Clinical and biologic implications of recurrent genomic aberrations in myeloma.
By R. Fonseca, E. Blood, M. Rue, D. Harrington, M. Oken, R. Kyle, G. Dewald, B. V. Van Ness, S. V. Van Wier, K. Henderson and 2 more. Blood, 2003
660 citations recorded by the source corpus.
Subfields: Genetics, Hematology, Molecular Biology
View Paper: https://www.semanticscholar.org/paper/12f34108a5494986fbb6acceecae94ef8d3b2a48
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Citations in the corpus
- Promiscuous mutations activate the noncanonical NF-kappaB pathway in multiple myeloma. (2007, methodology): “FISH The cIg-FISH method was performed as previously described(Fonseca et al., 2003a).”
- Understanding multiple myeloma pathogenesis in the bone marrow to identify new therapeutic targets (2007, background): “, whereas patients presenting with t(11;14) have a longer survival relative to all other genetic subtype”
- Management of newly diagnosed symptomatic multiple myeloma: updated Mayo Stratification of Myeloma and Risk-Adapted Therapy (mSMART) consensus guidelines. (2009, background): “The prognostic relevance of these genetic abnormalities has been examined in multiple studies in the context of different therapies.(32,37-43) In general, patients with hyperdiploidy and those with t(11;14) appear to have a relatively better outcome, whereas those with t(4;14), t(14;16), and del 17p”