Myxofibrosarcomas contain large numbers of infiltrating immature dendritic cells. (1/10)
Myxofibrosarcoma is a malignant tumor with distinctive histologic features and is believed to be derived from fibroblasts. The function of infiltrating myeloid cells in myxofibrosarcoma is poorly understood. It previously has been shown that a combination of dendritic morphologic features and expression of the C-type lectin, dendritic cell-specific intercellular adhesion molecule-3 grabbing nonintegrin (DC-SIGN), is useful for identifying DC populations in tissue sections. In the present study, we found that 3% to 61% (median, 22%) of cells in myxofibrosarcomas express DC-SIGN and have dendritic morphologic features. These DC-SIGN--positive cells are not in cell cycle and are consistent with infiltrating DCs. The percentage of DCs in myxofibrosarcomas is independent of tumor grade. It previously has been shown that DC-SIGN--positive cells are either immature DCs or DCs that predominantly activate TH2 cells, both subsets likely to give rise to ineffective antitumor responses. The DC-SIGN--positive DCs that we have identified in myxofibrosarcoma may, therefore, be involved in the induction of ineffective immune responses or even tolerance to tumor antigens. (+info)Population pharmacokinetics of melphalan in paediatric blood or marrow transplant recipients. (2/10)
AIM: To develop a population pharmacokinetic model for melphalan in children with malignant diseases and to evaluate limited sampling strategies for melphalan. METHODS: Melphalan concentration data following a single intravenous dose were collected from 59 children with malignant diseases aged between 0.3 and 18 years. The data were split into two sets: the model development dataset (39 children, 571 concentration observations) and the model validation dataset (20 children, 277 concentration observations). Population pharmacokinetic modelling was performed with the NONMEM software. Stepwise multiple linear regression was used to develop a limited sampling model for melphalan. RESULTS: A two-compartment model was fitted to the concentration-vs.-time data. The following covariate population pharmacokinetic models were obtained: (i) Clearance (l h(-1)) = 0.34.WT - 3.17.CPT + 0.0377.GFR, where WT = weight (kg), CPT = prior carboplatin therapy (0 = no, 1 = yes), and GFR = glomerular filtration rate (ml min(-1) 1.73 m(-2)); (ii) Volume of distribution (l) = 1.12 + 0.178.WT. Interpatient variability (coefficient of variation) was 27.3% for clearance and 33.8% for volume of distribution. There was insignificant bias and imprecision between observed and model-predicted melphalan concentrations in the validation dataset. A three-sample limited sampling model was developed which adequately predicted the area under the concentration-time curve (AUC) in the development and validation datasets. CONCLUSIONS: A population pharmacokinetic model for melphalan has been developed and validated and may now be used in conjunction with pharmacodynamic data to develop safe and effective dosing guidelines in children with malignant diseases. (+info)Evaluation of carboplatin pharmacokinetics in pediatric oncology by means of inductively coupled plasma mass spectrometry. (3/10)
Carboplatin is widely used in pediatric oncology to treat different tumors. Aim of the present study was to assess the potential of sector field inductively coupled plasma mass spectrometry (SF-ICPMS) in evaluating the area under the plasma platinum concentration vs time curve in pediatric patients presenting solid tumors and treated with carboplatin 349-1000 mg m-2. Seventeen patients were enrolled and 23 courses of chemotherapy were evaluated. Plasma was ultrafiltered and free carboplatin was measured in ultrafiltrates as platinum by SF-ICP-MS. Comparison was made between different equations to obtain a target AUC. Limits of detection and of quantification, intra- and inter-day repeatability of the measurements, recovery of the 'free-carboplatin' confirmed SF-ICP-MS as a reliable technique in the quantification of serum platinum in anticancer carboplatin-based therapies. (+info)Myofibroblastic sarcomas: a clinicopathological study of 20 cases. (4/10)
BACKGROUND: Myofibroblastic sarcoma was used to be a controversial neoplasm. This study investigated the clinicopathological features of 20 cases of myofibroblastic sarcoma arising in different locations. METHODS: The paraffin-embedded tissue samples from 20 cases of patients with myofibroblastic sarcoma were stained immunohistochemically, and 5 cases examined by electron microscopy. Student's t test was used to analyze the difference of Ki-67 labeling index between grade 1 and grade 2 myofibroblastic sarcomas. RESULTS: Histologically, the tumors were composed of slender spindle cells with eosinophilic cytoplasm, and fusiform, tapering, wavy, or plump ovoid; vesicular nuclei and a small central eosinophilic nucleoli. Immunohistochemically, the tumor cells expressed smooth muscle actin (18/20), muscle specific actin (16/20), fibronectin (20/20) and desmin (2/20). Ultrastructurally, the tumor cells revealed abundant rough endoplasmic reticulum and longitudinally arranged fine filaments with focal densities in the cytoplasm. A clinical follow-up of 19 patients showed that 2 cases experienced local recurrence and distant metastasis 6 months to 4 years after the initial operation. Nine cases recurred locally 17 to 46 months after the initial excision, and 9 cases were alive with no evidence of disease. CONCLUSIONS: Myofibroblastic sarcomas, which exhibit diverse histological appearance, can easily be misdiagnosed as benign tumors. Myofibroblastic sarcomas are local destructive lesions with frequent recurrence, and may metastase distantly. (+info)Primary high-grade myofibroblastic sarcoma arising from the pericardium. (5/10)
Primary pericardial sarcomas are very rare. A 62-year-old Japanese man presented with cardiac tamponade. Echocardiography, computed tomography and magnetic resonance imaging revealed massive pericardial effusion and a large tumor in the pericardial cavity, attached to the pericardium of the left ventricular posterolateral free wall. Surgical excision of the tumor was performed and histopathological and immunohistochemical examinations identified high-grade myofibroblastic sarcoma. Because of local recurrence soon after surgery, the patient received adjuvant chemotherapy, including doxorubicin and ifosfamide, and subsequent radiotherapy. As of 6 months after completing radiotherapy, the patient was alive and no disease progression or distant metastases were evident. This may be the first report of primary high-grade myofibroblastic sarcoma arising from the pericardium. (+info)Myofibroblastic sarcoma vs nodular fasciitis: a comparative study of chromosomal imbalances. (6/10)
(+info)Carcinosarcoma ex non-recurrent pleomorphic adenoma composed of TTF-1 positive large cell neuroendocrine carcinoma and myofibrosarcoma: apropos a rare Case. (7/10)
(+info)Continuous internalization of tumor necrosis factor receptors in a human myosarcoma cell line. (8/10)
The cell dynamics of the receptor for tumor necrosis factor (TNF) were examined in TNF-sensitive KYM cells derived from human myosarcoma. With receptor synthesis inhibited by cycloheximide, the half-life of the surface TNF receptor was 2 h in the absence of TNF and 30 min in its presence, suggesting that the TNF receptor is non-recycling and that its internalization is accelerated by TNF. During cell incubation with TNF receptor degradation suppressed by chloroquine, the number of surface TNF receptors remained approximately constant, but the total number of surface and internal TNF receptors increased gradually, at 3 h reaching 1.5 times the initial number, thus suggesting continuous synthesis, externalization, internalization, and degradation of the TNF receptor in the absence of cycloheximide. On cell incubation with 125I-TNF, the intracellular quantity of the pulse-labeled TNF-receptor complex promptly increased, reaching a maximum at 20 min, and then gradually declined, thus confirming that the TNF receptor is internalized as a TNF-receptor complex in the presence of TNF. During incubations with protein synthesis suppressed by cycloheximide following surface TNF receptor digestion by trypsin, TNF receptors reappeared on the cell surface, increasing in number to a peak at 60 min and gradually decreasing, and cells previously exposed to cycloheximide with or without TNF showed no recurrence of surface TNF receptors, suggesting that the TNF receptor is non-recycling. The results of the study thus suggest that the TNF receptor is continuously internalized and degraded intracellularly by lysosomes without being recycled regardless of the presence or absence of TNF and, further, that its internalization is accelerated when it is part of the TNF-receptor complex. (+info)Myosarcoma is a type of soft tissue sarcoma that arises from the muscle cells, often characterized by malignant tumors with local invasion and potential for distant metastasis.
Myosarcoma is a type of cancer that arises from the muscle tissue. It's a subtype of sarcoma, which is a broader category of malignancies that develop in the body's connective tissues (such as bones, muscles, tendons, cartilages, nerves, and blood vessels).
Myosarcomas specifically originate from the muscle cells, and they can occur in both smooth muscles (those we cannot consciously control, like the ones in the walls of our digestive system) and skeletal muscles (the ones we can voluntarily control). They are relatively rare tumors, accounting for about 1% of all adult malignancies.
The symptoms of myosarcoma depend on the location and size of the tumor. A common sign is a painless mass or swelling that grows over time. As the tumor advances, it may cause pain, limit movement, and eventually affect nearby organs and tissues. Treatment typically involves surgical removal of the tumor, often followed by radiation therapy and/or chemotherapy to kill any remaining cancer cells and reduce the risk of recurrence. The prognosis for myosarcoma varies depending on the stage at diagnosis, the patient's overall health, and other factors.