Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P15088 (mast cell)
 14,925 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The accumulation of malignant ascites is a significant cause of morbidity and mortality in patients with intraabdominal malignancies. However, the cause of malignant ascites is unknown. In this study, we used the rat cremaster muscle preparation to determine if and how malignant ascites could produce protein leakage from normal blood vessels which would lead to fluid accumulation in the peritoneal cavity. The rat cremaster muscle, with nerves and blood vessels to the animal intact, was prepared for microscopic observations of the microcirculation. Serum albumin was tagged to fluorescein isothiocyanate and injected into the rat. Fluorescent microscopy was used to quantitate leakage of the tagged albumin into the interstitial tissue. Malignant ascites was collected from a patient with metastatic breast cancer. The ascites fluid was placed on the cremaster muscle and it induced protein leakage from the normal blood vessels of this tissue. Protein leakage was partially blocked by diphenhydramine (10(-4) M) and by mast cell depletion with compound 48/80. There was a high level of C3a in the malignant ascites solution but C3a did not increase during the exposure period. These data suggest that activated complement in malignant ascites may release histamine from mast cells to cause protein leakage of the normal vasculature. The movement of protein into the peritoneal cavity would be followed by water, thus increasing the volume of the ascites and exacerbating the clinical condition.
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PMID:Human malignant ascites and histamine-induced protein leakage from the normal microcirculation. 325 8

Aggressive systemic mastocytosis is a rare hematologic neoplastic disease that presents with a poor prognosis and low survival rate. It typically manifests with symptoms associated to mast cell release of bioactive substances, causing anaphylaxis, flushing, autonomic and hemodynamic instability, gastric distress and headache. Moreover, more than 95% of cases are related to a mutation in codon 816 of the KIT gene, located on human chromosome 4q12 which codes for a type III receptor tyrosine kinase. We present a 78 year-old Hispanic man diagnosed with the aggressive subtype of systemic mastocytosis, who had an atypical manifestation and a KIT negative variant. The diagnosis was confirmed based on pathologic and serologic findings which included mast cell infiltration of the spleen and bone marrow, malignant ascites and an unusually elevated serum tryptase.
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PMID:Case Report: Unusual Manifestation of KIT Negative Systemic Mastocytosis. 2885 75