Haemangiopericytoma in the distal third of the arm. (1/145)

A 49-year-old woman had a haemangiopericytoma in the distal third of the arm, which is an extremely rare location. There was no recurrence of the tumor 5 years after wide margin surgical excision.  (+info)

Measurement of telomerase activity in dog tumors. (2/145)

Telomeres are specific structures present at the end of liner chromosomes. DNA polymerase can not synthesize the end of liner DNA and, as a result, the telomeres become progressively shortened by successive cell divisions. To overcome the end replication problem, telomerase adds new telomeric sequences to the end of chromosomal DNA. The enzyme activity is undetectable in most normal human adult somatic cells, in which shortening of the telomere is thought to limit the somatic-cell life span. In contrast to normal somatic cells, many human tumors possess telomerase activity. The present study looked at whether telomerase activity might serve as a marker for canine tumors. Telomerase activity was measured using the telomeric repeat amplification protocol assay. Normal dog somatic tissues showed little or no telomerase activity, while normal testis exhibited a high level of telomerase activity. We measured telomerase activity in tumor samples from 45 dogs; 21 mammary gland tumors, 16 tumors developed in the skin and oral cavity, 7 vascular tumors and 1 Sertoli cell tumor. Greater than 95% of the tumor samples contained telomerase activity (3-924 U/2 micrograms protein). The results obtained in this study indicated that telomerase should be a useful diagnostic marker for a variety of dog tumors, and it may serve as a target for antitumor chemotherapy.  (+info)

Haemangiopericytoma of kidney: a report of 2 cases. (3/145)

Haemangiopericytoma is a rare neoplasm of the kidney. There are no unique radiological or clinical identifiers that can aid in preoperative diagnosis. Surgery is the only reliable therapy, as both chemotherapy and radiotherapy have proven ineffective in several series. The outcome is difficult to predict, the only reliable predictor is presence or absence of metastasis. The rarity of this lesion prompts the report of these two cases.  (+info)

Liver angiosarcoma and hemangiopericytoma after occupational exposure to vinyl chloride monomer. (4/145)

Various malignant tumors of the liver, especially liver angiosarcoma, have been described after occupational exposure to vinyl chloride monomer. We present the case records and pathologic findings of two plastic industry workers who had been exposed to high concentrations of vinyl chloride. These workers developed hepatic neoplasms, angiosarcoma, or hemangiopericytoma. We discuss the histogenesis of these tumors; the common vascular origin and the mutual transformation of these two tumors suggest that the hemangiopericytoma may also have developed during occupational exposure to high concentrations of vinyl chloride monomer.  (+info)

Solitary fibrous tumor arising from the falx cerebri--case report. (5/145)

A 50-year-old female was admitted with headache and visual disturbance. Neuroimaging demonstrated a well-demarcated large tumor attached to the falx cerebri. The tumor was totally removed by surgery. Histological examination showed that the tumor consisted of spindle cells with no pattern in the collagenous background. Staghorn-like blood vessels were common. Immunohistochemical study showed the tumor cells were strongly positive for CD34 and vimentin, but negative for epithelial membrane antigen. The diagnosis was solitary fibrous tumor arising from the falx cerebri. Solitary fibrous tumor is rare within the cranial cavity, and can be distinguished from meningioma and hemangiopericytoma by the histological, ultrastructural, and immunohistochemical findings.  (+info)

Prostaglandin D synthase (beta-trace) in meningeal hemangiopericytoma. (6/145)

The level of prostaglandin D synthase (PGDS), a major protein constituent of cerebrospinal fluid (CSF), is altered in various brain diseases, including meningitis. However, its role in the brain remains unclear. PGDS is mainly synthesized in the arachnoid cells, the choroid plexus and oligodendrocytes in the central nervous system. Among brain tumors, meningiomas showed intense immunoreactivity to PGDS in the perinuclear region. Thus, PGDS has been considered a specific cell marker of meningioma. In this study, we examined 25 meningeal hemangiopericytomas (HPCs) and found that 16 of the tumors (64%) showed immunoreactivity for PGDS in the perinuclear region. For comparison, 15 meningiomas, 14 soft-tissue HPCs, 1 mesenchymal chondrosarcoma, 3 choroid plexus papillomas, and 7 oligodendrogliomas were also examined. Meningiomas showed positive immunoreactivity for PGDS in 13 cases (80%). Except for one case located at the sacrum, none of the other soft-tissue HPCs showed immunostaining for PGDS. Mesenchymal chondrosarcoma arises in the bones of the skull, and its histological pattern resembles that of HPC; however, it showed no immunoreactivity for PGDS. Neither choroid plexus papillomas nor oligodendrogliomas were immunopositive for PGDS. These findings suggest that meningeal HPCs may have a unique molecular phenotype that is distinct from that of the soft-tissue HPCs. The origin of meningeal HPCs may be more closely related to the arachnoid cells.  (+info)

Recurrent congenital haemangiopericytoma in a child. (7/145)

A five-day-old boy was referred with a soft-tissue mass in his right upper arm. Plain radiographs and ultrasound demonstrated a lesion extending from the axilla to the elbow on the posterolateral aspect of the humerus. Open biopsy confirmed the diagnosis of congenital haemangiopericytoma. After MRI and selective angiography, excision biopsy was carried out, but no adjuvant therapy was administered. At further examination, four years and ten months later, he was noted to have three small nodules at the site of the original tumour. Excision biopsy confirmed this to be a local recurrence, although the lesion was less cellular with no appreciable mitotic activity. Congenital haemangiopericytoma is a rare cause of a soft-tissue mass in children. Most tumours are benign, and recurrence is uncommon. The treatment is controversial, but most centres recommend the use of adjuvant chemotherapy, combined with complete excision. We recommend treatment with doxorubicin. Orthopaedic surgeons should be familiar with this tumour since 30% to 50% of cases occur in the limbs.  (+info)

Cloning and characterization of FGF23 as a causative factor of tumor-induced osteomalacia. (8/145)

Tumor-induced osteomalacia (TIO) is one of the paraneoplastic diseases characterized by hypophosphatemia caused by renal phosphate wasting. Because removal of responsible tumors normalizes phosphate metabolism, an unidentified humoral phosphaturic factor is believed to be responsible for this syndrome. To identify the causative factor of TIO, we obtained cDNA clones that were abundantly expressed only in a tumor causing TIO and constructed tumor-specific cDNA contigs. Based on the sequence of one major contig, we cloned 2,270-bp cDNA, which turned out to encode fibroblast growth factor 23 (FGF23). Administration of recombinant FGF23 decreased serum phosphate in mice within 12 h. When Chinese hamster ovary cells stably expressing FGF23 were s.c. implanted into nude mice, hypophosphatemia with increased renal phosphate clearance was observed. In addition, a high level of serum alkaline phosphatase, low 1,25-dihydroxyvitamin D, deformity of bone, and impairment of body weight gain became evident. Histological examination showed marked increase of osteoid and widening of growth plate. Thus, continuous production of FGF23 reproduced clinical, biochemical, and histological features of TIO in vivo. Analyses for recombinant FGF23 products produced by Chinese hamster ovary cells indicated proteolytic cleavage of FGF23 at the RXXR motif. Recent genetic study indicates that missense mutations in this RXXR motif of FGF23 are responsible for autosomal dominant hypophosphatemic rickets, another hypophosphatemic disease with similar features to TIO. We conclude that overproduction of FGF23 causes TIO, whereas mutations in the FGF23 gene result in autosomal dominant hypophosphatemic rickets possibly by preventing proteolytic cleavage and enhancing biological activity of FGF23.  (+info)