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

Osteosarcomas were produced by the intratibial inoculation of New Zealand black rats with Moloney sarcoma virus (MSV) at 1 day and 4 days of age. Radiographic evidence of osteosarcoma development was first demonstrated at 10 to 15 days postinoculation in both groups. Subsequent radiographic and light and electron microscopic evaluation of tumor-bearing rats demonstrated that osteosarcomas in rats inoculated at Day 4 of age were more osteoproliferative osteosarcomas than those in rats inoculated on Day 1. Rats inoculated at 4 days of age lived longer, had more slowly growing osteosarcomas, and developed a consistent tumor-associated cachexia compared to tumor-bearing rats inoculated at Day 1. Both groups of rats had a 93% metastasis rate involving either sublumbar lymph nodes, lungs, or both. Tumor-bearing rats inoculated at 4 days of age had consistent elevations in both urinary hydroxyproline excretion (HOP/CR) and serum alkaline phosphatase levels, and in serum calcium levels at some time points. The high tumor incidence after a short latent period and the morphologic and biochemical similarities between the MSV-induced murine osteosarcoma and the osteosarcoma in human beings makes this discrete tumor and a valuable animal model for the evaluation of new therapeutic regimens.
 ...
PMID:Virus-induced animal model of osteosarcoma in the rat: Morphologic and biochemical studies. 18 16

A case of an osteoblastoma of the proximal femur with a unique local, massive reactive periostitis mimicking osteosarcoma or osteomyelitis and unique systemic manifestations is reported. The severe toxic manifestations included: massive weight loss, chronic fever, anemia, systemic periostosis, and other signs. Due to confusion as to diagnosis, lack of response to numerous antibiotic regimens, and severe cachexia with clinical signs of impending death, an amputation was performed. Pathologic study revealed an osteoblastoma. A thorough review of the case suggests that the signs and symptoms were possibly consequent to an immune response mounted against the tumor rather than to secondary infection, although the latter possibility cannot be completely excluded.
 ...
PMID:A case of osteoblastoma associated with severe systemic toxicity. 53 63

A transplantable ascites-forming osteosarcoma (J. H. 1-AOS) derived from the 35th generation of spontaneous osteosarcoma, J. H. 1-OS, grown in Fischer 344 syngeneic rats was established. Tumorigenicity, histochemical and ultrastructural characteristics were investigated. Rats carrying the ascites form osteosarcoma died of cachexia about 15 days after transplantation, 1.5-2.5 x 10(6) cells/ml of tumor cells generally being involved in the ascites and tumor nodules formed in the mesentery. After inoculation into the back subcutaneous space, tumor growth was very rapid. Small round cells were detected in the Giemsa stain smear, and although osteoid formation was histologically lacking, cell surface alkaline phosphatase activity was noted both light and electron microscopically. Polyacrylamide gel electrophoresis demonstrated that alkaline phosphatase (Al-p) extracted from this tumor was consistent with Al-p from rat fetal calvaria. Thus maintenance of osteogenic potential is suggested for these ascites osteosarcoma cells, indicating their usefulness for further studies of biological behaviors of this tumor type.
 ...
PMID:[Establishment and characterization of an ascites-forming rat osteosarcoma cell line]. 154 42

Between 1978 and 1986, atrial heart tumors were found in 21 of our patients, all of them subsequently underwent surgery. Pathological-histological examination in 20 patients confirmed the diagnosis of a myxoma; the one remaining case was a female patient with primary cardiogenic osteosarcoma. Of the 20 patients, 15 (75%) were females; in four female patients (20%) the tumor was localized in the right atrium. The main symptoms and findings were elevated erythrocyte sedimentation rates (80%), stress-induced dyspnea or paroxysmal dyspnea (71% resp.), and diastolic mitral or tricuspid murmurs (62%). The patient with osteosarcoma died of cachexia on the basis of generalized diffuse metastases. One female patient with a preoperative history of severe left ventricular impairment on the basis of dilative cardiomyopathy died 5 weeks after surgery. Relapse of atrial myxoma has not yet occurred during follow-up since 1978.
 ...
PMID:[Primary atrial heart tumors--a review of 21 cases]. 321 45

An osteogenic sarcoma of the tibia occurred in an eight-year-old boy with epidermolysis bullosa dystrophica hereditaria (EBDH) (Hallopeau-Siemens type). The patient had had the congenital skin disease since the time of birth. A painful swelling appeared in the proximal portion of his right tibia, which was diagnosed as osteogenic sarcoma on biopsy study. The patient died of massive pulmonary metastases and cachexia four months after the onset of the tumor. Osteogenic sarcoma in a patient with EBDH seems not to have been previously reported. EBDH has been known to be occasionally associated with squamous cell carcinoma. Whether an impairment of the patient's defense mechanism by the chronic skin disease might have enhanced the rapid progression of the associated bone malignancy is unknown.
 ...
PMID:Osteogenic sarcoma of the tibia in a patient with epidermolysis bullosa dystrophica. 342 8

The purpose of this study was to prospectively evaluate the use of ultrasonographically guided high-intensity focused ultrasound (HIFU) in the salvage of limbs in patients with osteosarcoma. Seven patients underwent HIFU ablation. Laboratory and radiologic examinations were performed after intervention. Changes in symptoms and survival time were noted at follow-up. No severe complications were observed, and preexisting severe pain disappeared in patients treated with HIFU. Alkaline phosphatase did not show statistically significant changes before and after HIFU treatment, although Alkaline phosphatase did change 1 mo and 2 mo after HIFU. Complete response of the tumor was achieved in three patients with osteosarcoma. Partial response was achieved in another three patients treated with HIFU. Pulmonary metastasis was noted in only one patient 5 mo after HIFU. The median survival time was 68 mo. All patients were alive 3 y after HIFU treatment. Five patients were alive at follow-up visits after 5 y. One patient died from cachexia and infection after 4 y, another patient died of cardiac arrest attack after 4 y. Three patients died of lung dysfunction from pulmonary metastases after 5 y. The five-year survival rate was 71.4%. The authors concluded that HIFU ablation was a safe and feasible method of treatment of osteosarcoma which salvages the limb, but large-scale randomized clinical trials are necessary for confirmation.
 ...
PMID:Osteosarcoma: limb salvaging treatment by ultrasonographically guided high-intensity focused ultrasound. 1944 2

Skeletal muscle atrophy in cancer cachexia is mediated by the interaction between muscle stem cells and various tumor factors. Although Notch signaling has been known as a key regulator of both cancer development and muscle stem cell activity, the potential involvement of Notch signaling in cancer cachexia and concomitant muscle atrophy has yet to be elucidated. The murine K7M2 osteosarcoma cell line was used to generate an orthotopic model of sarcoma-associated cachexia, and the role of Notch signaling was evaluated. Skeletal muscle atrophy was observed in the sarcoma-bearing mice, and Notch signaling was highly active in both tumor tissues and the atrophic skeletal muscles. Systemic inhibition of Notch signaling reduced muscle atrophy. In vitro coculture of osteosarcoma cells with muscle-derived stem cells (MDSCs) isolated from normal mice resulted in decreased myogenic potential of MDSCs, while the application of Notch inhibitor was able to rescue this repressed myogenic potential. We further observed that Notch-activating factors reside in the exosomes of osteosarcoma cells, which activate Notch signaling in MDSCs and subsequently repress myogenesis. Our results revealed that signaling between tumor and muscle via the Notch pathway may play an important role in mediating the skeletal muscle atrophy seen in cancer cachexia.
...
PMID:Notch Signaling Mediates Skeletal Muscle Atrophy in Cancer Cachexia Caused by Osteosarcoma. 2737 29

Patients with cancer have an increased risk of thromboembolism, which is the second leading cause of death in these patients. Several mechanisms of the prothrombotic state in these patients have been proposed. Among them are a platelet activation receptor, C-type lectin-like receptor 2 (CLEC-2), and its endogenous ligand podoplanin, which are the focus of this review. CLEC-2 is almost specifically expressed in platelets/megakaryocytes in humans. A membrane protein, podoplanin is expressed in certain types of cancer cells, including squamous cell carcinoma, brain tumor, and osteosarcoma, in addition to several normal tissues, including kidney podocytes and lymphatic endothelial cells but not vascular endothelial cells. In the bloodstream, podoplanin induces platelet activation by binding to CLEC-2 and facilitates hematogenous cancer metastasis and cancer-associated thrombosis. In an experimental lung metastasis model, the pharmacological depletion of CLEC-2 from platelets in mice resulted in a marked reduction of lung metastasis of podoplanin-expressing B16F10 cells. Control mice with B16F10 orthotopically inoculated in the back skin showed massive thrombus formation in the lungs, but the cancer-associated thrombus formation in CLEC-2-depleted mice was significantly inhibited, suggesting that CLEC-2-podoplanin interaction stimulates cancer-associated thrombosis. Thromboinflammation induced ectopic podoplanin expression in vascular endothelial cells or macrophages, which may also contribute to cancer-associated thrombosis. CLEC-2 depletion in cancer-bearing mice resulted in not only reduced cancer-associated thrombosis but also reduced levels of plasma inflammatory cytokines, anemia, and sarcopenia, suggesting that cancer-associated thrombosis may cause thromboinflammation and cancer cachexia. Blocking CLEC-2-podoplanin interaction may be a novel therapeutic strategy in patients with podoplanin-expressing cancer.
 ...
PMID:Platelets and cancer-associated thrombosis: focusing on the platelet activation receptor CLEC-2 and podoplanin. 3177 48

Patients with cancer have an increased risk of thromboembolism, which is the second leading cause of death in these patients. Several mechanisms of the prothrombotic state in these patients have been proposed. Among them are a platelet activation receptor, C-type lectin-like receptor 2 (CLEC-2), and its endogenous ligand podoplanin, which are the focus of this review. CLEC-2 is almost specifically expressed in platelets/megakaryocytes in humans. A membrane protein, podoplanin is expressed in certain types of cancer cells, including squamous cell carcinoma, brain tumor, and osteosarcoma, in addition to several normal tissues, including kidney podocytes and lymphatic endothelial cells but not vascular endothelial cells. In the bloodstream, podoplanin induces platelet activation by binding to CLEC-2 and facilitates hematogenous cancer metastasis and cancer-associated thrombosis. In an experimental lung metastasis model, the pharmacological depletion of CLEC-2 from platelets in mice resulted in a marked reduction of lung metastasis of podoplanin-expressing B16F10 cells. Control mice with B16F10 orthotopically inoculated in the back skin showed massive thrombus formation in the lungs, but the cancer-associated thrombus formation in CLEC-2-depleted mice was significantly inhibited, suggesting that CLEC-2-podoplanin interaction stimulates cancer-associated thrombosis. Thromboinflammation induced ectopic podoplanin expression in vascular endothelial cells or macrophages, which may also contribute to cancer-associated thrombosis. CLEC-2 depletion in cancer-bearing mice resulted in not only reduced cancer-associated thrombosis but also reduced levels of plasma inflammatory cytokines, anemia, and sarcopenia, suggesting that cancer-associated thrombosis may cause thromboinflammation and cancer cachexia. Blocking CLEC-2-podoplanin interaction may be a novel therapeutic strategy in patients with podoplanin-expressing cancer.
 ...
PMID:Platelets and cancer-associated thrombosis: focusing on the platelet activation receptor CLEC-2 and podoplanin. 3180 11