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dc.contributor.authorThomas, Anish
dc.contributor.authorMailankody, Sham
dc.contributor.authorKorde, Neha
dc.contributor.authorKristinsson, Sigurdur Y
dc.contributor.authorTuresson, Ingemar
dc.contributor.authorLandgren, Ola
dc.date.accessioned2013-09-19T14:31:07Z
dc.date.available2013-09-19T14:31:07Z
dc.date.issued2012-03-22
dc.date.submitted2013-09-19
dc.identifier.citationBlood 2012, 119(12):2731-7en_GB
dc.identifier.issn1528-0020
dc.identifier.pmid22310913
dc.identifier.doi10.1182/blood-2011-12-381426
dc.identifier.urihttp://hdl.handle.net/2336/301917
dc.descriptionTo access publisher's full text version of this article. Please click on the hyperlink in Additional Links field.en_GB
dc.description.abstractBased on small numbers, recent reports from 3 randomized trials have consistently demonstrated more hematologic malignancies in patients treated with lenalidomide as maintenance (vs placebo). This fact has prompted concern and highlighted the association between multiple myeloma and second malignancies. Furthermore, an excess of acute myeloid leukemia (AML) and myelodysplastic syndromes (MDS) after multiple myeloma has been known for over 4 decades. Most prior studies have been restricted because of small numbers of patients, inadequate follow-up, and limitations of ascertainment of second malignancies. Although the underlying biologic mechanisms of AML/MDS after multiple myeloma are unknown, treatment-related factors are presumed to be responsible. Recently, an excess risk of AML/MDS was found among 5652 patients with IgG/IgA (but not IgM) monoclonal gammopathy of undetermined significance, supporting a role for disease-related factors. Furthermore, there is evidence to suggest that polymorphisms in germline genes may contribute to a person's susceptibility to subsequent cancers, whereas the potential influence of environmental and behavioral factors remains poorly understood. This review discusses current knowledge regarding second malignancies after multiple myeloma and gives future directions for efforts designed to characterize underlying biologic mechanisms, with the goal to maximize survival and minimize the risk for second malignancies for individual patients.
dc.description.sponsorshipNational Cancer Institute of the National Institutes of Healthen_GB
dc.language.isoenen
dc.publisherAmer Soc Hematologyen_GB
dc.relation.urlhttp://dx.doi.org/10.1182/blood-2011-12-381426en_GB
dc.relation.urlhttp://www.ncbi.nlm.nih.gov/pmc/articles/PMC3327452/en_GB
dc.rightsArchived with thanks to Blooden_GB
dc.subject.meshHumansen_GB
dc.subject.meshLeukemia, Myeloid, Acuteen_GB
dc.subject.meshMultiple Myelomaen_GB
dc.subject.meshMyelodysplastic Syndromesen_GB
dc.subject.meshNeoplasms, Second Primaryen_GB
dc.subject.meshRisk Factorsen_GB
dc.titleSecond malignancies after multiple myeloma: from 1960s to 2010s.en
dc.typeArticleen
dc.contributor.departmentMultiple Myeloma Section, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA.en_GB
dc.identifier.journalBlooden_GB
dc.rights.accessOpen Access - Opinn aðganguren
html.description.abstractBased on small numbers, recent reports from 3 randomized trials have consistently demonstrated more hematologic malignancies in patients treated with lenalidomide as maintenance (vs placebo). This fact has prompted concern and highlighted the association between multiple myeloma and second malignancies. Furthermore, an excess of acute myeloid leukemia (AML) and myelodysplastic syndromes (MDS) after multiple myeloma has been known for over 4 decades. Most prior studies have been restricted because of small numbers of patients, inadequate follow-up, and limitations of ascertainment of second malignancies. Although the underlying biologic mechanisms of AML/MDS after multiple myeloma are unknown, treatment-related factors are presumed to be responsible. Recently, an excess risk of AML/MDS was found among 5652 patients with IgG/IgA (but not IgM) monoclonal gammopathy of undetermined significance, supporting a role for disease-related factors. Furthermore, there is evidence to suggest that polymorphisms in germline genes may contribute to a person's susceptibility to subsequent cancers, whereas the potential influence of environmental and behavioral factors remains poorly understood. This review discusses current knowledge regarding second malignancies after multiple myeloma and gives future directions for efforts designed to characterize underlying biologic mechanisms, with the goal to maximize survival and minimize the risk for second malignancies for individual patients.


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