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)

Six cases of vagal body tumor are reviewed. All first presented as painless neck masses with normal cranial nerve function. Otologic symptoms were infrequent, occurring only with temporal bone involvement. In true vagal paragangliomas, cranial nerve and auditory function is usually preserved until there is extensive disease of the skull base. Tumor progression after radiotherapy was documented in four patients, three of whom were treated with 4500 cGy or more. One patient was found to have regional lymph node metastases. The six patients had a total of 10 head and neck paragangliomas, illustrating the high incidence of synchronous and metachronous lesions. Because of the high incidence of multiple lesions, these tumors threaten lower cranial nerves bilaterally in many instances. Because cranial nerve function is preserved until late, and because vagal and accessory nerve paralysis is usually unavoidable with resection, we advocate conservative treatment in selected cases. It may be reasonable to postpone surgery until cranial nerve impairment becomes evident or other vital structures are threatened.
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PMID:Vagal body tumors. 190 12

The distribution of MHC antigens in human melanocytic lesions, i.e. HLA class I and HLA class II antigens is reviewed. HLA class I antigens have a broad distribution, but may be lost during tumor progression. In contrast, HLA class II antigen expression appears with neoplastic transformation. The mode of regulation of HLA antigens in melanoma lesions is complex. Immunohistochemical demonstration of HLA antigen expression in primary melanoma lesions and in locoregional metastases has prognostic relevance. Expression of HLA-DR in primary melanoma lesions is associated with an unfavorable prognosis, as is a decreased expression of HLA-A,B,C antigens in locoregional metastases.
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PMID:MHC antigens in human melanomas. 191 17

Thirty-seven patients who had undergone radical cystectomy and pelvic node dissection for pathologic stage pT2-4 and/or N+ disease received adjuvant chemotherapy involving the injection of cis-platinum alone or in its combination from June 1982 to April 1989. Adjuvant chemotherapy was performed using the following three protocols. Protocol 1 entails the administration of cis-platinum alone. Protocol 2, involving the administration of a combination of cis-platinum, adriamycin and 5-fluorouracil (CAF), was used for deeply invasive bladder cancer. Protocol 3, consisting of cis-platinum, vp-16 and adriamycin (CVA), was employed in patients with deeply invasive bladder cancer instead of protocol 2 from July 1987. Of the 37 patients, 27 were alive with no evidence of disease for an average of 42 months. One patient died as a result of factors unrelated to cancer. Local recurrence and/or distant metastases occurred in 9 patients and all died of cancer progression. The survival rate for all 37 patients at 87 months was 64.4%. The rates were 75% in pT2, 80% in pT3a, 50.8% in pT3b, and 44.4% in pT4. Although adjuvant chemotherapy combined with radical cystectomy seemed to be effective in cases with pathological stage pT3a or less, more intensive chemotherapy is needed in an attempt to improve poor prognosis in cases with pathological stages pT3b-4 or node involvement.
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PMID:Clinical evaluation of adjuvant chemotherapy for high stage bladder cancer. 194 68

Colorectal primary carcinomas and metastases from 20 Dukes' stage C or D patients were examined for the immunohistochemical localization and contents of various fucosylated N-acetyl-lactosamine oligomers by specific monoclonal antibodies (MAbs). MAbs used were SH1, specific for Lewis X antigen; FH4, specific for dimeric Lewis X antigen; FH6, specific for sialyl-dimeric Lewis X antigen; and KH1, specific for Lewis Y-Lewis X antigen. The distribution of the carbohydrate antigens identified by these MAbs was heterogeneous within the primary tumor as well as within the metastatic lesion. Examinations of serial sections indicated that areas within an individual tumor which were stained with one MAb were not always reactive with the other MAbs, although these four MAbs identify closely related structures. The degree of MAb reactivity with carcinoma sections was classified by percentage positive carcinoma cells, and primary tumors and metastases from the same patients were compared. An equivalent or higher proportion of carcinoma cells in the metastatic lesions were reactive with MAb FH6 than in the primary colon carcinomas, but each correlation was not seen with the other MAbs. Electrophoretic separation of tumor tissue extracts followed by staining with these MAbs revealed that a component having an approximate molecular weight of 1,000,000 is the major site for the binding of MAbs, FH6, FH4, and KH1. The electrophoretic mobility of the antigenic molecule on polyacrylamide gels as shown by direct MAb bindings was slightly different from that of a major sialomucin revealed by wheat germ agglutinin in the same tissues. MAb FH6 binding to a high molecular weight component was eliminated by prior treatment of the glycoprotein with mild acid or sialidase to remove sialic acid. Simultaneously, binding of MAb SH2, specific for dimeric Lex antigen, to this component increased. An extract was prepared from a liver metastasis, and high molecular weight components were isolated by gel filtration and then fractionated by DEAE-cellulose ion exchange chromatography. A fraction eluted from DEAE-cellulose between 0.10-0.25 M sodium chloride contained most of the MAb FH6 reactivity, as shown by antibody affinity chromatography. These results support a hypothesis that high molecular weight glycoproteins produced by colorectal carcinoma tissues are heterogeneous with regard to their carbohydrate chains and their antigenic structures may change during tumor progression.
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PMID:Sialyl-dimeric Lewis-X antigen expressed on mucin-like glycoproteins in colorectal cancer metastases. 197 61

48 patients with advanced sarcomas were treated with regional hyperthermia (RHT) and systemic chemotherapy (ifosfamide/VP-16). 92% of the patients had been pretreated before entering the study. Pretreatment consisted of chemotherapy (33/48), surgery (9/48) or surgery plus irradiation (2/48). Following the conventional treatment, the patients had either relapsed (30/48) or had shown progressive disease (14/48) at the primary site with or without metastases. In 43 patients the overall response rate [5 complete responders (CR) and 6 partial responders (PR)] was 26%, 17 patients revealed no change (NC) and 15 patients showed local tumor progression (PD). A significant correlation of tumor response (responders [CR + PR] versus non-responders [PD]) with intratumoral averaged temperatures could be observed.
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PMID:[Regional deep hyperthermia of sarcoma for improving local tumor control]. 198 80

A procedure that measures the amplification of oncogenes in human cancer cells is described. The cells were obtained by fine-needle biopsy to allow repeated sampling from individual metastases. A drawback was the low number of cells obtained, but this could be overcome by using a slot-blot hybridization technique to measure gene amplification. Two patients with mammary cancer (primary tumors or metastases), analyzed for the levels of amplification of the oncogene erb-B2, are described in detail. This technique is suitable for analyzing alterations occurring during cancer progression and for identifying subgroups of mammary cancer with different characteristics.
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PMID:Amplification of oncogenes in mammary carcinoma shown by fine-needle biopsy. 199 3

Between June 1987 and June 1989, 29 recurrent malignant gliomas or recurrent solitary brain metastases in 28 patients were treated in a Phase I study of interstitial irradiation and hyperthermia. Patient age ranged from 18 to 65 years, and the Karnofsky Performance Status scores ranged from 40 to 90%. There were 13 glioblastomas, 10 anaplastic astrocytomas, 3 melanomas, and 3 adenocarcinomas. Catheters were implanted stereotactically after computed tomography-based preplanning. Hyperthermia was administered before and after brachytherapy, using one to six 2450- or 915-MHz helical coil microwave antennas and one to three multisensor fiberoptic thermometry probes. The goal was to heat as much of the tumor as possible to 42.5 degrees C for 30 minutes. Within 30 minutes after the first hyperthermia treatment, implant catheters were afterloaded with high-activity iodine-125 seeds delivering tumor doses of 32.6 to 61.0 Gy. Most patients had no sensation of heating. Complications included seizures in 5 patients, reversible neurological changes in 9 patients, a scalp burn in 1, and infections in 3. Of 28 evaluable 2-month follow-up scans, 11 showed definite improvement in the radiological appearance of the tumor, 4 were slightly improved, 7 were stable, and 6 showed tumor progression. Ten patients underwent reoperation for persistent tumor and/or necrosis. Eleven of 28 patients are alive 40 to 97 weeks after treatment. Thirteen patients died of a brain tumor, 2 died of extracranial melanoma metastases, 1 died of new brain melanoma metastases, and 1 died of a pulmonary embolus. The median survival was 55 weeks overall. Median survival has not yet been reached for the anaplastic astrocytoma subgroup. We conclude that interstitial brain hyperthermia using helical coil microwave antennas is technically feasible. The level of toxicity is acceptable, and the computed tomographic response rate is encouraging.
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PMID:Interstitial irradiation and hyperthermia for the treatment of recurrent malignant brain tumors. 199 88

Sixty patients with metastatic renal cell carcinoma were entered into an ongoing randomized phase II study with lonidamine, 350 mg/m2 orally daily (arm A) and high dose tamoxifen, 150 mg/m2 orally daily for 6 months, afterwards 50 mg/m2 (arm B), until tumor progression. All patients had measurable disease and documented tumor progression prior to treatment. There were 1 complete and 1 partial remission among 19 evaluable patients in arm A (10.5%) and 2 complete and 1 partial remission among 25 evaluable patients (12%) in arm B. Objective responses were observed in pulmonary, nodal, and cutaneous metastases. In addition, in 63% and 64% tumor progression could be stopped in arm A and B, respectively. Median response duration was 100 days (range, 20-361) in arm A and 150 days (range, 28-355) in arm B. One year survival rate was 37.5% with lonidamine and 35% with tamoxifen. In arm A patients with tumor progression within 12 weeks after diagnosis of metastatic disease survived significantly shorter than patients with a longer interval (P less than 0.05). Nephrectomy or number and localization of metastatic sites failed to significantly influence probability of remission or survival. Toxicity was mostly mild to moderate. Four patients in the lonidamine arm had to discontinue treatment because of intolerable myalgias, which were immediately reversible. These data suggest that lonidamine and high-dose tamoxifen are moderately effective in widespread renal cell carcinoma where treatment intention is palliative.
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PMID:Lonidamine versus high-dose tamoxifen in progressive, advanced renal cell carcinoma: results of an ongoing randomized phase II study. 203 Nov 96

Lonidamine revealed synergistic effects with anthracyclines and alkylating agents in experimental investigations. It differs from conventional cytostatics by acting on the cell energy metabolism and also lacks their typical side effects; therefore it may be valuable to be combined with established chemotherapeutic regimens. Because in unselected patients the results of randomized studies may be influenced by differences in type and combination of prognostic factors, we defined strict entry criteria: no previous systemic palliative treatment, disease-free interval less than or equal to 2 years, measurable visceral metastases, number of tumor sites less than or equal to 2, no brain or bone metastases, World Health Organization performance status less than or equal to 2, age less than or equal to 55. In an ongoing rate, remission duration, time to treatment failure, and survival time in patients treated with vindesin 3 mg/m2 plus epirubicin 100 mg/m2 plus cyclophosphamide 600 mg/m2 (day 1, intravenous, repeated every 3 weeks) +/- lonidamine 600 mg/day orally. Eight of 12 patients achieved an objective remission (complete response 4, partial response 4), 1 patients had a stable disease, 2 patients experienced tumor progression; 1 patient is not yet evaluable for response. In spite of the intensity of the therapy no treatment interval prolongation was necessary. Main toxicities were myelosuppression, nausea, emesis, alopecia, and in patients treated with lonidamine, mild myalgia. The addition of lonidamine to polychemotherapy did not affect myelosuppression. Differences in remission rates or remission duration due to lonidamine could not yet be demonstrated.
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PMID:Lonidamine in high-risk breast cancer patients. 203 Nov 99

The natural progression of benign tumors to malignancy and metastasis is characterized by their ability to circumvent microenvironmental controls on cellular proliferation, diversity, and positioning, and evolve into heterogeneous phenotypes, a process that probably involves qualitative and quantitative changes in gene expression. The oncogenes and suppressor genes that can effect tumor progression may control important points in the regulation of sets of genes that are ultimately responsible for the cellular alterations seen in highly metastatic cells. Because many cancers metastasize nonrandomly to particular distant sites, their colonization properties cannot be explained by mechanical considerations, such as arrest of tumor cells in the first microcirculatory network encountered. Metastatic cells that show a high propensity to metastasize to certain organs adhere at higher rates to microvessel endothelial cells isolated from their target sites, invade into target tissue at higher rates, and respond better to paracrine growth factors from the target site. These properties depend on multiple tumor cell, host cell, and stromal molecules that are differentially expressed by particular tumor and organ cells and by the organ extracellular matrix. Together these tumor and host factors appear to determine the organ metastatic properties of malignant cells.
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PMID:Molecular mechanisms of cancer metastasis: tumor and host properties and the role of oncogenes and suppressor genes. 204 98


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