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Pasanen, A.

Publications and source records attributed to Pasanen, A..

4 recordsLinked to original sources

Explainable Machine Learning for Preoperative Relapse Prediction in Molecularly Stratified Endometrial Cancer: A Single-Center Finnish Cohort Study

Relapse risk in endometrial carcinoma (EC) is strongly influenced by molecular subtype, yet current WHO/ESGO classifications rely on postoperative data, limiting their utility for preoperative decision-making. We developed and compared interpretable machine learning (ML) models to predict relapse timing (none, [≤]6 months, >6 months) using exclusively preoperative multimodal data. In a retrospective cohort of 784 EC patients, we integrated clinicopathological, molecular, immunohistochemical, and systemic biomarkers and constructed four feature strategies: (1) Traditional (clinicopathology), (2) ESGO (guideline risk groups), (3) TP53 + MMRd (high-risk biology), and (4) POLE (low-risk biology). Classifiers (Random Forest (RF), Support Vector Machine (SVM), k-Nearest Neighbors (KNN), Gradient Boosting (GBM)) were trained with leakage-safe preprocessing and in-fold resampling; performance was evaluated via area under the curve (AUC), accuracy, recall, and F1 score, and interpretability via SHapley Additive exPlanations (SHAP). The RF-based Traditional model achieved the highest overall performance (F1 = 0.895, AUC = 0.84), while the GBM-based POLE model showed superior sensitivity (F1 = 0.886, AUC = 0.842). SHAP identified ARID1A loss, elevated CA125, thrombocytosis, and p16 expression among key predictors of relapse; while overlapping high-risk features across models included advanced stage, deeper myometrial invasion, elevated CA125, and positive cytology. These biologically coherent, explainable predictions support individualized risk stratification and may enhance preoperative decision-making, particularly for aggressive histology and high-risk molecular subtypes. Graphical abstract O_FIG O_LINKSMALLFIG WIDTH=184 HEIGHT=200 SRC="FIGDIR/small/686680v1_ufig1.gif" ALT="Figure 1"> View larger version (51K): org.highwire.dtl.DTLVardef@1be31cforg.highwire.dtl.DTLVardef@1b8496dorg.highwire.dtl.DTLVardef@1dca04corg.highwire.dtl.DTLVardef@19fe6bd_HPS_FORMAT_FIGEXP M_FIG C_FIG Workflow for Machine Learning (ML)-based relapse prediction in endometrial cancer. The schematic figure outlines the study pipeline from patient inclusion to clinical application. (A) A retrospective cohort of 784 EC patients was analyzed, integrating clinical, demographic, biomarker, and molecular data into a multimodal feature set. Patients were stratified into four molecular subgroups: NSMP, p53abn, MMRd, and POLEmut. Multiple ML algorithms (Random Forest, SVM, XGBoost, k-NN) were trained to predict relapse timing. (B) Model performance was evaluated using area under the curve (AUC) and accuracy metrics, with SHapley Additive exPlanations (SHAP) analysis applied to identify key predictive features across models. (C) SHAP-based interpretation was used to support individualized relapse risk stratification, enabling potential clinical decision-making for surveillance and therapy. HighlightsO_LIPre-operative XAI models predict relapse timing in EC with an AUC of up to 0.842. C_LIO_LIThe traditional model achieves a top accuracy of 0.797 using 22 features, while POLE maximizes sensitivity at 0.886. C_LIO_LISHAP explanations identify class-specific drivers such as stage, LVSI, size, cytology, CA125, and PR. C_LIO_LIEarly Relapse is associated with burden and aggressiveness, while Late Relapse relates to the spread and size of EC, while No Relapse indicates an inverse profile. C_LIO_LITransparent outputs facilitate risk-aligned surveillance and treatment planning before surgery. C_LI

cancer biology↗

Interpretable prognostic modeling of endometrial cancer

Endometrial carcinoma (EC) is one of the most common gynecological cancers in the world. In this work we apply Cox proportional hazards (CPH) and optimal survival tree (OST) algorithms to the retrospective prognostic modeling of disease-specific survival in 842 EC patients. We demonstrate that the linear CPH models are preferred for the EC risk assessment based on clinical features alone, while the interpretable, non-linear OST models are favored when patient profiles are enriched with tumor molecular data. By studying the OST decision path structure, we show how explainable tree models recapitulate existing clinical knowledge prioritizing L1 cell-adhesion molecule and estrogen receptor status indicators as key risk factors in the p53 abnormal EC subgroup. We believe that visually interpretable tree algorithms are a promising method to explore feature interactions and generate novel research hypotheses. To aid further clinical adoption of advanced machine learning techniques, we stress the importance of quantifying model discrimination and calibration performance in the development of explainable clinical prediction models.

bioinformatics↗

ctDNAtools: An R package to work with sequencing data of circulating tumor DNA

SummarySequencing of cell-free DNA (cfDNA) including circulating tumor DNA (ctDNA) in minimally-invasive liquid biopsies is rapidly maturing towards clinical utility for cancer diagnostics. However, the publicly available bioinformatics tools for the specialized analysis of ctDNA sequencing data are still scarce. Here, we present the ctDNAtools R package, which provides functionalities for testing minimal residual disease (MRD) and analyzing cfDNA fragmentation. MRD detection in ctDNAtools utilizes a Monte Carlo sampling approach to test ctDNA positivity through tracking a set of pre-detected reporter mutations in follow-up samples. Additionally, ctDNAtools includes various functionalities to study cfDNA fragment size histograms, profiles and fragment ends patterns. AvailabilityThe ctDNAtools package is freely available under MIT license at https://github.com/alkodsi/ctDNAtools.

bioinformatics↗

ESR1, WT1, WNT4, ATM and TERT loci are major contributors to uterine leiomyoma predisposition

Uterine leiomyomas (ULs) are benign tumors that are a major burden to womens health. A genome-wide association study on 5,417 UL cases and 331,791 controls was performed, followed by replication of the genomic risk in two cohorts. Effects of the identified risk alleles were evaluated in view of molecular and clinical features.\n\nFive loci displayed a genome-wide significant association; the previously reported TNRC6B, and four novel loci ESR1 (ER), WT1, WNT4, and ATM. The sixth hit TERT is also a conceivable target. The combined polygenic risk contributed by these loci was associated with MED12 mutation-positive tumors. The findings link genes for uterine development and genetic stability to leiomyomagenesis. While the fundamental role of sex hormones in UL aetiology has been clear, this work reveals a connection to estrogen receptor alpha on genetic level and suggests that determinants of UL growth associated with estrogen exposure have an inherited component.

genomics↗