Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0178874 (tumor progression)
 40,807 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A retrospective evaluation of 101 cases of secondary chondrosarcoma was performed. The results of the analysis of X-ray data showed chondrosarcoma to develop from osteocartilaginous exostosis or chondroma (53 and 47 cases, respectively). (One case lacked roentgenologic data). The former pattern of tumor development prevailed in patients under 40 years of age, while the latter one was more frequently observed in the older age group (68% of cases in each age bracket). Secondary chondrosarcoma was most frequently localized to long tubular and flat bones (48 and 34 patients, 47.53 and 33.66%, respectively). Roentgenologic diagnosis of early stage secondary chondrosarcoma was extremely difficult. Histologic examination showed degree I cell anaplasia in most cases. Surgery is the main procedure of treatment of secondary chondrosarcoma. Relapses were observed only in patients who had undergone sparing operations. The smaller the extent of surgery, the higher relapse rate was registered. Fifteen patients (14.87%) died of tumor progression. Sparing procedures were performed in 14 of them (93.3%).
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PMID:[Secondary chondrosarcoma]. 366 Jul 58

Chondromas and chondrosarcomas are cartilage-forming tumors that occur rarely in the spine. These neoplasms exist on opposite ends of the pathologic spectrum, ranging from the benign chondroma to the malignant, high-grade chondrosarcoma. Unlike other sarcomas, a patient's long-term prognosis is influenced by the grade of the tumor. A complete en bloc resection is the ideal method of surgical management. This method holds especially true for chondrosarcomas, and can result in prolonged survival. These tumors are resistant to conventional chemotherapy and radiation therapy. Hypofractionated stereotactic radiation therapy may slow tumor progression, although the long-term effect of this modality is unknown.
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PMID:Chondroma/Chondrosarcoma of the spine. 1815 48

The dysregulation of signal transducers and activators of transcription 3 (STAT3) has been reported to be associated with tumor progression, angiogenesis and metastasis. The purpose of this study was to analyze the clinical value of STAT3 expression in human osteosarcoma. First, semi-quantitative RT-PCR was performed to detect the expression of STAT3 mRNA in normal bone tissues, chondroma tissues and osteosarcoma tissues. Then, immunohistochemistry was performed to detect the expression of STAT3 protein in 76 osteosarcoma tissues and the relationship of STAT3 protein expression with clinicopathologic factors or prognosis of osteosarcoma patients. RNA interference (RNAi) technology was employed to inhibit STAT3 expression. MTT and flow cytometric assays were performed to analyze the effect of STAT3 inhibition on proliferation and apoptosis of osteosarcoma cells. Finally, the expression of STAT3-related target genes were also determined. Results showed that osteosarcoma tissues showed significantly higher expression levels of STAT3 mRNA than normal bone or chondroma tissues (P<0.05). Immunohistochemistry showed that the staining of STAT3 protein was mainly located in cytoplasm of osteosarcoma cells in osteosarcoma tissue samples. The high level of STAT3 protein was associated with poor tumor differentiation and presentation of metastasis (P=0.039 and 0.022). Moreover, the 5-year overall and relapse-free survival rates for osteosarcoma patients with high STAT3 expression were lower than those for patients with low STAT3 expression. In addition, the status of STAT3 protein expression was an independent prognostic factor for both disease-free survival (P=0.0235) and overall survival (P=0.0032). RNAi-mediated STAT3 inhibition could induce proliferation inhibition and apoptosis enhancement in osteosarcoma cells, which might be associated with inhibition of some anti-apoptosis genes. Overall, STAT3 plays crucial roles in osteosarcoma development and might become a potential molecular target for gene therapy of human osteosarcomas.
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PMID:Clinical value of signal transducers and activators of transcription 3 (STAT3) gene expression in human osteosarcoma. 2054 60