Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0042963 (vomiting)
 31,883 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We report a case of a 32-year-old lady with chronic myeloid leukemia (CML) on Imatinib for the past four years and in complete clinical, hematological and molecular remission who presented to us with sudden onset of headache, vomiting and diplopia following self discontinuation of Imatinib for a month. Investigations were suggestive of chronic phase CML (CML-CP) with massive thrombocytosis and magnetic resonance imaging (MRI) of the brain revealed subdural hematoma. Coagulation studies confirmed the diagnosis of Acquired von Willebrand disease (AvWD) 2A because of thrombocytosis. The patient also tested positive for mutation T315I in bcr-abl gene. Treatment of the patient with high dose of Imatinib and hydroxyurea led to normalisation of platelet counts, reversal of coagulation defect and subsidence of symptoms. The present case highlights the importance of diagnosis of AvWD to determine the cause of bleeding in CML and distinguish it from Imatinib-induced bleeding, as prompt treatment with Imatinib can achieve reversal of the condition.
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PMID:A rare case of chronic myeloid leukemia with acquired von Willebrand disease presenting as subdural hematoma. 2688 78

Colony stimulating factor-1 (CSF-1) is one of the most common proinflammatory cytokine responsible for various inflammatory disorders. It has a remarkable role in the development and progression of osteoarthritis, cancer and other autoimmune disease conditions. The CSF-1 acts by binding to the receptor, called colony stimulating factor-1 receptor (CSF-1R) also known as c-FMS resulting in the cascade of signalling pathway causing cell proliferation and differentiation. Interleukin-34 (IL-34), recently identified as another ligand for CSF-IR, is a cytokine protein. Both, CSF-1 and IL-34, although two distinct cytokines, follow the similar signalling pathway on binding to the same receptor, CSF-1R. Like CSF-1, IL-34 promotes the differentiation and survival of monocyte, macrophages and osteoclasts. This CSF-1R/c-FMS is over expressed in many cancers and on tumour associated macrophages, consequently, have been exploited as a drug target for promising treatment for cancer and inflammatory diseases. Some CSF-1R/c-FMS inhibitors such as ABT-869, Imatinib, AG013736, JNJ-40346527, PLX3397, DCC-3014 and Ki20227 have been successfully used in these disease conditions. Many c-FMS inhibitors have been the candidates of clinical trials, but suffer from some side effects like cardiotoxicity, vomiting, swollen eyes, diarrhoea, etc. If selectivity of cFMS inhibition is achieved successfully, side effects can be overruled and this approach may become a novel therapy for treatment of various therapeutic interventions. Thus, successful targeting of c-FMS may result in multifunctional therapy. With this background of information, the present review focuses on the recent developments in the area of CSF-1R/c-FMS inhibitors with emphasis on crystal structure, mechanism of action and various therapeutic implications in which c-FMS plays a pivotal role. The review on structure activity relationship of various compounds acting as the inhibitors of c-FMS which gives the selection criteria for the development of novel molecules is also being presented.
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PMID:Recent advances in colony stimulating factor-1 receptor/c-FMS as an emerging target for various therapeutic implications. 2967 8


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