Project description:In a two-stage study we investigated levels of Immunoglobulin G (IgG) reactivity in plasma from Myelodysplastic Syndrome (MDS) and Acute Myeloid Leukemia (AML) post MDS patients (59 and 16 cases respectively) as compared to healthy cohort (34). In Stage I we utilized high-throughput protein arrays (23 232 total signals, in duplicate) to identify proteins of high-interest. In Stage II we designed new protein arrays (352 total signals, in duplicate) to further focus on 25 of the proteins from Stage I and expanded to a larger cohort, including both male and female samples (161 MDS and 43 AML patients; 112 healthy controls). Stage I resulted in 35 proteins displaying increased IgG reactivity in patients as compared to the healthy controls (P< 4.3 x10-07, Bonferroni Corrected P<0.01). This protein subset included 14 proteins associated with cancer, 12 with apoptosis, and 3 with the NFAT Regulation canonical pathway. Using the focused arrays we performed a classification of MDS patients and healthy controls. Stage II subsequently identified a high-interest focused set of 3 proteins, namely AKT3, FCGR3A and ARL8B displaying aberrant increased reactivity in patient subgroups, in concordance with Stage I. Autoantibody reactivity against specific proteins provides complementary information to other known molecular signatures for MDS and may enhance our capabilities for detecting and classifying MDS. In the study presented here, MDS patients were classified into Stable, Transforming or AML post MDS (L) classes retrospectively. The different patients were compared to a healthy cohort to assess increased autoantibody reactivity to specific patients as opposed to healthy groups Stage 1 of Study: 111 Files Analyzed, 37 sMDS, 22 tMDS, 16 AML(L), 34 Healthy and 2 Negative Controls (used to eliminate non-plasma signals)
Project description:In a two-stage study we investigated levels of Immunoglobulin G (IgG) reactivity in plasma from Myelodysplastic Syndrome (MDS) and Acute Myeloid Leukemia (AML) post MDS patients (59 and 16 cases respectively) as compared to healthy cohort (34). In Stage I we utilized high-throughput protein arrays (23 232 total signals, in duplicate) to identify proteins of high-interest. In Stage II we designed new protein arrays (352 total signals, in duplicate) to further focus on 25 of the proteins from Stage I and expanded to a larger cohort, including both male and female samples (161 MDS and 43 AML patients; 112 healthy controls). Stage I resulted in 35 proteins displaying increased IgG reactivity in patients as compared to the healthy controls (P< 4.3 x10-07, Bonferroni Corrected P<0.01). This protein subset included 14 proteins associated with cancer, 12 with apoptosis, and 3 with the NFAT Regulation canonical pathway. Using the focused arrays we performed a classification of MDS patients and healthy controls. Stage II subsequently identified a high-interest focused set of 3 proteins, namely AKT3, FCGR3A and ARL8B displaying aberrant increased reactivity in patient subgroups, in concordance with Stage I. Autoantibody reactivity against specific proteins provides complementary information to other known molecular signatures for MDS and may enhance our capabilities for detecting and classifying MDS. In the study presented here, MDS patients were classified into Stable, Transforming or AML post MDS (L) classes retrospectively. The different patients were compared to a healthy cohort to assess increased autoantibody reactivity to specific patients as opposed to healthy groups Stage 2 of study: 633 Files analyzed for: 316 Patients in duplicate and a negative control. The proteins on the array were selected following a first stage using ProtoArrays
Project description:We have determined the whole genome sequence of an individual at high accuracy and performed an integrated analysis of omics profiles over a 1.5 year period that included healthy and two virally infected states. Omics profiling of transcriptomes, proteomes, cytokines, metabolomes and autoantibodyomes from blood components have revealed extensive, dynamic and broad changes in diverse molecular components and biological pathways that occurred during healthy and disease states. Many changes were associated with allele- and edit-specific expression at the RNA and protein levels, which may contribute to personalized responses. Importantly, genomic information was also used to predict medical risks, including Type II Diabetes (T2D), whose onset was observed during the course of our study using standard clinical tests and molecular profiles, and whose disease progression was monitored and subsequently partially managed. Our study demonstrates that longitudinal personal omics profiling can relate genomic information to global functional omics activity for physiological and medical interpretation of healthy and disease states. Plasma and serum from a virus infected timepoint (in triplicate) and 34 healthy contorl samples were collected and used to probe Invitrogen human protoarray v5.0.
Project description:This SuperSeries is composed of the following subset Series: GSE32691: Autoantibody profile timecourse of UNK GSE32874: Personal Omics Profiling Reveals Dynamic Molecular Phenotypes and Actionable Medical Risks Refer to individual Series
Project description:We compared repeatability and comparability of microRNA microarray using 5 different platforms. and compared microarray data generated from five different microRNA microarray platforms with quantitative RT-PCR. Our data suggested that the most accurate and repeatable methods for microRNA expression profiling are Agilent and Toray, and the numbers of detected microRNA at Toray are more than at Agilent. Keywords: repeatability, comparability, microRNA, microarray We compared repeatability and comparability of microRNA microarray using 5 different platforms (Agilent, Ambion, Exiqon, Invitrogen, and Toray). In addition, we compared microarray data generated from five different microRNA microarray platforms with quantitative RT-PCR.
Project description:Using Affymetrix gene chips of human foetal brain tissue from 8-12.5 post-conceptional weeks (PCW, equivalent to Carnegie stage (CS) 23, to Foetal stage (F) 4), we have identified a number of genes that exhibit gradients along the anterior-posterior axis of the neocortex.
Project description:CGH analysis of Drosophila polytene chromosomes. Drosophila polytene chromosomes were isolated from whole salivary glands dissected from roaming third-instar larvae or from ovaries dissected from adult females. Salivary gland has two biological repeats.
Project description:Mapping the Drosophila melanogaster 2R heterochromatin by CGH analysis of embryos lacking specific regions of 2R. Seven translocations with breakpoints in 2R heterochromatin were tested: 2219 (T(2;3)ftz[Rpl]), 130058 (T(Y;2)B[SV5]), 130093 (T(Y;2)B63), 130112 (T(Y;2)B238), 101579 (T(2;3)bxd[68]), 101988 (T(Y;2)G10), and 107387 (T(2;3)E(da)). To generate embryos deficient for smaller regions of 2R heterochromatin, T(2;Y) or T(2;3) translocation males were crossed to C(2)EN females. One eighth of the embryos that lack 2R were identified according to their failure in forming the ventral furrow during early gastrulation. All embryos were collected at room temperature.
Project description:Mapping the Drosophila melanogaster X heterochromatin by CGH analysis of embryos lacking specific regions of the X chromosome. Eight ChrX deficiencies and duplications were tested: 168 (Dp(1;Y)y[2]67g), 175 (Dp(1;Y)y[2]sc), 114n (Dp(1;Y)y[+]mal[126]), 114f (Df(1)fog[114]), 186n (Dp(1;Y)y[+]mal), 186f (Df(1)mal12), B2580 (Dp(1;Y)ct y[+]), B5280 (Dp(1;Y)ct[+]y[+]). To generate embryos lacking different portions of the X heterochromatin, two types of stocks were used: (1) males carrying a deficient X chromosome missing part of the heterochromatin (generally fog-) and a duplication on the Y chromosome that complements the deficiency, and (2) males carrying a duplication of X on the Y chromosome which covers part of the X heterochromatin. In both cases males were crossed to attached X females. In the first case, one quarter of embryos lack most of the X chromosome except the duplication of X on Y. These embryos were identified according to their defects during cellularization. Another quarter of the embryos carry the deficient X chromosome as their sole X chromosome. These embryos were identified according to their defects in posterior midgut formation during early gastrulation. In the second case, one quarter of embryos that lack most of the X chromosome except the duplication of X on Y were identified according to their defects in cellularization or posterior midgut formation. All embryos were collected at room temperature.
Project description:CGH analysis of translocations with breakpoints at the euchromatin/heterochromatin boundary. Three translocations with breakpoint at the euchromatin/heterochromatin boundary of 2L, 3L and X, respectively, were analyzed by CGH to distinguish heterochromatic sequences from euchromatic sequences. X: 101042(T(1;Y)B91); 2L: 130186 (T(Y;2)R146); and 3L: 102004(T(2;3)H31). To obtain embryos lacking the euchromatin portion of the chromosome arms, translocation males bearing breakpoint at the euchromatin/heterochromatin boundary of 2L, 3L and X were crossed to C(2)EN, C(3)EN or attached X females, respectively. All embryos were collected at room temperature.