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Zanfagnin, V.

Publications and source records attributed to Zanfagnin, V..

2 recordsLinked to original sources

Weak supervision of H&E slides reveals systems-level biology and functional states that govern therapeutic resistance

Precision oncology lacks scalable methods to identify the mechanisms that mediate therapeutic resistance for individual patients. Resistance often arises from focal cellular niches that are obscured by bulk profiling and costly to resolve with multi-omics. Here, we show that deep learning (DL), applied to routine histology, can localize focal tissue regions enriched for therapeutically relevant biology. Using 3111 breast cancer H&E slides with matched bulk transcriptomics, we trained weakly-supervised DL models to infer activities of immune, metabolic, and tumor-intrinsic phenotypes implicated in therapeutic resistance (AUROC>0.80; PCC>0.64). Accurate inference of these phenotypes should identify tissue regions enriched for the corresponding biological signal. Therefore, we validated phenotype inference and spatial localization with complementary analyses. Tissue-matched multiplexed immunofluorescence showed concordance between inferred immune states and corresponding cell fractions (p=0.006-0.106). Across multi-institutional cohorts, model-derived phenotypes recovered expected relationships with therapeutic outcomes (p<0.045). Finally, in a blinded evaluation, pathologists confirmed that model-derived high-attention regions were enriched for phenotype-specific morphology (p<2.408*10-5). Because evaluated phenotypes represent diverse mechanisms of resistance across therapeutic modalities, these findings provide a foundation for resistance-directed localization using therapeutic outcomes as supervision. By directing deep profiling toward model-prioritized regions, this framework could enable scalable nomination of candidate mediators of resistance for subsequent functional validation across real-world patient populations. One sentence summaryWeakly supervised deep learning localizes focal tissue regions enriched for therapeutically relevant biology in routine histology, thus offering a scalable strategy to study therapeutic resistance across large patient populations.

biophysics↗

YAP and collagen remodelling support cell proliferation and tumour aggressiveness in uterine leiomyosarcoma

Fibrillar collagen deposition, stiffness, and downstream signalling support the development of leiomyomas (LM), common benign mesenchymal tumours of the uterus, and are associated with aggressiveness in multiple carcinomas. Compared to epithelial carcinomas, however, the impact of fibrillar collagens on malignant mesenchymal tumours, including uterine leiomyosarcoma (LMS), remains elusive. In this study, we analyse the network morphology and density of fibrillar collagens combined with the gene expression of LMS, LM and normal myometrium (MM). We find that, in contrast to LM, LMS tumours present low collagen density and increased expression of collagen-remodelling genes, features associated with tumour aggressiveness. Using collagen-based 3D matrices, we show that the activity of MMP14, a central protein with collagen-remodelling functions particularly overexpressed in LMS, is necessary for LMS cell proliferation. In addition, we find that, unlike MM and LM cells, LMS proliferation and migration are not affected by collagen substrate stiffness. We demonstrate that LMS cell growth in low matrix adhesion microenvironments is supported by an enhanced basal YAP activity. Altogether, our results indicate that LMS cells acquire high collagen remodelling capabilities and are adapted to grow and migrate in low collagen and soft microenvironments. These results further suggest that matrix remodelling and YAP are potential therapeutic targets for this deadly disease.

cancer biology↗