocytomas tend to progress to grade IV astrocytoma, which is synonymous with glioblastoma multiforme (GBM). GBMs are characterized by marked neovascularity, increased mitosis, greater degree of cellularity and nuclear pleomorphism, and microscopic evidence of necrosis. Several genetic abnormalities have been associated with the development of GBM: In some cases, the abnormality is inherited (e.g., Li-Fraumeni syndrome); in others, genetic alteration appears to result from mutation into an oncogene or deterioration of the tumor-suppressor gene p53. A common, distinctive histopathologic feature of GBM is pseudopalisading. The most common imaging appearance of GBM is a large heterogeneous mass in the supratentorial white matter that exerts considerable mass effect. Less frequently, GBM can occur near the dura mater or in the corpus callosum, posterior fossa, and spinal cord. GBM typically contains central areas of necrosis, has thick irregular walls, and is surrounded by extensive, vasogenic edema, but the tumor may also have thin round walls, scant edema, or a cystic appearance with a mural nodule. GBMs most commonly metastasize from their original location by direct extension along white matter tracts; however, cerebrospinal fluid, subependymal, and hematogenous spread also can occur. Given the rapidly growing body of knowledge about GBM, the radiologist's role is more important than ever in accurate and timely diagnosis.
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PMID:Glioblastoma multiforme: radiologic-pathologic correlation. 894 45

Precise localization of subcortical targets contributes to the technical challenge of craniotomies. To address this challenge, the application of readily available stereotactic localization techniques to open craniotomies was investigated. Over a 2-year period, 62 consecutive stereotactic craniotomies were performed successfully using the CT-compatible Brown-Roberts-Wells (BRW) apparatus. Standard BRW hardware and software were employed. This series consists of craniotomies in 50 patients for resection of subcortical mass lesions. Targets were consistently and precisely localized by the stereotactic frame. Pathology revealed 32 metastases, 18 glial tumors, 5 nonglial tumors, and 7 nonneoplastic lesions. Histology differed from presumptive diagnoses by neurodiagnostic imaging studies in 30.6% of cases. The average volume of tumors resected was 55,903 mm3. Gross total resection of all solid tumor tissue was consistently confirmed by postoperative contrast-enhanced CT. Postoperatively, 38 patients with masses were neurologically improved, 22 were unchanged, and 2 were worse. Median postoperative survival for glioblastoma multiforme after adjuvant therapy was 58.7 weeks and for metastases was 39.2 weeks. There were no postoperative deaths. Overall surgical morbidity was 3.7%. CT-directed stereotactic craniotomy using the BRW system is a safe, efficacious, and readily available technique. It successfully confers the precision of stereotactic methodology on open microneurosurgical procedures.
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PMID:Tumor resection by stereotactic craniotomy using the Brown-Roberts-Wells system. 907 47

The telomeric repeat amplification protocol was used to detect expression of telomerase in primary intracranial tumors. Expression was confined to high-grade variants; 10 of 19 glioblastoma multiforme tumors and 5 of 5 primitive neuroectodermal tumors showed telomerase activity. Two of 8 anaplastic gliomas (1 anaplastic oligodendroglioma and 1 anaplastic oligoastrocytoma) were positive for telomerase. Of 16 meningiomas tested, only the 2 atypical variants were positive for telomerase. Two hemangiopericytomas of the central nervous system also showed expression of telomerase. Twenty-two pituitary adenomas (including 6 invasive variants), 2 low-grade gliomas, 2 ependymomas, and 8 nonneoplastic brain specimens were negative. It was concluded that expression of telomerase is found in most glioblastoma multiforme tumors; primitive neuroectodermal tumors appeared to be more uniformly positive. Expression of telomerase in atypical variants of meningioma and hemangiopericytomas of the central nervous system correlated with the potential for aggressive local growth and metastases. Despite the invasive tendency of some pituitary adenomas, telomerase was not detected in these tumors, which suggests that other pathways account for their aggressive behavior.
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PMID:Differential telomerase expression in human primary intracranial tumors. 912 67


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