Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0029463 (osteosarcoma)
 16,637 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Two murine monoclonal antibodies, 29-13 (IgG1) and 29-2 (IgG2a), generated against malignant fibrous histiocytoma plasma membranes immunoprecipitated a Mr 200,000 protein (p200), with an isoelectric point between 6.3 and 7.5. Two additional antibodies, 35-16 (IgG1) and 30-40 (IgG2a), generated against Ewing's sarcoma membranes, immunoprecipitated an acidic protein of Mr 160,000 (p160), with an isoelectric point between 5.8 and 6.7. Monoclonal antibodies 29-13 and 29-2 recognize a similar determinant(s) on p200 while 35-16 and 30-40 recognize different determinants on p160. Monoclonal antibody 29-13 exhibited significant binding to membranes isolated from fibrosarcoma and aggressive fibromatosis; moderate binding to osteosarcoma, hemangiopericytoma, and malignant fibrous histiocytoma; and minimal to no binding to other soft tissue sarcoma plasma membranes. The p200 protein was not expressed in 16 other malignant tumors and in only 3 of 35 normal human tissue specimens. High levels of p200 were selectively expressed by leiomyosarcoma, Ewing's sarcoma, and fibrosarcoma cells as well as neonatal fibroblasts in vitro, but not by other carcinoma cell lines or B-lymphoblasts. The p160 protein appeared to be selectively expressed by Ewing's sarcoma with little or no expression on other sarcomas, carcinomas, or normal tissues. However, the p160 antigen was expressed in Ewing's sarcoma, leiomyosarcoma, melanoma, 4 of 9 carcinomas, and neonatal fibroblasts in vitro. The affinity of MoAbs 29-13, 29-2, 35-16, and 30-40 ranged from 5.3 x 10(8) to 4.7 x 10(9) M-1 for sarcoma membranes with approximately 5 x 10(4) binding sites/sarcoma cell.
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PMID:Monoclonal antibody identification and characterization of two human sarcoma-associated antigens. 206 31

Small, round, blue-cell tumors (SRCT), including rhabdomyosarcoma, Ewing's sarcoma of bone and soft tissue, mesenchymal chondrosarcoma, small cell osteosarcoma, hemangiopericytoma, neuroblastoma, peripheral neurectodermal tumor (peripheral neuroepithelioma of bone and soft tissue), and the malignant small cell tumor of the thoracopulmonary region described by Askin (Askin's tumor), are often difficult to distinguish by light microscopy. We have evaluated the cytogenetics of these tumors by studying 24 tumor explants in short-term culture and 22 tumor cell lines. In Ewing's sarcoma (a tumor of unknown histogenesis), and in peripheral neuroepithelioma and Askin's tumor (tumors with evidence of neural origin), we have observed an indistinguishable t(11;22) translocation.
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PMID:Cytogenetic characterization of selected small round cell tumors of childhood. 300 99

From February 1982 to December 1983, 42 patients affected by neoplasms of the limbs were treated at the Istituto Nazionale Tumori of Milan by hyperthermic antiblastic perfusion in extracorporeal circulation at the temperature of 40-41 degrees C for 1 h. Thirty-two were affected by melanoma, 4 by osteogenic sarcoma, 2 by squamous-cell carcinoma, 1 by liposarcoma, 1 by hemangiopericytoma, 1 by clear-cell sarcoma and 1 by Kaposis's sarcoma. As regards the immediate response, a complete plus partial remission rate of 88% without any major complication was obtained. The follow-up period is too short for any considerations about overall survival. However, because of these good clinical results we consider this method able to locally control the evolution of neoplasms of the extremities, allowing in many cases a limb salvage.
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PMID:Hyperthermic antiblastic perfusion in the treatment of cancer of the extremities. 404 37

Sixteen cases of mandibular tumors or paramandibular soft tissue tumors with mandibular involvement are reported. These include such rare mandibular tumors or tumor-like conditions as melanotic progonoma, intraosseous haematoma secondary to von Willebrand's disease, post-irradiation osteosarcoma, monostotic eosinophilic granuloma, aneurysmal bone cyst and osseous hemangiopericytoma. Three cases of cherubism, one of fibrous dysplasia or aggressive fibromatosis and one of central giant cell reparative granuloma are also reported. The soft tissue tumors comprise round cell sarcoma, parotid adeno-carcinoma with generalised metastases, embryonal rhabdo-myo-sarcoma, neuro-fibro-sarcoma and congenital cystic hygroma. In all the cases the disease was well advanced when the patient presented for X-ray examination. The specific X-ray diagnosis of mandibular and paramandibular tumors in childhood is more difficult than that of similar tumors in other parts of the body.
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PMID:Mandibular and para-mandibular tumors in children. Report of 16 cases. 627 31

The relative rarity and anatomical position of retrorectal tumors may lead to difficulty in diagnosis and surgical treatment. The clinical features and management of 20 such tumors (chordoma 8, neurilemmoma 3, teratoma 3, hemangiopericytoma 1, chondrosarcoma 1, osteosarcoma 1, dermoid 1, lipoma 1, and undifferentiated sarcoma 1) have therefore been reviewed. Low back or sacral pain was present in 18 patients and, although all tumors were palpable on rectal examination, pain had been present for a median of 12 months before diagnosis. Mean tumor size was 9.4 cm (range: 2.5-17 cm). Sacral bone destruction was demonstrated radiographically in all chordomas and three sarcomas, but in none of the benign tumors. Three patients had undergone previous partial removal of their tumors. Surgical resection was carried out using a combined abdominal and transsacral approach in 13, a transsacral approach in the right lateral position in four and transabdominally in three. There was one operative death following secondary operation for chbrdoma. Four of 12 patients with malignant tumors are alive and well at seven months to eight years. One died of a myocardial infarct without recurrence at 11 years. For small benign tumors, the right lateral position permits maximal flexibility for resection either by the transsacral, transabdominal or a combined approach. For bulky or malignant tumors, a combined abdominal transsacral approach in the right lateral position permits vascular control and provides good exposure for protection of vital structures and wide resection.
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PMID:Abdominosacral approach for retrorectal tumors. 692 81

The C/EBP-homologous transcription factor CHOP (GADD153) is inducible by growth inhibition or DNA damage, and has been shown to be oncogenically activated by the specific (12;16) translocation in human myxoid liposarcoma. We have now found CHOP amplification in two sarcoma cell lines with previously reported amplification of the nearby GLI gene. Among 98 other human sarcomas of various types, CHOP was amplified in a hemangiopericytoma, a liposarcoma, and two osteosarcoma. High constitutive expression levels of CHOP were observed in tumors with gene amplification, but also in some other samples. The nearby MDM2 gene, which codes for a protein that may inactivate wild-type p53, has previously been reported to be frequently amplified in sarcoma. In our sarcoma panel, MDM2 was amplified in 9 cases. MDM2 and CHOP were co-amplified in two of these, whereas the two osteosarcomas had amplified CHOP but not MDM2. CHOP was amplified in both cell lines with GLI amplification, and MDM2 only in one. No mutations in the TP53 gene have been found in samples with amplification of MDM2. In contrast, the cell line in which CHOP but not MDM2 was amplified had mutated TP53, suggesting that selection of this amplicon was not mediated through p53 inactivation.
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PMID:The protooncogene CHOP/GADD153, involved in growth arrest and DNA damage response, is amplified in a subset of human sarcomas. 782 48

Oncogenic osteomalacia is an unusual and rare clinicopathologic syndrome characterized by mesenchymal tumors that apparently produce osteomalacia and biochemical abnormalities consisting of hypophosphatemia, normocalcemia, and increased levels of alkaline phosphatase. We collected from the Mayo Clinic files and from our consultation files the records for 17 cases of osteomalacia associated with bone lesions. There were five cases of fibrous dysplasia, three of hemangiopericytoma, and two of phosphaturic mesenchymal tumor. There was one case each of osteosarcoma, chondroblastoma, chondromyxoid fibroma, malignant fibrous histiocytoma, giant cell tumor, metaphyseal fibrous defect, and hemangioma. In this study we can figure out that the most common characteristic histologic features of our cases were hemangiopericytomatous vascular proliferation, fine lace-like stromal calcification, and stromal giant cells. In most of the cases, the clinical and biochemical symptoms and signs resolved soon after complete resection of the lesion. When the lesion recurred or metastasized, the symptoms and signs also recurred.
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PMID:Oncogenic osteomalacia: a clinicopathologic study of 17 bone lesions. 784 76

We reviewed the clinical course and the results of various treatment modalities of 80 patients with rare pulmonary neoplasms, who constituted 0.8% of all patients with primary lung cancer treated at the Mayo Clinic from 1980 through 1990. The 50 male and 30 female patients had a median age of 60 years (range, 20 to 87). The histopathologic types of these rare pulmonary neoplasms were non-Hodgkin's lymphoma (41%), carcinosarcoma (20%), mucoepidermoid carcinoma (15%), malignant fibrous histiocytoma (5%), malignant melanoma (4%), fibrosarcoma (4%), leiomyosarcoma (4%), angiosarcoma (2%), hemangiopericytoma (2%), osteosarcoma (1%), and blastoma (1%). Follow-up was complete in all 80 patients, and the median duration of follow-up was 59 months (range, 15 to 130). Of the 80 patients, 63 (79%) underwent pulmonary resection. Of the other 17 patients, 8 underwent only bronchoscopy for diagnosis, 4 had unresectable disease at thoracotomy, 3 had metastatic disease on initial assessment, and 2 had mediastinal involvement detected on mediastinoscopy. Fifty-four patients (68%) received chemotherapy or radiation treatment (or both). The overall 5-year survival was 39%. The strongest factors that influenced survival were cell type and extent of disease at time of initial examination.
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PMID:Rare pulmonary neoplasms. 838 92

Oncogenic osteomalacia is a condition where renal phosphate wasting occurs causing defective mineralisation, in the presence of a tumor. Cultures of cells were established from a hemangiopericytoma resected from a patient with oncogenic osteomalacia. Conditioned media from the cells inhibited phosphate uptake in opossum kidney cells and stimulated of cAMP in rat osteosarcoma cells, a standard parathyroid hormone (PTH)-like assay. This cAMP stimulation was suppressed by the PTH analogue, 3-34 bPTH and also by heat and trypsin treatment of the media. Tests of conditioned media for PTH and parathyroid hormone related protein (PTHrP) immunoreactivity were negative, however, and no hybridisation to probes for PTH, PTHrP or human stanniocalcin was detected in tumor cell RNA on Northern blot. These data support the hypothesis that tumors responsible for oncogenic osteomalacia produce a humoral substance that reduces renal phosphate reabsorption and provide evidence that the factor may act via PTH/PTHrP receptors.
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PMID:Characteristics of tumor cell bioactivity in oncogenic osteomalacia. 902 20

Osteosarcoma, chondrosarcoma and tumors of the Ewing group are the most frequently observed primary malignant bone tumors. In an Internet homepage recently constructed for the Orthopedic Hospital Rizzoli Bologna, Italy, these tumors have represented the majority of 4423 malignant bone tumors in the archives of this institution since 1920 (http:/(/)www.tizeta.it/rizzoli). Malignant fibrous histiocytoma, fibrosarcoma, hemangioendothelioma, malignant hemangiopericytoma and giant-cell tumors are diagnosed less frequently. Since the introduction of modern molecular and cytogenetic techniques, knowledge of genetic aberrations in malignant bone tumors has steadily increased. However, so far only for the group of Ewing tumors has a recurrent chromosomal marker, the translocation t(11;22) (q24;q12), been identified.
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PMID:[Cytogenetic and molecular genetic changes in malignant primary bone tumors]. 970 Jul 67


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