David B. Solit

SLC25A28 is a synthetic lethal vulnerability in nucleotide excision repair-deficient cancers

This study identifies SLC25A28 as a synthetic lethal target in NER-deficient cancers, showing its loss impairs cell viability and increases oxidative stress.

Integrated Clinicogenomic Risk Modeling for Metachronous Second Primary Cancers

The paper develops and validates a clinicogenomic risk model to predict second primary cancers in cancer survivors using genetic, clinical, and lifestyle factors.

Integrated histopathologic modeling of detailed tumor subtypes and actionable biomarkers

The paper develops Mosaic, a machine learning system that classifies tumors into detailed subtypes and identifies molecular phenotypes using histopathologic and genomic data from a large patient cohort.

Tumor suppressor heterozygosity and homologous recombination deficiency mediate resistance to front-line therapy in breast cancer

The paper identifies how germline and somatic mutations interact to cause resistance to CDK4/6 inhibitors in breast cancer and proposes a sequential treatment strategy using PARP inhibitors.

Clonal evolution during metastatic spread in high-risk neuroblastoma

This study traces clonal evolution in high-risk neuroblastoma using genomic data from 470 samples, showing metastatic clones can remain dormant and later cause relapses.

Enhanced specificity of high sensitivity somatic variant profiling in cell-free DNA via paired normal sequencing: design, validation, and clinical experience of the MSK-ACCESS liquid biopsy assay

The paper describes the development and clinical application of MSK-ACCESS, a liquid biopsy assay that improves the specificity of somatic variant detection in cell-free DNA by using paired normal sequencing.

Oncologic Therapy Shapes the Fitness Landscape of ClonalHematopoiesis

The paper shows oncologic therapy increases clonal hematopoiesis with DDR mutations, which predicts risk of therapy-related myeloid neoplasms.

Perturbation biology models predict c-Myc as an effective co-target in RAF inhibitor resistant melanoma cells

The paper uses perturbation biology to predict c-Myc as a co-target with BRAF/MEK inhibitors to overcome RAF inhibitor resistance in melanoma.