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Graziano, C.

Publications and source records attributed to Graziano, C..

2 recordsLinked to original sources

Knowledge-informed multimodal cfDNA analysis improves sensitivity and generalization in cancer detection

Liquid biopsy offers a minimally invasive opportunity to detect and monitor cancers through analysis of cell-free DNA (cfDNA). However, current approaches face challenges of limited sensitivity at low tumor fractions, technical variability, and poor generalization across cohorts. Tumor-informed targeted methods offer high specificity but suffer from low sensitivity due to random sampling, tumor evolution and adaptation (including resistance mechanisms), and other sources of heterogeneity. Conversely, tumor-naive genome-wide methods can increase sensitivity but often sacrifice specificity, particularly at low tumor fractions. We developed Fragmentomics Analysis for Tumor Evaluation with AI (Fate-AI), a multimodal framework that integrates fragmentomic and methylation-derived features from low-pass whole-genome sequencing (LPWGS) and cell-free methylated DNA immunoprecipitation and high-throughput sequencing (cfMeDIP-seq). It employs a knowledge-informed strategy to select recurrently altered genomic regions and tissue-specific methylation loci to combine the advantages of tumor-naive approaches with the specificity of tumor-informed approaches. This approach derives robust per-sample normalized features that mitigate batch effects and enhance cross-cohort reproducibility. We evaluated Fate-AI on a total of 1,219 plasma samples spanning ten cancer types and healthy controls from multiple laboratories and sequencing centers, including 432 newly profiled cases (280 with both cfMeDIP-seq and LPWGS) together with 787 samples from four independent public datasets. Fate-AI achieved superior sensitivity and specificity compared to state-of-the-art methods, detecting tumor-derived signals at fractions as low as 10-5 in experimental dilutions. Fate-AI scores correlated with disease stage and tracked longitudinal progression, anticipating relapse months before clinical progression. Furthermore, Fate-AI enabled tissue-of-origin classification, with AUCs ranging from 0.84 to 0.97 across six cancer types. Collectively, our results demonstrate that Fate-AI provides a sensitive, generalizable, and clinically actionable platform for early detection, minimal residual disease monitoring, and tissue-of-origin classification, supporting its potential as a liquid biopsy framework in precision oncology.

cancer biology↗

HDAC9 structural variants disrupting TWIST1 transcriptional regulation lead to craniofacial and limb malformations

Structural variants (SVs) can affect protein-coding sequences as well as gene regulatory elements. However, SVs disrupting protein-coding sequences that also function as cis-regulatory elements remain largely uncharacterized. Here, we show that craniosynostosis patients with SVs containing the Histone deacetylase 9 (HDAC9) protein-coding sequence are associated with disruption of TWIST1 regulatory elements that reside within HDAC9 sequence. Based on SVs within the HDAC9-TWIST1 locus, we defined the 3 HDAC9 sequence (~500Kb) as a critical TWIST1 regulatory region, encompassing craniofacial TWIST1 enhancers and CTCF sites. Deletions of either Twist1 enhancers (eTw5-7{Delta}/{Delta}) or Ctcf site (Ctcf{Delta}/{Delta}) within the Hdac9 protein-coding sequence in mice led to decreased Twist1 expression and altered anterior\posterior limb expression patterns of Shh pathway genes. This decreased Twist1 expression results in a smaller sized and asymmetric skull and polydactyly that resembles Twist1+/- mouse phenotype. Chromatin conformation analysis revealed that the Twist1 promoter region interacts with Hdac9 sequences that encompass Twist1 enhancers and a Ctcf site and that interactions depended on the presence of both regulatory regions. Finally, a large inversion of the entire Hdac9 sequence (Hdac9INV/+) in mice that does not disrupt Hdac9 expression but repositions Twist1 regulatory elements showed decreased Twist1 expression and led to a craniosynostosis-like phenotype and polydactyly. Thus, our study elucidated essential components of TWIST1 transcriptional machinery that reside within the HDAC9 sequence, suggesting that SVs, encompassing protein-coding sequence, such as HDAC9, could lead to a phenotype that is not attributed to its protein function but rather to a disruption of the transcriptional regulation of a nearby gene, such as TWIST1.

genomics↗