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• 2015 AML-ETO WGS analysis result

  This data is belong to 2015 AML-ETO patients' genome data which is aligned to human reference(human_g1k_v37.fasta). There are 10 paired tumor/normal samples from SNUH. All samples has passed QC and recalibration steps while aligning to reference.

  Dataset EGAD00001004011

• There are 22 pairs of LAML cases in this project which belongs to LAML-CN. The library is constructed by the Illumina protocol.

  There are 22 pairs of LAML cases in this project which belongs to LAML-CN.The library is constructed by the Illumina protocol.

  Dataset EGAD00001003317

• RNA-seq of Ewing sarcoma tumors (ICGC)

  Ewing sarcoma (ES) is a primary bone tumor initiated by an EWSR1-ETS gene fusion. To characterize the transcriptome of Ewing sarcoma, RNA-seq was performed.

  Study EGAS00001003333

• There are 66 pairs of LAML cases(complete genomics) in this project which belongs to LAML-CN.The library is constructed by the Completes Genomics protocol.

  There are 66 pairs of LAML cases(complete genomics) in this project which belongs to LAML-CN..The library is constructed by the Completes Genomics protocol.

  Dataset EGAD00001003310

• 2015_AML Whole exome sequencing analysis result

  This data is belong to 2015 whole exome sequenced AML data which is aligned to human reference(human_g1k_v37.fasta). There are 40 paired NR samples from Chunnam University. All samples has passed QC and recalibration steps while aligning to reference.

  Dataset EGAD00001003587

• 2018 AML-ETO WGS analysis result

  This data is belong to 2018 AML-ETO patients' genome data which is aligned to human reference(human_g1k_v37.fasta). There are 12 paired tumor/normal samples from SNUH. All samples has passed QC and recalibration steps while aligning to reference.

  Dataset EGAD00001003912

• 2014 sequenced AML-WGS analysis result

  This data is belong to 2014 AML-WGS patients' genome data which is aligned to human reference(human_g1k_v37.fasta). There are 10 paired tumor/normal samples from SNUH. All samples has passed QC and recalibration steps while aligning to reference.

  Dataset EGAD00001003925

• Genome-Wide Discovery of Novel Breast Cancer Predisposing Mutations

  Cancer risk shows clear heritability, but the inherited genetic factors remain largely unknown. This project will seek to identify new genes in which mutations confer hereditary risk for early onset breast cancer, with important implications for both biological understanding and clinical prediction and prevention. Identifying cancer predisposing mutations can provide new biological insights and significantly impact important clinical decision making regarding treatment, surveillance and preventive approaches. Examples include the BRCA1 breast cancer susceptibility gene, which affects treatment decisions (surgical management), surveillance (frequent breast MRI) and prevention (oophorectory for prevention of ovarian cancer). Hereditary early onset breast cancer patients commonly present to Cancer Genetics clinics, but the majority of these patients do not have identifiable mutations in known candidate genes. Here, we will perform whole exome sequencing to discover novel cancer susceptibility genes. The patients have been recruited from Memorial Sloan Kettering Cancer Center (PIs Kenneth Offit and Zsofia Stadler) and Massachusetts General Hospital (PI Daniel Haber). All exome sequencing was performed at the Broad Institute of Harvard and MIT; samples sequence capture was performed using Agilent SureSelect Human All Exon Kit v2 and sequencing was performed on an Illumina HiSeq 2000 or 2500.

  Study phs000822

• Epigenetic Biomarkers of Aging

  The aim of the study was to discover new epigenetic biomarkers of aging. We used a genome-wide screen for genetic loci showing consistent changes of DNA methylation with progressive aging. Blood DNA samples from 19 apparently healthy individuals aged 22-80 years obtained from the NINDS repositories were analyzed for DNA methylation using Reduced Representation Bisulfite Sequencing. We followed the New England Biolabs (NEB) protocol for methylated adaptors as described previously. Briefly, 1 microgram of genomic DNA was spiked with 100 picograms of lambda phage DNA as the unmethylated standard and digested with MspI endonuclease at C’CGG sites. Ends of restriction fragments were filled in, 3’-dA tailed and methylated adaptors were ligated to the ends of restriction fragments. Bisulfite treatment using the Epitect kit (Qiagen) followed. Bisulfite-converted libraries were amplified using EpiMark Taq DNA polymerase (NEB) and primers with dual barcode indices. The libraries were pooled and sequenced on Illumina HiSeqX instrument using paired end reads of 150 bases. We used Bismark v0.23.1 to align the sequences to hg19 human genome assembly. We used methylKit v1.22.0 to analyze differential methylation in individuals of different ages.

  Study phs003046

• Resistance Development in Basal Cell Nevus Syndrome through the Basal to Squamous Transition

  While basal cell carcinomas (BCCs) arise from ectopic hedgehog pathway activation and can be treated with pathway inhibitors, sporadic BCCs display high resistance rates, while tumors arising in Gorlin syndrome patients with germline Patched (PTCH1) mutations are uniformly suppressed by inhibitor therapy. In rare cases, Gorlin syndrome patients on long-term inhibitor therapy will develop individual resistant tumor clones that rapidly progress, but the basis of this resistance remains unstudied. Here we report a case of a Smoothened inhibitor (SMOi)-resistant tumor arising in a Gorlin patient on suppressive SMOi for nearly a decade. Using a combination of multi-omics and spatial transcriptomics, we define the tumor populations at the cellular and tissue level to conclude that Gorlin tumors can develop resistance to SMOi through the previously described basal to squamous cell carcinoma transition (BST). Intriguingly, through spatial whole exome genomic analysis, we nominate PCYT2, ETNK1, and the phosphatidylethanolamine biosynthetic pathway as novel genetic suppressors of BST resistance. These observations provide a general framework for studying tumor evolution and provide important clinical insight into mechanisms of resistance to SMOi for not only Gorlin syndrome but sporadic BCCs as well.

  Study phs003415