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• Genomics to select patients with metastatic breast cancer for targeted therapy (microarray_agilent)

  Cancer progression is driven in part by genomic alterations located in oncogenes or tumor suppressor genes. The genomic characterization of cancers has shown a large interpatient heterogeneity regarding the driver alterations, leading to the concept that generating a genomic profiling by multigene sequencing in patients with cancer could allow selecting effective targeted therapies. While this concept has been broadly implemented in daily practice, there is no evidence that such approach improves patient outcome, and how to optimally select the therapy to administer. A genomic profiling using next generation sequencing and copy number analyses was performed 1462 patients with Her2-non overexpressing metastatic breast cancer included in SAFIR02 Breast trial. 238 of these patients were randomized in two trials between a targeted therapy matched to genomic alteration and a maintenance chemotherapy. The trial shows that targeted therapies matched to genomics improves progression free survival (PFS) when genomic alterations are classified level I/II according to ESMO Scale for Clinical Actionability of Molecular Targets (ESCAT) (adjusted HR: 0.41, 90% CI: 0.27-0.61, p<0.001), but not when alterations are classified beyond level II (unadjusted HR: 1.15, 95% CI: 0.76-1.75). This trial provides evidence that the treatment decision led by genomics should be driven by a framework of target actionability in patients with mBC.

  Study EGAS00001005587

• Exome Sequencing of Chordoma Cases

  Chordoma is a rare tumor that is believed to develop from notochord remnants. We previously identified germline duplication of the TBXT gene as a major susceptibility mechanism in several chordoma families. Currently, we are using whole exome sequencing to identify additional susceptibility genes in chordoma families without TBXT duplication as well as in sporadic cases.

  Study phs001280

• Native American Ancient DNA sequencing

  The morphology of the first humans in the Americas (Paleoamericans) differs from that of Native Americans, and has raised the question of whether or not there are also differences in origin or genetics. A few populations who survived until relatively recently have been suggested to retain Paleoamerican morphology. One of these populations is from La Jolla. Here, we have generated genome sequence data from four La Jolla individuals in order to investigate these questions This data is part of a pre-publication release. For information on the proper use of pre-publication data shared by the Wellcome Trust Sanger Institute (including details of any publication moratoria), please see http://www.sanger.ac.uk/datasharing/

  Dataset EGAD00001002144

• Exome sequencing of early and late passage Patient Derived Xenogratf Tumoroids with matched Patient Derived Xenogratfs and matched normal liver

  The breadth and depth at which cancer models are interrogated contribute to successful translation of drug discovery efforts to the clinic. In colorectal cancer (CRC), model availability is limited by a dearth of large-scale collections of patient-derived xenografts (PDXs) and paired tumoroids from metastatic disease, the setting where experimental therapies are typically tested. XENTURION is a unique open-science resource that combines a platform of 129 PDX models and a sister platform of 129 matched PDX-derived tumoroids (PDXTs) from patients with metastatic CRC, with accompanying multidimensional molecular and therapeutic characterization. This specific dataset is focused on a comparison of early and late passage tumoroids transcriptomes. In this study we focused our attention on early (passage 3) and late (passage 8-12) PDXTs with their matched PDXs and normal liver

  Study EGAS50000000185

• Small cell number RNA-seq (400 cells per sample)

  Transcriptional profiles for stemB and proB cells harvested from either primary or secondary xenografts. This dataset contains six types of samples: - diagnostic stemB cells harvested from primary xenografts - diagnostic proB cells harvested from primary xenografts - relapse stemB cells harvested from secondary xenografts injected with stemB cells from primary xenografts - relapse proB cells harvested from secondary xenografts injected with stemB cells from primary xenografts - relapse stemB cells harvested from secondary xenografts injected with proB cells from primary xenografts - relapse proB cells harvested from secondary xenografts injected with proB cells from primary xenografts

  Dataset EGAD50000001830

• IL7-receptor expression is frequent in T-cell acute lymphoblastic leukemia and predicts sensitivity to JAK-inhibition

  T-cell acute lymphoblastic leukemia (T-ALL) is an aggressive hematological malignancy with a dismal prognosis related to refractory/relapsing diseases, raising the need for new targeted-therapies. Activating mutations of the IL7-receptor pathway genes (IL7Rp) play a proven leukemia-supportive role in T-ALL. JAK-inhibitors such as ruxolitinib have recently demonstrated preclinical efficacy. However, prediction markers for sensitivity to JAK-inhibitors are still lacking. Herein, we show that IL7R (CD127) expression is more frequent (~70%) than IL7Rp-mutations in T-ALL (~30%). We compared the so-called non-expressers (no IL7R-expression/IL7Rp-mutation), expressers (IL7R-expression without IL7Rp-mutation) and mutants (IL7Rp-mutations). Integrative multi-omics analysis outlined IL7R-deregulation in virtually all T-ALL subtypes, at the epigenetic-level in non-expressers, genetic-level in mutants, and post-transcriptional level in expressers. Ex-vivo data using primary-derived xenografts support that IL7Rp is functional whenever the IL7R is expressed, regardless of the IL7Rp mutational status. Consequently, ruxolitinib impaired T-ALL survival in both expressers and mutants. Interestingly, we show that expressers displayed ectopic IL7R-expression and IL7Rp-addiction conferring a deeper sensitivity to ruxolitinib. Conversely, mutants were more sensitive to venetoclax than expressers. Overall, combination of ruxolitinib and venetoclax resulted in synergistic effects in both groups. We illustrate the clinical relevance of this association by reporting achievement of complete remission in two patients with refractory/relapsed-T-ALL. This provides proof of concept for translation of this strategy into clinics as bridge to transplant. Altogether, IL7R-expression can be used as a biomarker for sensitivity to JAK-inhibition, thereby expanding the fraction of T-ALL patients eligible to ruxolitinib up to nearly ~70% of T-ALL.

  Study EGAS00001007144

• TONIC-Trial-cfDNA-Project

  Cell-free DNA (cfDNA) is an emerging technology to predict and monitor response to cancer treatment, including immune checkpoint blockade (ICB). However, data on cfDNA dynamics during ICB in metastatic triple negative breast cancer (mTNBC) are limited. While most applications of cfDNA involve assays that focus on mutation detection, mTNBC and multiple other cancer types are driven by copy number alterations (CNAs). We evaluate cfDNA-based copy number profile abnormality (CPA) score as a potential biomarker for monitoring ICB response in mTNBC, analyzing data from 87 patients enrolled in stage 1 and stage 2 of the TONIC-trial. We find significant concordance between cfDNA-based and tissue-based CNA profiles. Additionally, responders show a decrease in CPA scores upon ICB at week 6 (3 cycles of nivolumab). These findings underscore the potential of cfDNA-based CNA dynamics as a non-invasive biomarker for ICB early response assessment in patients with mTNBC.

  Study EGAS50000001308

• Precision Medicine for Dilated Cardiomyopathy in European and African Ancestry

  The DCM Precision Medicine Study is a multi-site consortium-based cross-sectional study of families with an embedded open-label randomized controlled trial. The aims of the study are to test the hypothesis that dilated cardiomyopathy (DCM) has a substantial genetic basis and to evaluate the effectiveness of a family communication intervention in improving the uptake of preventive screening and surveillance in at-risk first-degree relatives. The Study goal was to recruit 1,300 individuals (600 non-Hispanic African ancestry, 600 non-Hispanic European ancestry, and 100 Hispanic; 50% female) meeting rigorous diagnostic criteria for idiopathic DCM (probands) and 2,600 of their relatives. The probands were inpatients or outpatients identified by heart failure and cardiac transplant cardiovascular physicians and clinical research personnel in heart failure/heart transplant programs at sites in the DCM Consortium. The DCM phenotype was selected for this study because of its prevalence and its prior inclusion in the development of virtually all pharmacotherapy for non-ischemic heart failure from reduced ejection fraction. Study procedures included obtaining family history, cardiac history, medical record review, surveys, and blood sample collection. Exome data from 1219 idiopathic DCM probands and 127 idiopathic DCM relatives are included in dbGaP.

  Study phs002641

• National Sleep Research Resource (NSRR): Hispanic Community Health Study/Study of Latinos

  The Hispanic Community Health Study / Study of Latinos (HCHS/SOL) is a multi-center epidemiologic study in Hispanic/Latino populations to determine the role of acculturation in the prevalence and development of disease, and to identify risk factors playing a protective or harmful role in Hispanics/Latinos. The study is sponsored by the National Heart, Lung, and Blood Institute (NHLBI) and six other institutes, centers, and offices of the National Institutes of Health (NIH) contributed to the first phase of the project. Raw polysomnography data are available from the HCHS/SOL Baseline visit and raw actigraphy data are available from the Sueño Ancillary visit. Primary HCHS/SOL data can be requested through dbGaP phs000810 Hispanic Community Health Study /Study of Latinos (HCHS/SOL).

  Study phs003543

• Acquisition of additional mutations drives accelerated progression of NPM1 positive CMML to AML

  This data is part of a pre-publication release. For information on the proper use of pre-publication data shared by the Wellcome Trust Sanger Institute (including details of any publication moratoria), please see http://www.sanger.ac.uk/datasharing/ We performed exome sequencing on serial samples from a patient with CMML who progressed to AML. The exome sequencing suggests that NPM1, TET2 and DNMT3a mutations were present in the dominant clone in the CMML sample and that NRAS is a new subclonal mutation in the AML sample. Diagnostic data shows the presence of a FLT3-ITD mutation in the AML sample, which is likely to have driven progression. Here we are performing re-sequencing of the putative driver and some passenger mutations which appear to be in the same clone to validate these mutations and to verify the relative quantification of these abnormalities .

  Dataset EGAD00001002194