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10.1111/bjh.13897 http://scihub22266oqcxt.onion/10.1111/bjh.13897 C5409813!5409813!26659815     free     free     free Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Br+J+Haematol 2016 ; 172 (5): 735-44 Nephropedia Template TP {{tp|p=26659815|t=2016. Clonal architecture of CXCR4 WHIM-like mutations in Waldenström Macroglobulinaemia |pdf=|usr=}}{{26659815}} gab.com Text Clonal architecture of CXCR4 WHIM-like mutations in Waldenström Macroglobulinaemia JO: Br J Haematol http://www.kidney.de/pget.php?&tw=1&pmid=26659815 #FOAvip CXCR4WHIM somatic mutations are distinctive to Waldenstrom Macroglobulinaemia (WM), and impact disease presentation and treatment outcome. The clonal architecture of CXCR4WHIM mutations remains to be delineated. We developed highly sensitive allele-specific polymerase chain reaction(AS-PCR) assays for detecting the most common CXCR4WHIM mutations (CXCR4S338X C>A and C>G) in WM. The AS-PCR assays detected CXCR4S338X mutations in WM and IgM monoclonal gammopathy of unknown significance (MGUS) patients not revealed by Sanger sequencing. By combined AS-PCR and Sanger sequencing, CXCR4WHIM mutations were identified in 44/102 (43%), 21/62 (34%), 2/12 (17%) and 1/20 (5%)untreated WM, previously treated WM, IgM MGUS and marginal zonelymphoma patients, respectively, but no chronic lymphocytic leukaemia, multiple myeloma, non-IgM MGUS patients or healthy donors. Cancer cellfraction analysis in WM and IgM MGUS patients showed CXCR4S338X mutations were primarily subclonal, with highly variable clonal distribution(median 35·1%, range 1·2?97·5%). Combined AS-PCR and Sangersequencing revealed multiple CXCR4WHIM mutations in many individual WM patients, including homozygous and compound heterozygous mutations validated by deep RNA sequencing. The findings show thatCXCR4WHIM mutations are more common in WM than previously revealed, and are primarily subclonal, supporting their acquisition after MYD88L265P in WM oncogenesis. The presence of multiple CXCR4WHIM mutations within individual WM patients may be indicative of targeted CXCR4 genomic instability. Twit Text FOAVip Clonal architecture of CXCR4 WHIM-like mutations in Waldenström Macroglobulinaemia ????Br J Haematol http://www.kidney.de/pget.php?&tw=1&pmid=26659815 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26659815 #FOAvip English Wikipedia <ref>{{Cite pmid|26659815}}</ref> Clonal architecture of CXCR4 WHIM-like mutations in Waldenström Macroglobulinaemia #MMPMID26659815 Xu L; Hunter ZR; Tsakmaklis N; Cao Y; Yang G; Chen J; Liu X; Kanan S; Castillo JJ; Tai YT; Zehnder JL; Brown JR; Carrasco RD; Advani R; Sabile JM; Argyropoulos K; Palomba ML; Morra E; Trojani A; Greco A; Tedeschi A; Varettoni M; Arcaini L; Munshi NM; Anderson KC; Treo SP Br J Haematol 2016[Mar]; 172 (5): 735-44 PMID26659815show ga CXCR4WHIM somatic mutations are distinctive to Waldenstrom Macroglobulinaemia (WM), and impact disease presentation and treatment outcome. The clonal architecture of CXCR4WHIM mutations remains to be delineated. We developed highly sensitive allele-specific polymerase chain reaction(AS-PCR) assays for detecting the most common CXCR4WHIM mutations (CXCR4S338X C>A and C>G) in WM. The AS-PCR assays detected CXCR4S338X mutations in WM and IgM monoclonal gammopathy of unknown significance (MGUS) patients not revealed by Sanger sequencing. By combined AS-PCR and Sanger sequencing, CXCR4WHIM mutations were identified in 44/102 (43%), 21/62 (34%), 2/12 (17%) and 1/20 (5%)untreated WM, previously treated WM, IgM MGUS and marginal zonelymphoma patients, respectively, but no chronic lymphocytic leukaemia, multiple myeloma, non-IgM MGUS patients or healthy donors. Cancer cellfraction analysis in WM and IgM MGUS patients showed CXCR4S338X mutations were primarily subclonal, with highly variable clonal distribution(median 35·1%, range 1·2?97·5%). Combined AS-PCR and Sangersequencing revealed multiple CXCR4WHIM mutations in many individual WM patients, including homozygous and compound heterozygous mutations validated by deep RNA sequencing. The findings show thatCXCR4WHIM mutations are more common in WM than previously revealed, and are primarily subclonal, supporting their acquisition after MYD88L265P in WM oncogenesis. The presence of multiple CXCR4WHIM mutations within individual WM patients may be indicative of targeted CXCR4 genomic instability. äClonal architecture of CXCR4 WHIM-like mutations in Waldenström Macrog(epmc).pdf DeepDyve Pubget Overpricing