Nicholas Stong

Vandana Shashi 17 collaborations

None None 12 collaborations

David B Goldstein 9 collaborations

Kelly Schoch 8 collaborations

Jennifer A Sullivan 7 collaborations

Erin Flynt 5 collaborations

Anjan Thakurta 5 collaborations

Allyn McConkie-Rosell 5 collaborations

Jennifer Sullivan 4 collaborations

Boris Keren 4 collaborations

Cyril Mignot 4 collaborations

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Joan Jasien 3 collaborations

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Eric W Klee 3 collaborations

Kerstin Wenzl 3 collaborations

Joseph P Novak 3 collaborations

Vivekananda Sarangi 3 collaborations

Maria Ortiz 3 collaborations

C Chris Huang 3 collaborations

Matthew J Maurer 3 collaborations

Brian K Link 3 collaborations

Susan L Slager 3 collaborations

Stephen M Ansell 3 collaborations

Thomas M Habermann 3 collaborations

Rebecca L King 3 collaborations

James R Cerhan 3 collaborations

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Anne J Novak 3 collaborations

Rolph Pfundt 3 collaborations

Mohamad A Mikati 3 collaborations

Marie T McDonald 3 collaborations

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Affiliations

Publications (33)

Heterozygous variants in MYBPC1 are associated with an expanded neuromuscular phenotype beyond arthrogryposis.

Heterozygous loss-of-function variants of MEIS2 cause a triad of palatal defects, congenital heart defects, and intellectual disability.

CSNK2B: A broad spectrum of neurodevelopmental disability and epilepsy severity.

Multiomic Analysis Identifies a High-Risk Metabolic and TME Depleted Signature that Predicts Early Clinical Failure in DLBCL.

Transcriptomic classification of diffuse large B-cell lymphoma identifies a high-risk activated B-cell-like subpopulation with targetable MYC dysregulation.

De novo variants in TCF7L2 are associated with a syndromic neurodevelopmental disorder.

The microRNA processor DROSHA is a candidate gene for a severe progressive neurological disorder.

Whole-genome analysis identifies novel drivers and high-risk double-hit events in relapsed/refractory myeloma.

ETV4-Dependent Transcriptional Plasticity Maintains MYC Expression and Results in IMiD Resistance in Multiple Myeloma.

Alternative transcripts in variant interpretation: the potential for missed diagnoses and misdiagnoses.

A pathogenic variant in the SETBP1 hotspot results in a forme-fruste Schinzel-Giedion syndrome.

Improved Pathogenic Variant Localization via a Hierarchical Model of Sub-regional Intolerance.

A comprehensive iterative approach is highly effective in diagnosing individuals who are exome negative.

Rare deleterious de novo missense variants in Rnf2/Ring2 are associated with a neurodevelopmental disorder with unique clinical features.

The location of the t(4;14) translocation breakpoint within the NSD2 gene identifies a subset of patients with high-risk NDMM.

TSPEAR variants are primarily associated with ectodermal dysplasia and tooth agenesis but not hearing loss: A novel cohort study.

Autism and developmental disability caused by KCNQ3 gain-of-function variants.

SSBP1 mutations cause mtDNA depletion underlying a complex optic atrophy disorder.

Whole-exome sequencing in the evaluation of fetal structural anomalies: a prospective cohort study.

Epileptic encephalopathy with features of rapid-onset dystonia Parkinsonism and alternating hemiplegia of childhood: a novel combination phenotype associated with ATP1A3 mutation.

Coding and noncoding variants in EBF3 are involved in HADDS and simplex autism.

Expanding the phenotypic spectrum of ARCN1-related syndrome.

Ancestry adjustment improves genome-wide estimates of regional intolerance.

Late-onset pattern macular dystrophy mimicking

A case-control collapsing analysis identifies retinal dystrophy genes associated with ophthalmic disease in patients with no pathogenic ABCA4 variants.

Missense Variants in the Histone Acetyltransferase Complex Component Gene TRRAP Cause Autism and Syndromic Intellectual Disability.

Expanding the Spectrum of BAF-Related Disorders: De Novo Variants in SMARCC2 Cause a Syndrome with Intellectual Disability and Developmental Delay.

Clinical sites of the Undiagnosed Diseases Network: unique contributions to genomic medicine and science.

De novo variants in SNAP25 cause an early-onset developmental and epileptic encephalopathy.

Integrative multi-omics identifies high risk multiple myeloma subgroup associated with significant DNA loss and dysregulated DNA repair and cell cycle pathways.

The best of both worlds: Blending cutting-edge research with clinical processes for a productive exome clinic.

Multiomic analysis identifies a high-risk signature that predicts early clinical failure in DLBCL.

Pharmacodynamic changes in tumor and immune cells drive iberdomide's clinical mechanisms of activity in relapsed and refractory multiple myeloma.

Réseau de co-auteurs