Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:Q86TM3 (cage)
 29,987 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Desmoid tumor are rare connective tissue tumors currently considered as sarcoma of low grade malignancy. They are most often encountered in young women of child-bearing years. Abdominal localisation is the most frequent site. The main aim of treatment is to avoid recurrences. We report a case of desmoid tumor developing in the thoracic cage in a patient who had been operated on six years earlier for an epidermoid carcinoma of bronchus.
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PMID:[Desmoid tumor of the thoracic wall]. 812 23

In recent years, significant progress has been made in identifying characteristic chromosomal rearrangements associated with several solid tumor types, notably sarcomas, a relatively rare subset of human cancer. Most sarcomas analyzed have been found to be characterized by recurrent chromosome translocations that are specific to histological types. We have reviewed published reports of chromosomal aberrations in benign and malignant soft tissue tumors and found an incidence of specific translocations in these neoplasms that ranged from 20% to 93% within histological tumor types. Identification of recurrent chromosomal abnormalities in benign tumors has resulted in a reappraisal of the general concept that benign tumors have a normal (diploid) chromosome constitution. The variety of recurrent changes present in the different tumor types attests to the cytogenetic diversity inherent in these tumors. The chromosomal rearrangements in each of the tumor types were unique and did not correspond to cancer-associated aberrations known from other solid or hematopoietic malignancies. Cytogenetics thus provides an essential adjunct to diagnostic surgical pathology in the case of malignant soft tissue tumors, which often present substantial diagnostic challenges. In addition, it represents another approach to determine the histogenetic origin of some tumors and identifies sites of gene deregulation for molecular analysis. Indeed, recent molecular analyses of several sarcoma-associated translocations have identified novel genes and novel mechanisms of their dysregulation.
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PMID:Chromosomal aberrations in soft tissue tumors. Relevance to diagnosis, classification, and molecular mechanisms. 820 53

Interleukin-1 (IL-1) induces anorexia via direct action in the brain, and its participation in the pathogenesis of cancer-associated anorexia has been hypothesized. Because the functional ablation of the ventromedial nucleus of hypothalamus (VMH), where IL-1 receptors have been detected, reverses cancer-associated anorexia in tumor-bearing (TB) rats, we hypothesize that cancer anorexia involves the direct effect of IL-1 on the VMH. To test this hypothesis, we investigated whether the intra-VMH injection of the IL-1 receptor antagonist (IL-1ra) improves food intake in anorectic TB rats. Sixteen Fischer rats (approximately 300 g/BW) were injected s.c. with 10(6) trypan-blue viable methylcholanthrene sarcoma cells, and then individually caged. Chow and water were freely available, and food intake was recorded throughout the study. Normal food intake was measured in 8 more rats, injected s.c. with normal saline. Tumor developed in all rats. When TB rats became anorectic, they were randomly assigned to either treatment or control groups. Using stereotaxic techniques, 25 ng of IL-1ra dissolved in normal saline (TB-IL-1ra; n = 8), or an equal volume of normal saline (TB-NS; n = 8) was injected bilaterally into the VMH. After surgery, rats were caged and changes in food intake recorded. At study's end, rats were sacrificed and brains removed for histological confirmation of injection sites. In the TB-NS group, food intake decreased with the occurrence of anorexia. In contrast, the intra-VMH injection of IL-1ra reduced the severity of cancer anorexia, significantly improving food intake in TB-IL-1ra rats. Data indicate that centrally acting IL-1 plays a significant role in the development of cancer anorexia.
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PMID:Relationship between interleukin-1 and cancer anorexia. 874 51

Tumor necrosis factor (TNF) is a highly cytotoxic cytokine. However, due to its severe side effects, the only clinical situation allowing its administration in humans is isolated limb perfusion (ILP). Early studies have shown that TNF alone is of limited efficacy even at high doses via ILP, and that a chemotherapeutic agent needs to be added. The most commonly used drug in this setting is melphalan which is considered to be synergistic with TNF. However, since melphalan has not been commonly used in sarcoma, we believed that confirmation of its synergistic effect with TNF in an experimental sarcoma model could prove valuable for future drug choice. B16F10 melanoma and CT26 colon carcinoma cells were injected subcutaneously (s.c.) into mice, while GF fibrosarcoma cells were injected s.c. into the hindleg of Wistar rats. The animals were then divided into four treatment groups: TNF alone, melphalan alone, TNF and melphalan, and 0.9% NaCl controls. Mice were treated with intraperitoneal injections and rats by ILP. TNF dosage was 20 microgram for mice and 200 microgram for rats. Melphalan was given at 5-10 mg/kg for both mice and rats. Results showed synergism of TNF and melphalan in both modes of therapy. In the systemic administration groups (mice carrying B16F10 and CT26 tumors), tumors increased in size in all but the combined TNF-melphalan group. In the regional delivery groups (rats carrying GF sarcoma cells treated via ILP), there was a 16% decrease in tumor volume in rats treated with TNF alone, a 29% decrease in rats treated with melphalan, and a 75% decrease in the combined TNF-melphalan group. In conclusion, TNF and melphalan proved to be highly synergistic in both systemic and regional delivery. This fact makes melphalan an adequate choice for TNF perfusion in advanced limb malignancies.
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PMID:Synergism of tumor necrosis factor-alpha and melphalan in systemic and regional administration: animal study. 977 89

In this study, we developed a mouse model of adoptive immunotherapy reflecting immune recognition of syngeneic tumor cells naturally expressing an endogenous rejection Ag. Specifically, in a pulmonary metastases model, we examined the potency and maintenance of an antitumor CD8(+) CTL response in vivo, as well as its effectiveness against an "extensive" tumor burden. The approach taken was to first generate tumor-specific CTL from mice challenged with the CMS4 sarcoma coadministered with anti-CTLA4 mAb, which has been shown to facilitate the induction of Ag-specific T cell responses in vivo. An H-2L(d)-restricted nonamer peptide, derived from an endogenous murine leukemia provirus was identified as a CMS4-reactive CTL epitope based upon the following: CTL cross-recognition of another syngeneic tumor cell line (CT26 colon carcinoma) previously characterized to express that gene product; sensitization of Ag-negative lymphoblasts or P815 targets with the peptide; and by cold target inhibition assays. In vivo, the adoptive transfer of CMS4-reactive CTL (> or =1 x 10(6)) resulted in nearly the complete regression of 3-day established lung metastases. Furthermore, mice that rejected CMS4 following a single adoptive transfer of CTL displayed antitumor activity to a rechallenge 45 days later, not only in the lung, but also at a s.c. distal site. Lastly, the adoptive transfer of CTL to mice harboring extensive pulmonary metastases (> 150 nodules) led to a substantial reduction in tumor burden. Overall, these data suggest that the adoptive transfer of tumor-specific CTL may have therapeutic potential for malignancies that proliferate in or metastasize to the lung.
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PMID:Regression of extensive pulmonary metastases in mice by adoptive transfer of antigen-specific CD8(+) CTL reactive against tumor cells expressing a naturally occurring rejection epitope. 1159 51

Very soon after their original identification in HeLa cells in 1983, HMGA proteins appeared as interesting cancer-related molecules. Indeed, they were immediately noted as a sub-class of High Mobility Group proteins induced in fibroblast or epithelial cells transformed with sarcoma viruses. After more than 20 years, the association between HMGA protein expressions and cellular transformation has been largely confirmed and HMGA are among the most widely expressed cancer-associated proteins. Nevertheless, their functional contribution to tumour development and progression is far from being completely understood. Furthermore, although HMGA1 expression has been reported to be inducible by a number of factors and circumstances, the question of how their expression is deregulated in cancer is even less clear and somehow has been ignored from most researchers. An active AP1 site is the only characterized element of the HMGA1 human promoter, that remains a rather complicated and unexplored source of information to answer this question. Following the indication that c-Myc might bind and activate the mouse HMGA1 gene promoter, we have demonstrated that HMGA1 is a new target for MYCN in human neuroblastomas. In this report, we overview part of the current information on HMGA1 and focus our attention on the analysis of its human promoter.
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PMID:Molecular mechanism of HMGA1 deregulation in human neuroblastoma. 1592 78

Dysadherin is a cancer-associated cell membrane glycoprotein, which downregulates E-cadherin and promotes metastasis. We studied the clinicopathological features in 72 cases of epithelioid sarcoma and in six cases of malignant rhabdoid tumor, and also assessed the immunohistochemical expression of dysadherin, E-cadherin and MIB-1 in epithelioid sarcoma and malignant rhabdoid tumor cases. In addition, we compared dysadherin mRNA expression between epithelioid sarcoma and malignant rhabdoid tumor cell lines, using RT-PCR and real-time quantitative RT-PCR analysis. Immunohistochemical dysadherin expression was more frequently observed in proximal-type epithelioid sarcoma (71%) in comparison with distal-type epithelioid sarcoma (36%) (P = 0.037). Furthermore, seven proximal-type epithelioid sarcoma cases mimicking malignant rhabdoid tumor (histologically classified as the large cell type, accompanied by frequent rhabdoid cells and located in deep soft tissue) were all positive for dysadherin (100%), whereas dysadherin expression was not detected at all in any of the true six malignant rhabdoid tumors (0%). Cell lines established from proximal-type epithelioid sarcoma revealed significantly higher levels of dysadherin mRNA expression, compared with the levels seen in malignant rhabdoid tumor cell lines by real-time quantitative RT-PCR (P = 0.0433). Epithelioid sarcoma patients with dysadherin expression survived for a significantly shorter time than those without dysadherin expression (P = 0.001). In multivariate analysis, dysadherin immunopositivity (P = 0.0004) was one of the two independent adverse prognostic factors. We conclude that dysadherin expression in epithelioid sarcoma is a significant poor prognostic factor and that it is a powerful diagnostic marker for distinguishing epithelioid sarcoma, including the proximal-type epithelioid sarcoma, from malignant rhabdoid tumor. In epithelioid sarcoma, especially in proximal-type epithelioid sarcoma, increased cell disadhesion and motility by dysadherin plays an important role to acquire aggressive biological behavior. However, in malignant rhabdoid tumor, cell growth cycle that is regulated by hSNF5/INI1 gene seems to be critical to lethal biological behavior rather than dysadherin.
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PMID:Prognostic significance of dysadherin expression in epithelioid sarcoma and its diagnostic utility in distinguishing epithelioid sarcoma from malignant rhabdoid tumor. 1655 75

Tumor necrosis factor (TNF) is an extraordinarily pleiotropic cytokine with a central role in immune homeostasis, inflammation, and host defense. Dependent on the cellular context, it can induce such diverse effects as apoptosis, necrosis, angiogenesis, immune cell activation, differentiation, and cell migration. These processes are of great relevance in tumor immune surveillance, and also play crucial roles in tumor development and tumor progression. It is therefore no surprise that TNF in a context-dependent manner displays pro- and antitumoral effects. Modulation of the activity of the TNF-TNF receptor system thus offers manifold possibilities for cancer therapy. In fact, TNF in combination with melphalan is already an established treatment option in the therapy of advanced soft tissue sarcoma of the extremities and many preclinical data suggest that TNF neutralization could also be exploited to fight cancer or cancer-associated complications.
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PMID:The role of TNF in cancer. 1913 69

We describe a previously healthy, non-leukaemic young male presenting with neurological deficit and a pathological dislocation of D8 over D9 vertebra. The magnetic resonance imaging showed an enhancing soft tissue tumour. His basic laboratory workup as well as a bone marrow biopsy was normal. Through a single midline posterior approach, he underwent a decompressive laminectomy of D8 and D9 vertebra, anterior column reconstruction with a meshed titanium cage and posterior pedicle screw instrumentation. The histological diagnosis of granulocytic sarcoma was confirmed by appropriate immuno-histochemical studies. He received postoperative radiotherapy following which his wound dehiscesed and the tumour fungated and spread to his left thigh. He declined chemotherapy and unfortunately expired 9 months later. This case is presented to draw attention to the unusual presentation and to stress that granulocytic sarcoma should be kept in mind when making the differential diagnosis in patients with signs of spinal cord compression even in non-leukaemic individuals.
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PMID:Pathological dislocation of the dorsal spine following granulocytic sarcoma in a non-leukaemic patient. 1968 54

We report a case of fatal evolution of neurofibromatosis in a young boy. A laminectomy was performed when he was 9 years old. A secondary hyperkyphosis led to many surgeries resulting in recurrent malunions. When he was 23 years old, a breakage of his rods was treated by a new instrumentation and a T12-L1 interbody cage fitted with rh-BMP. Five months later, he developed a huge posterior tumour on his back. The biopsy diagnosed a neurofibrosarcoma. The growth of the tumour was extremely rapid. He died after several months from a septic shock. NF1 is characterised by neurofibromas that have a possibility of malign degeneration and conversion to a sarcoma. However, the chronology, rapidity of evolution and the exceptional volume of the tumour made us wonder whether the BMP had a part of responsibility as osteoinductor in the malignant degeneration, in this particular case, of neurofibromatosis. It seemed important to point out this case to the medical community.
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PMID:Could an osteoinductor result in degeneration of a neurofibroma in NF1? 2044 13


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