Project description:The DNA isolated from 44 either frozen or FFPE Neuroendocrine Neoplasm (NEN) was analysed by NGS, to identify genes more likely to be subject to sequence variations among 523 cancer-related ones.
Project description:Plasma DNA from 558 malignancies, 263 benign and borderline tumors and 367 healthy control samples were collected and subjected to random short-gun whole genome sequencing.
Project description:This study aims to investigate the DNA methylation patterns at transcription factor binding regions and their evolutionary conservation with respect to binding activity divergence. We combined newly generated bisulfite-sequencing experiments in livers of five mammals (human, macaque, mouse, rat and dog) and matched publicly available ChIP-sequencing data for five transcription factors (CEBPA, HNF4a, CTCF, ONECUT1 and FOXA1). To study the chromatin contexts of TF binding subjected to distinct evolutionary pressures, we integrated publicly available active promoter, active enhancer and primed enhancer calls determined by profiling genome wide patterns of H3K27ac, H3K4me3 and H3K4me1.
Project description:Chronic myeloid leukemia (CML) epitomizes successful targeted therapy, with 86% of patients in the chronic phase treated with tyrosine kinase inhibitors (TKIs) attaining remission. However, resistance to TKIs occurs during treatment, and patients with resistance to TKIs progress to the acute phase called Blast Crisis (BC), wherein the survival is restricted to 7-11 months. About 80 % of patients in BC are unresponsive to TKIs. This issue can be addressed by identifying a molecular signature which can predict resistance in CML-CP prior to treatment as well as by delineating the molecular mechanism underlying resistance. Herein, we report genomic analysis of CML patients and imatinib-resistant K562 cell line to achieve the same. WGS was performed on imatinib-sensitive and -resistant K562 cells. Library preparation was done by 30x WGS KAPA PCR-Free v2.1 kit, and Illumina HiSeq X sequencer was used for 2 x 150 bp paired-end sequencing. Our study identified accumulation of aberrations on chromosomes 1, 3, 7, 16 and 22 as predictive of occurrence of resistance. Further, recurrent amplification in chromosomal region 8q11.2-12.1 was detected in highly resistant K562 cells as well as CML patients. The genes present in this region were analyzed to understand molecular mechanism of imatinib resistance.
Project description:LexA is a transcriptional repressor for genes requiring expression primarily during SOS response in response to stress such as that caused by DNA alkylating agent Mitomycin C (MMC). LexA undergoes self-cleavage under stress conditions thereby lifting the repression on genes whose expression is required for stress response. In our experiment LexA binding sites in the genome were determined in untreated and MMC treated (overnight, 14h) cultures using a LexA-3xFLAG strain and anti-FLAG monoclonal antibodies. Wild type Streptomyces venezuelae (unFLAGged LexA) cultures, with and without MMC treatment were used as negative controls.
Project description:The enhancer binding protein VnfA1 of Azotobacter vinelandii has two paralogs as well VnfA2 and VnfA3. This experiment was carried out to compare the binding sites of VnfA1 and VnfA3 under conditions of vanadium availability and its absence. This is important for the regulation of expression of alternative nitrogenase isoenzymes in response to metal availability.
Project description:Whole genome sequencing of the Arabidopsis thaliana dot5-1 transposon insertion line described in Petricka et al 2008 The Plant Journal 56(2): 251-263.
Project description:We aim at understanding how ionizing radiations (IR) increase the risk of developing myeloid leukemia. We recently showed that IR leads to the derepression of retroelements. We demonstrated that retroelements expression in aged HSCs is regulated by the heterochromatin repressive histone mark H3K9me3. However, the mechanisms by which IR specifically triggers retroelements expression in HSCs are unknown. We hypothesized that retroelements derepression is due to IR-induced heterochromatin changes. To answer this question, we performed H3K9me3 ChIP-seq experiments in hematopoietic stem cells sorted from mice one month after they were irradiated and compared them to controls hematopoietic stem cells sorted from non-irradiated mice.
Project description:The analysis identifies differentially occupied genomic regions of H2Bub1, H3K79me3, and H3K27ac by RNF40 silencing in HCC1806 cells
