Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.6.1.3 (ATPase)
 65,361 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Three cases of so-called pulmonary sclerosing hemangioma have been studied for endothelial markers (alkaline phosphatase, adenosine triphosphatase, factor VIII-related antigen, and Ulex europaeus I lectin), for intermediate filaments (keratin, vimentin), and for carcinoembryonic and epithelial membrane antigen. Not one of the neoplasms expressed endothelial markers, carcinoembryonic antigen, or keratin reactivity. The tumor cells showed a positive reaction for epithelial membrane antigen and vimentin. The findings exclude an endothelial origin for this group of tumors and favored an epithelial origin as the probable genesis of the neoplastic proliferation.
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PMID:Sclerosing hemangioma of the lung. An immunohistochemical study of intermediate filaments and endothelial markers. 253 67

A total of five haemangiosarcomata and two benign haemangiomas arising in the mammary gland have been studied electron microscopically and by histochemical techniques. Malignant tumors were mainly composed of endothelial cells reactive to alkaline phosphatase and adenosine triphosphatase, and of pericytes and undifferentiated mesenchymal elements. A juvenile haemangioma showed a more structured wall with an increase of endoplasmic reticulum and filaments, and a diminution of membrane modulations and rod-like tubular bodies. A cavernous haemangioma showed an ultrastructure very similar to normal vessels. The ultrastructural and histochemical data suggest a blood vessel origin of mammary angiosarcomas and show that vascular neoplasms of the breast, benign or malignant, are composed of a combined proliferation of the different cell types present in the vessel wall, as described in other organs.
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PMID:Vascular tumors of the mammary gland. A histochemical and ultrastructural study. 646 Nov 25

The natural course of the pathologic features in striated muscle was studied in a full-term infant with myotubular myopathy. At 5 days of age a muscle biopsy revealed that more than 90 percent of muscle fibers fulfilled histologic, histochemical and electron microscopic criteria of fetal myotubes. The infant died unexpectedly at 9 months of age from spontaneous rupture of a multifocal cavernous hemangioma of the liver. Postmortem examination revealed that progressive maturation of the fetal muscle had not occurred postnatally, and more than 90 percent of myofibers were still apparent myotubes. This maturational arrest was generalized to all striated muscles. The only changes detected since the neonatal period were hypertrophy of the small population of large fibers, but with minor cytoarchitectural alterations, and loss of the incomplete histochemical differentiation with ATPase stains or dedifferentiation not attributed to postmortem diffusion. Involvement of the gubernaculum testis accounted for the undescended testicles. The brain and spinal cord appeared normal. Evidence of degenerating and regenerating axons in the sciatic nerve suggested that the etiology of this maturational arrest of fetal muscle may be neurogenic.
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PMID:Neonatal myotubular myopathy: neuropathy and failure of postnatal maturation of fetal muscle. 732 11