0.01; p 0.001; p 0.0001. The connection in between MRD and individual mutations was examined utilizing a four-fold contingency table and Fisher’s precise test. To this end, each and every mutation was coded as a binary (wildtype or mutant) variable as previously described6. Minimal residual illness was defined as detection of 0.1 of cells that stained for AML-associated surface markers by flow cytometry as described above. There were 144 sufferers with complete mutational and MRD data, summarized in Supplementary Table 1. To make sure that family-wise error rate is controlled in the 5 level we used a resampling-based process to adjust the p-values. This technique is much more powerful than standard step-down Holm system, taking into account the discreteness along with the multivariate distribution in the test statistics60. The resulting p-values not simply manage the marginal (comparison-wise) false good rate at the nominal amount of 5 but also the all round (family-wise) error price at five . In other words, if none of the mutations were linked with MRD, the probability of locating at the very least one association is much less than five . See also Supplementary Table 1.Author Manuscript Author Manuscript Author Manuscript Author ManuscriptSupplementary MaterialRefer to Net version on PubMed Central for supplementary material.TRAIL/TNFSF10, Rhesus Macaque AcknowledgmentsThis perform was supported by NCI K99 grant CA178191 and Lauri Strauss Leukemia Foundation award to OAG, by NCI K08 grant CA169055 and an American Society of Hematology (ASHAMFDP-20121) under the ASH-AMFDP partnership using the Robert Wood Johnson Foundation to FEG-B, by a Hyundai Hope On Wheels award to BS, by a Gabrielle’s Angel Fund grant to RLL and AMM, by NCI grant CA172636 to RLL and AMM, and by the Samuel Waxman Cancer Analysis Center. ASM is supported by NIH grants T32GM007739 and F30CA18349. AMM can be a Burroughs Wellcome Clinical Translational Scholar, and is supported by the Sackler Center for Biomedical and Physical Sciences. RLL is really a LLS Scholar. PBS is supported by the Austrian Analysis Foundation (#P27132) as well as the Oesterreichische Nationalbank (OeNB) Anniversary Fund (#15936). MSKCC cores employed in these research are supported by the P30 Core Grant CA008748. ECOG-ACRIN Integrated Leukemia Translational Research Center is funded by NCI U10 grant CA180827 to EMP et al. The authors are grateful to C. Sheridan, J. Gandara and Y. Neelamraju for technical assistance, to Weill Cornell Medicine Epigenomics Core for sequencing services, to H. Erdjument-Bromage (MSKCC Proteomics Core), to S.CD45 Protein supplier Zha (Columbia University Healthcare Center) and to A.PMID:23310954 Ciccia (Columbia University Healthcare Center) for important reading from the manuscript and useful suggestions.
HHS Public AccessAuthor manuscriptJ Mol Biol. Author manuscript; readily available in PMC 2017 April 24.Published in final edited kind as: J Mol Biol. 2016 April 24; 428(8): 1617636. doi:10.1016/j.jmb.2016.02.008.Author Manuscript Author Manuscript Author Manuscript Author ManuscriptHigh-resolution mapping with the folding transition state of a WW domainKapil Dave, Marcus J er Houbi Nguyen, Jeffery W. Kelly and Martin Gruebele,Centerfor Biophysics and Computational Biology, University of Illinois at Urbana-Champaign, Urbana, IL 61801 USA of Chemistry along with the Skaggs Institute for Chemical Biology, The Scripps Study Institute, 10550 North Torrey Pines Road BCC255, La Jolla, CA 92037, USA of Physics and Division of Chemistry, University of Illinois at UrbanaChampaign, Urbana, IL 61801 USAepartment�DepartmentAbstractFast-.
