{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,4,3]],"date-time":"2026-04-03T03:40:48Z","timestamp":1775187648309,"version":"3.50.1"},"reference-count":51,"publisher":"Wiley","issue":"S1","license":[{"start":{"date-parts":[[2015,6,22]],"date-time":"2015-06-22T00:00:00Z","timestamp":1434931200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American J Hematol"],"published-print":{"date-parts":[[2015,7]]},"abstract":"<jats:p>Data emerging from the International Collaborative Gaucher Group (ICGG) Gaucher Registry together with other contemporary clinical surveys have revealed a close association between Gaucher disease and non\u2010Hodgkin's B\u2010cell lymphoma and myeloma and Gaucher disease and Parkinson's disease. Several possible explanations for increased B\u2010cell proliferation and neoplasia in Gaucher disease have been proposed, including the possible influence of sphingosine (derived from the extra lysosomal metabolism of glucosylceramide), gene modifiers, splenectomy and immune system deregulation induced by cytokines, chemokines, and hydrolases released from Gaucher cells. Parkinson's disease is frequently seen in the otherwise\u2010healthy relatives of Gaucher disease patients leading to the finding that <jats:italic>GBA<\/jats:italic> mutations represent a genetic risk factor for Parkinson's disease. The mechanism of the association between <jats:italic>GBA<\/jats:italic> mutations and Parkinson's disease has yet to be elucidated but the pathogenesis appears distinct from that of Gaucher disease. Several pathogenic pathways have been proposed including lysosomal and\/or mitochondrial dysfunction. The effect of Gaucher disease specific therapies on the incidence of cancer or Parkinson's disease are not clear and will likely be evaluated in future ICGG Gaucher Registry studies. Am. J. Hematol. 90:S25\u2013S28, 2015. \u00a9 2015 Wiley Periodicals, Inc.<\/jats:p>","DOI":"10.1002\/ajh.24057","type":"journal-article","created":{"date-parts":[[2015,6,22]],"date-time":"2015-06-22T06:50:07Z","timestamp":1434955807000},"source":"Crossref","is-referenced-by-count":30,"title":["Gaucher disease and comorbidities: B\u2010cell malignancy and parkinsonism"],"prefix":"10.1002","volume":"90","author":[{"given":"Timothy M.","family":"Cox","sequence":"first","affiliation":[{"name":"Department of Medicine University of Cambridge  United Kingdom"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Barry E.","family":"Rosenbloom","sequence":"additional","affiliation":[{"name":"Cedars\u2010Sinai\/Tower Hematology Oncology Beverly Hills California"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Roger A.","family":"Barker","sequence":"additional","affiliation":[{"name":"Department of Clinical Neurosciences University of Cambridge  United Kingdom"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"311","published-online":{"date-parts":[[2015,6,22]]},"reference":[{"key":"e_1_2_6_2_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.bcmd.2003.10.007"},{"key":"e_1_2_6_3_1","doi-asserted-by":"publisher","DOI":"10.1007\/s00277-008-0441-8"},{"key":"e_1_2_6_4_1","doi-asserted-by":"publisher","DOI":"10.1182\/blood-2004-12-4672"},{"key":"e_1_2_6_5_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.bcmd.2005.03.004"},{"key":"e_1_2_6_6_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.bcmd.2005.08.004"},{"key":"e_1_2_6_7_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.mayocp.2012.06.014"},{"key":"e_1_2_6_8_1","doi-asserted-by":"publisher","DOI":"10.1001\/archinte.167.11.1189"},{"key":"e_1_2_6_9_1","doi-asserted-by":"publisher","DOI":"10.1002\/ajh.21362"},{"key":"e_1_2_6_10_1","doi-asserted-by":"crossref","first-page":"e242","DOI":"10.5858\/2003-127-e242-SLAIAP","article-title":"Splenic lymphoma arising in a patient with Gaucher disease. 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