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Fagin, J.

Publications and source records attributed to Fagin, J..

2 recordsLinked to original sources

Integrated histopathologic modeling of detailed tumor subtypes and actionable biomarkers

Accurate cancer subtyping with accompanying molecular characterization is critical for precision oncology. While machine learning approaches have been applied to both digital pathology and cancer genomics, previous work has been limited in sample size and has typically aggregated granular cancer subtypes into coarse groupings, likely obfuscating informative molecular and prognostic associations and phenotypic variation of more detailed tumor subtypes. Accordingly, we collated 378,123 hematoxylin and eosin (H&E)-stained whole-slide images (WSIs) with matched targeted DNA clinical sequencing results and OncoTree detailed cancer subtypes from a real-world cohort of 71,142 patients. Using this scaled, granular dataset and a cancer subtype knowledge graph, we developed Mosaic: a family of calibrated machine learning models using H&E WSI embeddings to classify tumors and identify molecular phenotypes across 163 detailed subtypes. The cancer subtyping module (Aeon) achieved an area under the receiver operating characteristic curve (AUROC) of 0.992 overall, with 161/163 subtypes reaching an AUROC [≥] 0.90 and improved performance over a state-of-the-art genomics-based classifier. The genomic inference module (Paladin) achieved an AUROC [≥] 0.80 for 167 pairs of detailed subtypes and genomic targets. We further used the learned histopathologic representations to i) identify key associations of the histopathologic embeddings with clinical biomarkers; ii) identify unsupervised sub-clusters of tumors with genomic determinants of tumor phenotype; iii) specify granular diagnoses for cancers of unknown primary, evaluated by genomic associations and expected clinical outcome distributions; iv) annotate functional significance for variants of uncertain significance (VUS); and v) identify cases that mimic the phenotypic effect of known DNA variants on H&E in the absence of detectable DNA alterations. Taken together, this work advances our understanding of phenotypic variation of granular tumor subtypes, their relevance to enhanced diagnostics, and their potential utility in risk stratification with multimodal machine learning in cancer.

cancer biology↗

Oncologic Therapy Shapes the Fitness Landscape of ClonalHematopoiesis

Clonal hematopoiesis (CH) is frequent in cancer patients and associated with increased risk of therapy related myeloid neoplasms (tMN). To define the relationship between CH, oncologic therapy, and tMN progression, we studied 24,439 cancer patients. We show that previously treated patients have increased rates of CH, with enrichment of mutations in DNA Damage Response (DDR) genes (TP53, PPM1D, CHEK2). Exposure to radiation, platinum and topoisomerase II inhibitors have the strongest association with CH with evidence of dose-dependence and gene-treatment interactions. We validate these associations in serial sampling from 525 patients and show that exposure to cytotoxic and radiation therapy imparts a selective advantage specifically in hematopoietic cells with DDR mutations. In patients who progressed to tMN, the clone at CH demarcated the dominant clone at tMN diagnosis. CH mutational features predict risk of therapy-related myeloid neoplasm in solid tumor patients with clinical implications for early detection and treatment decisions.

genetics↗