Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023473 (chronic myeloid leukemia)
 18,916 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

ICO-G-2 hybridoma clone was obtained after fusion of spleen cells from BALB/c mice immunized with cells from a patient with acute myelomonoblastic leukemia (AMML) and P3 X 63 Ag8.653 cells, using 50% polyethyleneglycol, molecular weight 1500 KD. The antigen with a molecular weight of 100 KD was present only on polymorphonuclear neutrophils and eosinophils of the peripheral blood. The antigen expression was also found on the majority of myeloid precursors and some nuclear erythroid cells. CFU-GM did not express the antigen. Monoclonal antibodies ICO-G-2 reacted with blast cells of some patients with AML, AMML and CML. The antibodies did not react with cells from patients with AMonL, CMonL, ALL, CLL and LSA. Such pattern of reactivity makes these monoclonal antibodies useful for the differential diagnosis of acute nonlymphocytic leukemias and CML in blast crisis.
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PMID:[Monoclonal antibodies to the antigen of myeloid cells]. 362 Jun 54

Imatinib mesylate (Glivec; Novartis AG, Basel, Switzerland) is a tyrosine kinase inhibitor which is used in the treatment of oncologic diseases like chronic myeloid leukemia and gastrointestinal stroma tumor (GIST). Among cutaneous side effects, bullous reactions are rare. The authors describe the case of a 66-year-old woman developing blistering and skin fragility on her hands, foot, lower legs, and back after intake of imatinib for treatment of GIST. Biopsy showed vacuolar alteration at the dermoepidermal junction (DEJ) associated with a few lymphocytes and a subepidermal blister. The upper papillary dermis below the vacuolar alteration and below the blister showed hyalinization and loss of elastic microfibrils. Direct immunofluorescence was negative for deposits of immunoglobulins. Immunofluorescence on cryosections revealed loss of laminin and collagen IV in vacuoles at the DEJ. Electron microscopy showed dissolution of lamina lucida and lamina densa of the basement membrane below as well as next to the vacuoles and blister. In conclusion, the authors present the first patient with GIST with blistering and skin fragility due to imatinib therapy. As a pathophysiological explanation the authors propose loss of laminin and collagen IV at the DEJ leading to basement membrane instability and blistering. This case also suggests additional features reminiscent of lichen sclerosus induced by imatinib, a drug which is actually known for its antifibrotic effects.
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PMID:Blistering and Skin Fragility Due to Imatinib Therapy: Loss of Laminin and Collagen IV as a Possible Cause of Cutaneous Basement Membrane Instability. 2921 Jul 15