Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.4.21.4 (trypsin)
 42,187 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Two monoclonal antibodies, M32-1 (Ig-G1,k) and M39-2 (IgM,k), were prepared against high molecular weight (greater than 650 kDa) cytosol antigens (HMW-CA) of a human adenocarcinoma of the colon (GW-39). These monoclonal antibodies appeared to bind to determinants on two distinct high molecular weight colon antigens. One was shown by gel filtration to be a 650 kDa glycoprotein (gp650) containing at least one 300 kDa antigenic subunit (gp300). The other antigen eluted from a S-300 Sephacryl column at a molecular size of 600 kDa (gp600) and was resistant to dissociation by detergents, salts and chaotropic agents. The differential sensitivity of these two high molecular weight glycoproteins to treatment with trypsin, chondroitinase ABC, HNO2, endoglycosidase H and 2-mercaptoethanol suggest that monoclonal antibodies M39-1 and M39-2 react with distinct antigenic determinants located on two separate, high molecular weight, colon antigens. Since these antigens are only detected in extracts prepared from normal mucosa, well-differentiated tumors or margins of well-differentiated tumors, their expression appears to be related to a well-differentiated cell phenotype.
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PMID:Characterization of two monoclonal antibodies that recognize high molecular weight colon antigens. 292 Mar 72

We report the case of capecitabine-induced ventricular fibrillation arrest, possibly secondary to type I Kounis syndrome. A 47-year-old man with a history of T3N1 moderately differentiated adenocarcinoma of the colon, status-post sigmoid resection, was started on adjuvant capecitabine approximately five months prior to presentation of cardiac arrest secondary to ventricular fibrillation. An electrocardiogram (EKG) revealed ST segment elevation on the lateral leads and the patient was taken emergently to the cardiac catheterization laboratory. The catheterization revealed no angiographically significant stenosis and coronary artery disease was ruled out. After ruling out other causes of cardiac arrest, the working diagnosis was capecitabine-induced ventricular fibrillation arrest. As such, an inflammatory work up was sent to evaluate for the possibility of a capecitabine hypersensitivity, or Kounis syndrome, and is the first documented report in the literature to do so when evaluating Kounis syndrome. Immunoglobulin E (IgE), tryptase, and C-reactive protein were normal but histamine, interleukin (IL)-6, and IL-10 were elevated. Histamine elevation supports the suspicion that our patient had type I Kounis syndrome. Naranjo adverse drug reaction probability scale indicates a probable adverse effect due to capecitabine with seven points. A case of capecitabine-induced ventricular fibrillation arrest is reported, with a potential for type 1 Kounis syndrome as an underlying pathology supported by immunologic work up.
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PMID:Capecitabine-induced ventricular fibrillation arrest: Possible Kounis syndrome. 2587 Jan 82