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Francesca Khani

Publications and source records attributed to Francesca Khani.

2 recordsLinked to original sources

Improving PI-RADS Prediction and Prostate Cancer Detection from Multiparametric MRI with Anatomical Guidance

Accurate prediction of Prostate Imaging Reporting and Data System (PI-RADS) scores from multiparametric MRI (mpMRI) remains challenging, more so than clinically significant prostate cancer (csPCa) detection. Given the importance of lesion location in PI-RADS scoring, we evaluated whether incorporating prostate zonal masks improves PI-RADS prediction and csPCa detection across multiple architectures (3D ResNet-18, ResNet-50, and ViT) using a large-scale internal dataset. Anatomical guidance generally improved performance across architectures, with the best results achieved by ResNet-18 with 2-zone guidance for PI-RADS prediction (QWK = 0.511) and ResNet-50 with 5-zone guidance for csPCa detection (AUC = 0.809). Fine-tuned results on external datasets further demonstrated the benefits of anatomical guidance. Furthermore, models with anatomical guidance improved the utility of model-predicted PI-RADS scores for PI-RADS-based csPCa detection (positive defined as PI-RADS>=3). Combining model-predicted and expert-assigned PI-RADS scores significantly increased the AUC from 0.711 to 0.756 (p < 0.05), suggesting that AI-derived PI-RADS scores may provide complementary information to expert assessment for csPCa detection. Overall, our findings highlight the value of incorporating prostate zonal anatomy into deep learning-based prostate MRI assessment.

cs.CV↗

Causes of evolutionary divergence in prostate cancer

Cancer progression involves the sequential accumulation of genetic alterations that cumulatively shape the tumour phenotype. In prostate cancer, tumours can follow divergent evolutionary trajectories that lead to distinct subtypes, but the causes of this divergence remain unclear. While causal inference could elucidate the factors involved, conventional methods are unsuitable due to the possibility of unobserved confounders and ambiguity in the direction of causality. Here, we propose a method that circumvents these issues and apply it to genomic data from 829 prostate cancer patients. We identify several genetic alterations that drive divergence as well as others that prevent this transition, locking tumours into one trajectory. Further analysis reveals that these genetic alterations may cause each other, implying a positive-feedback loop that accelerates divergence. Our findings provide insights into how cancer subtypes emerge and offer a foundation for genomic surveillance strategies aimed at monitoring the progression of prostate cancer.

q-bio.GN↗