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• noninvasive lung cancer subtyping

  Accurate diagnosis of lung cancer is important for treatment decision-making. Currently, the gold standard for diagnosing histological subtypes of lung cancer relies on tumor biopsies. Recently, liquid biopsy, particularly cell-free DNA (cfDNA), has shown promising results in cancer detection and classification. In this study, we investigated the potential of cfDNA methylome for the noninvasive classification of lung cancer histological subtypes. Specifically, we focused on the two most prevalent lung cancer subtypes, lung adenocarcinoma and lung squamous cell carcinoma. Using a fragment-based marker discovery approach, we identified robust subtype-specific methylation markers from tumor samples. These markers were successfully validated in independent cohorts and associated with subtype-specific transcription activity. Leveraging these markers, we constructed a subtype classification model using cfDNA methylation profiles, achieving an AUC of 0.808 in the cross-validation and an AUC of 0.747 in the independent validation. Additionally, tumor copy number variations inferred from cfDNA methylome analysis revealed potential implications for treatment selection. In summary, our study demonstrates the potential of cfDNA methylome analysis for noninvasively lung cancer subtyping, offering insights for cancer monitoring and early detection.

  Study EGAS00001007717

• Single Cell RNA-Seq Reveals Malignant and Stromal Programs Associated with Metastasis in Head and Neck Cancer

  This study of head and neck cancer aimed to profile individual malignant, stromal, and immune cells in treatment-naive oral cavity squamous cell carcinoma, with or without matched metastatic cervical lymph nodes. Clinical and pathologic information was collected on all patients, in addition to a fresh biopsy sample from the primary tumor and/or metastatic lymph node at the time of initial surgery. Biopsy specimens were processed for single cell RNA-seq (scRNA-seq) and/or whole exome sequencing (WES). A total of ~6,000 single cells from 18 participants were included in the final dataset. Stromal and immune cells had consistent expression programs across patients. Conversely, malignant cells varied within and between tumors in their expression of signatures related to cell cycle, stress, hypoxia, epithelial differentiation, and partial epithelial-to-mesenchymal transition (p-EMT). One of the top scoring genes in this program was TGFβ-induced (TGFBI), implicating the classic EMT regulator TGFβ. Cells expressing the p-EMT program spatially localized to the leading edge of primary tumors. By integrating single-cell transcriptomes with bulk expression profiles for hundreds of tumors, we refined Head and Neck Squamous Cell Carcinoma (HNSCC) subtypes by their malignant and stromal composition, and established p-EMT as an independent predictor of nodal metastasis, grade, and adverse pathologic features. Our results provide insight into the HNSCC ecosystem and define stromal interactions and a p-EMT program associated with metastasis.

  Study phs001474

• The clonal and mutational evolution spectrum of primary triple negative breast cancers

  Primary triple negative breast cancers (TNBC) represent approximately 16% of all breast cancers and are a tumour type defined by exclusion,for which comprehensive landscapes of somatic mutation have not been determined. Here we show in 104 early TNBC cases, that at the time of diagnosis these cancers exhibit a wide and continuous spectrum of genomic evolution, with some exhibiting only a handful of somatic aberrations in a few pathways, whereas others contain hundreds of somatic events and multiple pathways implicated. Integration with matched whole transcriptome sequence data revealed that only 36% of mutations are expressed. By examining single nucleotide variant (SNV) allelic abundance derived from deep re-sequencing (median > 20,000 fold) measurements in 2414 somatic mutations, we determine for the first time in an epithelial tumour, the relative abundance of clonal genotypes among cases in the population. We show that TNBC vary widely and continuously in their clonal frequencies at the time of diagnosis, with basal subtype TNBC exhibiting more variation than non-basal TNBC. Although p53 and somatic mutations appear clonally dominant compared with other pathways, in some tumours their clonal frequencies are incompatible with founder status. Mutations in cytoskeletal and cell shape/motility proteins occurred at lower clonal frequencies, suggesting they occurred later during tumour progression. Taken together our results show that future attempts to dissect the biology and therapeutic responses of TNBC will require the determination of individual tumour clonal genotypes.

  Study EGAS00001000132

• Prematurity and Respiratory Outcomes Program (PROP) Core Database Protocol (PROP-BioLINCC)

  Data Access NOTE: Please refer to the "Authorized Access" section below for information about how access to the data from this accession differs from many other dbGaP accessions. Objectives: The Prematurity and Respiratory Outcomes Program (PROP) was performed to identify suitable predictors of respiratory outcomes that may serve as surrogate endpoints in future trials of prevention and therapy of respiratory diseases in preterm infants.Background: Acute and chronic respiratory morbidities are common in premature births, and can pose significant risk to the infant's health, particularly during the first two years of life. One such condition is bronchopulmonary dysplasia (BPD) where infants require oxygen therapy due to abnormal repair and impaired lung development after acute lung injury. BPD poses a high mortality risk, even in infants that survive the initial hospitalization. Regardless of BPD diagnosis, preterm infants frequently return for medical care due to symptoms of post-prematurity respiratory disease (PRD), which includes intermittent or chronic wheezing, cough without cold, poor growth, apnea and cyanosis, and lower respiratory tract infections. Impaired lung function can persist into adulthood, contributing to chronic respiratory diseases including asthma and emphysema.However, at the time of the PROP study, there were no objective measures to predict which preterm infants would have persistent respiratory problems after discharge from the hospital. Furthermore, improved survival rates of premature infants and the high prevalence of lasting respiratory morbidities highlight the need for more comprehensive strategies to address both short-term and long-term respiratory complications. Thus, the Prematurity and Respiratory Outcomes Program (PROP) was formed to investigate multiple research hypotheses on the molecular mechanisms that contribute to respiratory disease risk of premature neonates over the first year of life. Specifically, PROP investigators hypothesized that in survivors of extreme prematurity to 36 weeks postmenstrual age (PMA), specific biologic, physiologic and clinical data obtained during the initial hospitalization will predict respiratory morbidity between discharge and 1 year corrected age. Participants: A total of 835 infants were enrolled.Design: PROP was a collaboratively developed multicenter prospective cohort study of very preterm infants from birth through the time of discharge from the NICU and up to one year corrected age.Clinical data included maternal and infant demographics, co-morbidities, and daily infant respiratory, nutritional, and medication data until discharge. These were prospectively collected from birth using medical record review and family interviews. After discharge, phone interviews were conducted with the infant's main caregiver at 3, 6, 9 and 12 months corrected age to assess domains of respiratory morbidity. At 6 and 12 months corrected age, a survey of environmental respiratory irritant exposures and an assessment for gastroesophageal reflux disease were also completed. A standardized physical exam was performed at 36-40 weeks PMA and again at one year corrected age. The exam focused on anthropometrics, vital signs, and respiratory system signs. At 34-41 weeks PMA and within one week of anticipated discharge based on physiologic stability, a set of non-invasive respiratory assessments were performed to assess physiologic biomarkers in infants that were not mechanically ventilated or receiving non-invasive positive pressure ventilation. Respiratory inductance plethysmography (RIP) was performed before and after inhaled albuterol to assess potential airway reactivity. During the RIP study, continuous pulse oximetry was performed during quiet sleep in order to analyze oxygen desaturations and apneas. Standardized oxygen requirement challenge tests were performed at about 36 weeks PMA, and at about 40 weeks PMA if the infant was still hospitalized and was not eligible for, or failed, the previous challenge. Failure was defined as SpO2 20 seconds at any point in the testing. Infants breathing ambient air or that passed the 36 week challenge test underwent a hypoxia challenge consisting of a 15-minute trial of FiO2 of 0.15. Failure was defined as SpO2 The primary outcome was respiratory morbidity, as measured by the presence or absence of substantial post-prematurity respiratory disease (PRD) up to one year corrected age. PRD was classified as a positive response in at least one of four morbidity domains during at least two separate parental interviews. The domains were respiratory medications, hospitalizations for cardiopulmonary cause, respiratory symptoms, and home technology dependence (oxygen, ventilator, or CPAP/BiPAP). Mortality from a respiratory cause was also incorporated.

  Study phs004117

• RNAseq and ATACseq on HGSC lines, pre- and post-treatment with an epigenetic drug

  This study looked to determine changes in gene expression and chromatin accessibility of five HGSC cell lines, following treatment with a novel epigenetic drug. The epigenetic drug, HKMTi-1-005, is a compound with dual activity against H3K27 and H3K9 methylation. The cell lines used were PEO1, PEO4, PEA2, OVCAR5, OVCAR8.

  Study EGAS50000000047

• Genetic Susceptibility and Biomarkers of Platinum-Related Toxicities

  The Platinum Study is an R01-funded, multicenter study of testicular cancer survivors that characterizes both long-term cisplatin-induced peripheral neuropathy (CisIPN) and cisplatin-associated ototoxicity, i.e., permanent, bilateral hearing loss. We collected data abstracted from medical records (e.g., cumulative cisplatin dose), conducted audiometric examinations, and administered self-report questionnaires, which included CisIPN symptoms.

  Study phs001621

• Washington University Coronary Artery Disease Study

  The genetic basis of coronary artery disease in individuals of non-European ancestry is largely unknown. The Washington University Coronary Artery Disease Study (WUCADS) recruited participants of non-European ancestry with and without coronary artery disease to address this question. Whole genome sequencing in WUCADS was performed at the McDonnell Genome Institute at Washington University.

  Study phs001227

• Determinants of Asthma Following RSV Bronchiolitis in Early Life

  The goal of the RSV Bronchiolitis in Early Life (RBEL) study is to determine how specific genetic, biologic, and immunologic characteristics interact to predispose individuals to develop asthma. Participants were carefully recruited by selecting a prospective cohort of 206 infants with severe respiratory syncytial virus (RSV) bronchiolitis who were at substantial risk of developing asthma.

  Study phs001009

• Loss of RREB1 in pancreatic beta cells reduces cellular insulin content and affects endocrine cell gene expression

  Genome-wide studies have uncovered multiple independent signals at the RREB1 locus associated with altered type 2 diabetes (T2D) risk and related glycemic traits. However, little is known about the function of the zinc finger transcription factor RREB1 in glucose homeostasis or how changes in its expression and/or function influence diabetes risk. We studied its function using three transcriptomic strategies, profiling gene expression when RREB1 is knocked out or knocked down in the Endo-betaH1 cell line, in addition to the in vitro differentiation in hiPSCs.

  Dataset EGAD00001009740

• Whole exome sequencing data of patients with resectable esophageal adenocarcinoma treated with neoadjuvant atezolizumab and chemoradiation (PERFECT)

  Whole exome sequencing was performed on matched tumor and normal DNA of patients with resectable esophageal adenocarcinoma that particpated in the PERFECT trial. The PERFECT trial is an open-label, single-arm, multicenter, phase II feasibility study (NCT03087864) investigating the safety and efficacy of atezolizumab, combined with neoadjuvant chemoradiotherapy and subsequent esophagectomy.

  Study EGAS00001006504