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• SIGi001-A-2 / SAMEA4451116 WGS data

  The iPSC line SIGi001-A-2 / SAMEA4451116 has undergone whole genome sequencing. Whole genome sequencing was done using Illumina HiSeq X Five platform with a reference genome of GRCh38. Raw data as FASTQ files and analysed data as CRAM files are available for this sample, in this dataset. The iPSC line SIGi001-A-2 is available for research use at www.EBiSC.org.

  Dataset EGAD50000001077

• SIGi001-A-12 / SAMEA104237570 WGS data

  The iPSC line SIGi001-A-12 / SAMEA104237570 has undergone whole genome sequencing. Whole genome sequencing was done using Illumina HiSeq X Five platform with a reference genome of GRCh38. Raw data as FASTQ files and analysed data as CRAM files are available for this sample, in this dataset. The iPSC line SIGi001-A-12 is available for research use at www.EBiSC.org.

  Dataset EGAD50000001076

• SIGi001-A-11 / SAMEA4451118 WGS data

  The iPSC line SIGi001-A-11 / SAMEA4451118 has undergone whole genome sequencing. Whole genome sequencing was done using Illumina HiSeq X Five platform with a reference genome of GRCh38. Raw data as FASTQ files and analysed data as CRAM files are available for this sample, in this dataset. The iPSC line SIGi001-A-11 is available for research use at www.EBiSC.org.

  Dataset EGAD50000001075

• SIGi001-A-10 / SAMEA4451117 WGS data

  The iPSC line SIGi001-A-10 / SAMEA4451117 has undergone whole genome sequencing. Whole genome sequencing was done using Illumina HiSeq X Five platform with a reference genome of GRCh38. Raw data as FASTQ files and analysed data as CRAM files are available for this sample, in this dataset. The iPSC line SIGi001-A-10 is available for research use at www.EBiSC.org.

  Dataset EGAD50000001074

• SIGi001-A-1 / SAMEA4451096 WGS data

  The iPSC line SIGi001-A-1 / SAMEA4451096 has undergone whole genome sequencing. Whole genome sequencing was done using Illumina HiSeq X Five platform with a reference genome of GRCh38. Raw data as FASTQ files and analysed data as CRAM files are available for this sample, in this dataset. The iPSC line SIGi001-A-1 is available for research use at www.EBiSC.org.

  Dataset EGAD50000001073

• BIONi010-C-2 / SAMEA4342705 WGS data

  The iPSC line BIONi010-C-2 / SAMEA4342705 has undergone whole genome sequencing. Whole genome sequencing was done using Illumina HiSeq X Five platform with a reference genome of GRCh38. Raw data as FASTQ files and analysed data as CRAM files are available for this sample, in this dataset. The iPSC line BIONi010-C-2 is available for research use at www.EBiSC.org.

  Dataset EGAD50000001068

• BIONi010-C-5 / SAMEA4452061 WGS data

  The iPSC line BIONi010-C-5 / SAMEA4452061 has undergone whole genome sequencing. Whole genome sequencing was done using Illumina HiSeq X Five platform with a reference genome of GRCh38. Raw data as FASTQ files and analysed data as CRAM files are available for this sample, in this dataset. The iPSC line BIONi010-C-5 is available for research use at www.EBiSC.org.

  Dataset EGAD50000001062

• SIGi001-A-7 / SAMEA4448730 WGS data

  The iPSC line SIGi001-A-7 / SAMEA4448730 has undergone whole genome sequencing. Whole genome sequencing was done using Illumina HiSeq X Five platform with a reference genome of GRCh38. Raw data as FASTQ files and analysed data as CRAM files are available for this sample, in this dataset. The iPSC line SIGi001-A-7 is available for research use at www.EBiSC.org.

  Dataset EGAD50000001060

• National Sleep Research Resource (NSRR): Cleveland Family Study (CFS)

  The Cleveland Family Study (CFS) is a family-based study of sleep apnea, consisting of 2,284 individuals (46% African American) from 361 families studied on up to 4 occasions over a period of 16 years. The study began in 1990 with the initial aims of quantifying the familial aggregation of sleep apnea. National Institutes of Health (NIH) renewals provided expansion of the original cohort, including increased minority recruitment, and longitudinal follow-up, with the last exam occurring in February 2006. The CFS was designed to provide fundamental epidemiological data on risk factors for sleep disordered breathing (SDB). The sample was selected by identifying affected probands who had laboratory diagnosed obstructive sleep apnea. All first-degree relatives, spouses and available second-degree relatives of affected probands were studied. In addition, during the first 5 study years, neighborhood control families were identified through a neighborhood proband, and his/her spouses and first-degree relatives. Each exam, occurring at approximately 4-year intervals, included new enrollment as well as follow up exams for previously enrolled subjects. For the first three visits, data, including an overnight sleep study, were collected in participants' homes while the last visit occurred in a general clinical research center (GCRC). Phenotypic characterization of the entire cohort included overnight sleep apnea studies, blood pressure, spirometry, anthropometry and questionnaires. Currently, data of 710 individuals are available for use through BioData Catalyst (with genotype data available through dbGaP).The National Sleep Research Resource (NSRR) is a NIH-supported sleep data repository that offers free access to large collections of de-identified physiological signals and related clinical data from a large range of cohort studies, clinical trials and other data sources from children and adults, including healthy individuals from the community and individuals with known sleep or other health disorders. The goals of NSRR are to facilitate rigorous research that requires access to large or more diverse data sets, including raw physiological signals, to promote a better understanding of risk factors for sleep and circadian disorders and/or the impact of sleep disturbances on health-related outcomes. Data from over 15 data sources and more than 40,000 individual sleep studies, many linked to dozens if not hundreds of clinical data elements, are available (as of Feb. 2022). Query tools are available to identify variables of interest, and their meta-data and provenance.

  Study phs002715

• RNA-seq data of bone marrow CD34-positive cells from 57 patients with myelodysplastic syndromes (MDS) and 5 healthy individuals (62 participants in total)

  Genetic mutations in hematopoietic neoplasms, seen in disease-specific and non-specific ways, are key drivers in pathogenesis. Typically, these mutations alone don't cause neoplasms; rather, multiple mutations or breakdowns in regulatory mechanisms occur, progressing the disease through stages. Genetic mutation patterns vary even within subtypes, suggesting shared gene expression abnormalities from different mutations may drive neoplasm development. Identifying these "common factors" is vital for effective molecular-targeted therapy development. Our study aims to elucidate neoplasm pathogenesis by analyzing patient genetic abnormalities, pinpointing "common factors" in each subtype for novel targeted therapy development.

  Study JGAS000724

• Whole genome sequencing of pancreatic cystic fluid for early detection and diagnosis of pancreatic cancer

  Pancreatic cancer (PC) is a leading cause of cancer-related deaths globally. Accurate PC detection at early or premalignant stage, when surgery is effective, would increase survival rates and prevent unnecessary surgery or surveillance. Molecular diagnostic attempts using PCy fluid (PCyF), as a liquid biopsy, to analyze common mutations associated with PC development are yet to contribute to early diagnosis. Whole genome sequencing (WGS) is utilized in various cancers, PC inclusive, for detecting genetic changes associated with carcinogenesis, but not in PCyF due to technical limitations, including isolated DNA purity. The goal of the study was to achieve high quality of WGS from PCyF from 9 patients to enable development of signatures of malignancy. The WGS was performed using Illumina sequencing. Experimental design was at a 50x depth.

  Dataset EGAD50000000869

• National Eye Institute (NEI) Genetic Epidemiology of Age-Related Macular Degeneration in the Old Order Amish

  Identifying genetic risk loci for Age-Related Macular Degeneration is important. Most of the loci identified to date have been found through the interrogation of common variants. This study initiates the identification of rare variants in a founder population, the Amish, and will use genotyping of known risk loci and ultimately use the whole exome chip to assess the association of Age-related Macular Degeneration with coding variants. We will further refine the Age-Related Macular Degeneration phenotype through the use of modern imaging, the OCT, to visualize the early anatomic signs of Age-Related Macular Degeneration. We hypothesize there are endophenotypes associated with specific genotypes that can be used to determine Age-related Macular Degeneration progression. These endophenotypes are hypothesized to be influenced by a combination of common and rare variants. We will relate these endophenotypes to genotypes to define the role of genetics in the progression of Age-Related Macular Degeneration and a new risk profile incorporating genotypic information.

  Study phs001361

• Widespread hypertranscription in aggressive human cancers

  Cancers are often defined by the dysregulation of specific transcriptional programs; however, the importance of global transcriptional changes is less understood. Hypertranscription is the genome-wide increase in RNA output. Hypertranscription’s prevalence, underlying drivers and prognostic significance are undefined in primary human cancer. This is due in part to limitations of expression profiling methods, which assume equal RNA output between samples. Here, we developed a computational method to directly measure hypertranscription in 7,494 human tumors, spanning 31 cancer types. Hypertranscription is ubiquitous across cancer, especially in aggressive disease. It defines patient subgroups with worse survival, even within well-established subtypes. Our data suggest that loss of transcriptional suppression underpins the hypertranscriptional phenotype. Single-cell analysis reveals hypertranscriptional clones, which dominate transcript production regardless of their size. Finally, patients with hypertranscribed mutations have improved response to immune checkpoint therapy. Our results provide fundamental insights into gene dysregulation across human cancers and may prove useful in identifying patients that would benefit from novel therapies.

  Study EGAS00001006365

• Heart Failure Network - Imaging from Nitrate's Effect on Activity Tolerance in Heart Failure with Preserved Ejection Fraction (HFN NEAT-Imaging)

  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: To determine the effect of isosorbide mononitrate on daily activity in patients with heart failure and preserved ejection fraction.Background: Nitrates are commonly prescribed for symptom relief in patients with heart failure. Early studies in patients with heart failure with a reduced ejection fraction concluded that long-acting nitrates improves activity tolerance; however, approximately half of heart failure patients have preserved ejection fraction. The effects of nitrates in patients with heart failure and a preserved ejection fraction have not been extensively studied and the overall effect of nitrates on activity tolerance in such patients is uncertain.Subjects: There were a total of 110 patients enrolled with 51 patients assigned to receive isosorbide mono-nitrate first and placebo second, and 59 patients assigned to receive placebo first and isosorbide mononitrate second.Design: Enrolled subjects underwent baseline assessments, including echocardiography, quality-of-life scores, 6-minute walk test distance, and NT-proBNP levels. Subjects were also supplied with two kinetic activity monitors containing high-sensitivity triaxis accelerometers, to be worn 24 hours per day. The accelerometer measurements were expressed as arbitrary accelerometer units and stored every 15 minutes equaling 96 data points per day. The 15-minute cumulative accelerometer units were totaled over a 24-hour period to provide daily accelerometer units.Subjects were assigned to one of two treatment groups: 6 weeks of placebo first with crossover to 6 weeks of isosorbide mononitrate, or 6 weeks of isosorbide mononitrate first with crossover to 6 weeks of placebo. The study drugs were prepared as 30-mg tablets of isosorbide mononitrate and matching placebo. During each 6-week period, patients were instructed to take no study drug for the first 2 weeks followed by one tablet (30 mg daily) for 1 week, two tablets (60 mg once daily) for 1 week, and four tablets (120 mg once daily) until the next study visit, for a treatment duration of at least 2 weeks and up to 4 weeks. After each 6-week period, patients returned to the study center to repeat end-point assessments. The primary outcome for the study was the comparison of average daily accelerometer units during the period in which patients were receiving the 120-mg dose of isosorbide mononitrate compared to the period in which patients received the placebo. Other secondary end points included the 6-minute walk distance and the post-walk Borg dyspnea score, scores on the Kansas City Cardiomyopathy Questionnaire and the Minnesota Living with Heart Failure Questionnaire, and NT-proBNP levels. In addition, subjects completed a questionnaire indicating in which period (first, second, no preference) they felt better. Conclusions: Patients were active for fewer hours of the day during the 120-mg phase of receipt of isosorbide mononitrate as compared with placebo. Furthermore, during all study-drug regimens combined (30 mg to 120 mg), patients were less active during receipt of isosorbide mononitrate as compared with placebo. There was no significant effect of isosorbide mononitrate on secondary outcomes.

  Study phs004254

• Chromatin accessibility in human monocyte differentiation

  This dataset consists of ATAC-seq data from human monocytes, monocyte-derived dendritic cells or monocyte-derived macrophages as well as monocyte-derived cells that were subjected to siRNA treatment targeting TET2, IRF4 and EGR2. In total, it includes 26 samples.

  Dataset EGAD00001006601

• METABRIC: Data from Pereira et al (2016), The somatic mutation profiles of 2433 breast cancers refine their genomic and transcriptomic landscapes. Nat Comms 7.

  The genomic landscape of breast cancer is complex, and inter- and intra-tumour heterogeneity are important challenges in treating the disease. In this study, we sequence 173 genes in 2433 primary breast tumours that have copy number aberration (CNA), gene expression, and long-term clinical follow-up data. We identify 40 mutation-driver (Mut-driver) genes, and determine associations between mutations, driver CNA profiles, clinical-pathological parameters, and survival. We assess the clonal states of Mut-driver mutations, and estimate levels of intratumour heterogeneity using mutant allele fractions. Associations between PIK3CA mutations and reduced survival are identified in three subgroups of ER-positive cancer (defined by amplification of 17q23, 11q13-14 or 8q24). High levels of intratumour heterogeneity are in general associated with worse outcome, but highly aggressive tumours with 11q13-14 amplification have low levels of intratumour heterogeneity. These results emphasise the importance of genome-based stratification of breast cancer, and have important implications for designing therapeutic strategies.

  Study EGAS00001001753

• AVENIO Expanded ctDNA panel sequence alignments (BAMs) from plasma DNA of lung cancer patients from the OSCILLATE trial

  The AVENIO ctDNA Expanded Kit is a next-generation sequencing (NGS) liquid biopsy assay with a 77 gene panel (192 kb) containing genes in U.S. National Comprehensive Cancer Network (NCCN) Guidelines and emerging cancer biomarkers. This pan-cancer assay was applied to 100 plasma samples from patients with lung cancer undergoing treatment in the OSCILLATE trial. After 150 bp paired-end sequencing, reads were aligned to the human genome reference with the AVENIO Oncology Analysis Software. These files are the sorted non-deduplicated alignments generated by the analysis software used for subsequent variant, indel and CNV calling.

  Study EGAS50000000103

• Molecular subtypes of pancreatic neuroendocrine tumors mutated in MEN1/DAXX/ ATRX explain biological variability

  Pancreatic Neuroendocrine Tumors (PanNETs) most probably arise from the islets of Langerhans, although direct evidence is still lacking. About 40% of non-functioning (NF) PanNETs harbour mutations in MEN1, often in conjunction with alterations in DAXX/ATRX. Despite the homogeneous genetic background, the ADM (mutation in DAXX/ATRX and MEN1) group is heterogeneous regarding molecular features and response to treatment. To explore the molecular and clinical heterogeneity within this group, we integrated transcriptomic and DNA methylation data from 36 and 93 samples, respectively. Using a multi-omic approach we described a two-level hierarchy separating PanNET subtypes mutated in MEN1, DAXX and ATRX. First, DNA methylation discriminates ADM-PanNET from PanNET mutated in MEN1 only (α-like). Compared to α-like, all ADM tumors exhibit DNA methylation changes at enhancer and lowly methylated regions as well as at peri-centromeric and telomeric regions, associated with alternative lengthening of telomeres, increased chromosomal instability, and enhanced proliferative capacity. At a second level, transcriptomic analysis revealed three distinct ADM subtypes: ADM hypoxic, ADM NST (No Special Type), and ADM immunosuppressive. The ADM hypoxic subtype is characterized by strong hypoxia signature, likely regulated epigenetically. The ADM NST subtype appears to be primarily driven by epigenetic changes that promote proliferation. The ADM immunosuppressive is highly enriched in immune component and strong metastasis-like signature. While all the three subtypes are highly associated with liver metastasis formation and invasion, the ADM immunosuppressive are significantly smaller (<2.5 cm p.value=0.023) despite displaying aggressive molecular features. By defining these three novel ADM subtypes, our study provides a refined framework for understanding PanNET heterogeneity. This classification underscores potential diagnostic markers and highlights distinct biological vulnerabilities that may inform the development of subtype-tailored therapeutic strategies.

  Study EGAS00001008272

• Transrenal DNA Analysis

  Urinary cell-free DNA (ucfDNA) is an emerging marker in liquid biopsy. However, the characteristics of transrenal DNA and urinary-tract DNA are not fully understood. Therefore, we investigated the fragmentomic features and demonstrated the potential clinical utilities of ucfDNA in the current study.

  Study EGAS50000000766

• PAGE: The Charles Bronfman Institute for Personalized Medicine (IPM) BioMe BioBank

  The Institute for Personalized Medicine (IPM) BioMe Biobank is a consented, EMR-linked medical care setting biorepository of the Mount Sinai Medical Center (MSMC) drawing from a population of over 70,000 inpatients and 800,000 outpatient visits annually. MSMC serves diverse local communities of upper Manhattan, including Central Harlem (86% African American), East Harlem (88% Hispanic Latino), and Upper East Side (88% Caucasian/white) with broad health disparities. IPM BioMe Biobank populations include 28% African American, 38% Hispanic Latino predominantly of Caribbean origin, 23% Caucasian/White. IPM BioMe Biobank disease burden is reflective of health disparities with broad public health impact. Biobank operations are fully integrated in clinical care processes, including direct recruitment from clinical sites waiting areas and phlebotomy stations by dedicated Biobank recruiters independent of clinical care providers, prior to or following a clinician standard of care visit. Recruitment currently occurs at a broad spectrum of over 30 clinical care sites. This study is part of the Population Architecture using Genomics and Epidemiology (PAGE) study (phs000356).

  Study phs000925

• Genome-Wide Association Study of Endometrial Cancer in the Epidemiology of Endometrial Cancer Consortium (E2C2)

  Endometrial cancer, the most common gynecological malignancy in the United States, has both an environmental and genetic component. To this end, we conducted a genome-wide association study to identify genes involved in endometrial cancer using studies from the NCI-supported Epidemiology of Endometrial Cancer Consortium (E2C2). For the discovery stage we included samples from 6 cohort and 7 case control studies through 2007. The total number of cases genotyped were 2,307, white women of European descent, and 2,307 matched controls using the Illumina HumanOmniExpress platform. We conducted the replication using the Infinium HumanExome BeadChip, which successfully genotyped 177,139 variants in 1055 cases and 1778 controls from four ethnically diverse studies that are part of the Epidemiology of Endometrial Cancer Consortium (E2C2). The overall goal is to determine whether certain genotypes are predictive of future endometrial cancer risk, and whether the genotypes interact with established endometrial risk factors.

  Study phs000893

• Familial psychosis associated with a missense mutation at MACF1 gene combined with the rare duplications DUP3p26.3 and DUP16p23.3, affecting the CNTN6 and CDH13 genes

  Psychosis is a highly heritable and heterogeneous psychiatric condition. Its genetic architecture is thought to be the result of the joint effect of common and rare variants. Families with high prevalence are an interesting approach to shed light on the rare variant's contribution without the need of collecting large cohorts. To unravel the genomic architecture of a family enriched for psychosis, with four affected individuals, we applied a system genomic approach based on karyotyping, genotyping by whole-exome sequencing to search for rare single nucleotide polymorphisms (SNPs) and SNP array to search for copy-number variants (CNVs). We identified a rare non-synonymous variant, g.39914279 C>G, in the MACF1 gene, segregating with psychosis. Rare variants in the MACF1 gene have been previously detected in SCZ patients. Besides, two rare CNVs, DUP3p26.3 and DUP16p23.3, were also identified in the family affecting relevant genes (CNTN6 and CDH13, respectively). We hypothesize that the co-segregation of these duplications with the rare variant g.39914279 C>G of MACF1 gene precipitated with schizophrenia and schizoaffective disorder.

  Study EGAS00001004791

• NHLBI TOPMed: Outcome Modifying Genes in Sickle Cell Disease (OMG)

  Sickle cell disease (SCD) is caused by homozygosity for a single mutation of the beta hemoglobin gene. Despite the constancy of this genetic abnormality, the clinical course of patients with SCD is remarkably variable. SCD can affect the function and cause the failure of multiple organ systems through the pathophysiologic processes of vaso-occlusion and hemolysis. These pathophysiological processes are complex and expected to impact multiple organ systems in a variety of ways. This study, therefore, was designed to identify genetic factors that predispose SCD patients to develop specific end-organ complications and to experience more or less severe clinical courses. We enrolled > 700 patients with Hb SS, Hb S-beta0 thalassemia and HbSC being followed primarily at three southeastern U.S. regional institutions (Duke University Medical Center, University of North Carolina Medical Center, and Emory University Medical Center). Medical information obtained included the presence or absence of specific targeted outcomes (overall disease severity as well as specific types of end organ damage). Clinical data include medical status (history, physical, examination, and laboratory results) and information regarding potentially confounding environmental factors. Limited plasma samples are available for correlative studies (e.g. of cytokine levels, coagulation activation). Targeted SNP for candidate gene analysis as well as GWAS has been performed on most samples. Whole genome sequencing has been conducted through the TOPMed Consortium. The subjects in this analysis were collected as part of a larger study, "Outcome Modifying Genes in Sickle Cell Disease" (OMG-SCD) aimed at identifying genetic modifiers for sickle cell disease. More information about the study can be found in Elmariah et al. (2014), PMID: 24478166. Clinical and genetic data have been used to identify genetic characteristics predisposing patients with SCD to a more or less severe overall clinical course as well as to individual organ-specific complications. It is anticipated that identification of such genetic factors will reveal new therapeutic targets individualized to specific complications of SCD, leading to improved outcomes and increased life expectancy for patients with SCD.

  Study phs001608

• Successful BRAF/MEK-inhibition in a young patient with BRAF V600E-mutated extrapancreatic acinar cell carcinoma (HIPO-021)

  Pancreatic acinar cell carcinoma (PAC) is a rare disease with a poor prognosis. Treatment options for metastatic PAC are limited and often follow chemotherapeutic regimens for pancreatic ductal adenocarcinoma. Although recurrent genomic alterations, such as BRAF fusions and defects in genes involved in homologous recombination DNA repair, have been described in PAC, data on the clinical efficacy of molecularly guided, targeted treatment are scarce. Here we describe the case of a 27-yr-old patient with BRAF V600E-mutated PAC who was successfully treated with a combination of BRAF and MEK inhibitors. The patient presented to our clinic with abdominal pain and weight loss. Imaging showed extensive retroperitoneal disease as well as mediastinal lymphadenopathy. Because of elevated alpha-fetoprotein (AFP) levels and inconclusive histologic findings, a germ cell tumor was suspected; however, PEI chemotherapy was unsuccessful. A repeat biopsy yielded the diagnosis of PAC and treatment with FOLFIRINOX was initiated. Comprehensive molecular profiling within the MASTER (Molecularly Aided Stratification for Tumor Eradication Research) precision oncology program revealed a somatic BRAF V600E mutation and a germline PALB2 stop-gain mutation. Therapy was therefore switched to BRAF/MEK inhibition, resulting in almost complete remission and disease control for 12 mo and a remarkable improvement in the patient's general condition. These results indicate that BRAF alterations are a valid therapeutic target in PAC that should be routinely assessed in this patient population.

  Study EGAS00001004282

• Mutation-specific non-canonical pathway of PTEN as a distinct therapeutic target for glioblastoma

  PTEN is one of most frequently altered tumor suppressor genes in malignant tumors. The dominant negative effect of PTEN alteration suggests that aberrant function of PTEN mutation might be more disastrous than deletion, the most frequent genomic event in glioblastoma (GBM). This study aimed to understand the functional properties of various PTEN missense mutations and to investigate their clinical relevance. The genomic landscape of PTEN alteration was analyzed using the Samsung Medical Center GBM cohort and validated via The Cancer Genome Atlas dataset. Several hot-spot mutations were identified, and their subcellular distributions and phenotypes were evaluated. We established a library of cancer cell lines that over-express these mutant proteins using the U87MG and patient-derived cell models lacking functional PTEN. PTEN mutations were categorized into two major subsets: missense mutations in the phosphatase domain and truncal mutations in the C2 domain. We determined the subcellular compartmentalization of four mutant proteins (H93Y, C124S, R130Q, and R173C) from the former group and found that they had distinct localizations; those associated with invasive phenotypes (‘edge mutations’) localized to the cell periphery, while the R173C mutant localized to the nucleus. Invasive phenotypes derived from edge substitutions were unaffected by an anti-PI3K/Akt agent but were disrupted by microtubule inhibitors. PTEN mutations exhibit distinct functional properties with regard to their subcellular localization. Further, some missense mutations (‘edge mutations’) in the phosphatase domain caused enhanced invasiveness associated with dysfunctional cytoskeletal assembly, thus suggesting it to be a potent therapeutic target.

  Study EGAS00001004753