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Orbital exenteration in the management of orbital and periorbital tumours: Factors related to treatment outcomes

Journal of Plastic, Reconstructive and Aesthetic Surgery 2025年 105卷 260-269页

作者： Niinimäki, Paula Määttänen, Maria Vuola, Jyrki Kivelä, Tero T. Mäkitie, Antti A. Uusitalo, Marita Department of Ophthalmology University of Helsinki and Helsinki University Hospital Helsinki Finland University of Helsinki Finland Department of Plastic Surgery Helsinki University Hospital and University of Helsinki Finland Department of Otorhinolaryngology – Head and Neck Surgery Helsinki University Hospital and University of Helsinki Helsinki Finland Research Program in Systems Oncology Faculty of Medicine University of Helsinki Helsinki Finland

The aim of this study was to evaluate the indications for surgery, patient and healthcare delays, ophthalmic status, challenges of management, complications, disease-free survival (DFS), and overall survival (OS) of patients treated by orbital exenteration at a tertiary care centre. Patients who underwent orbital exenteration during an 18-year period (2005–2022) were identified from the Helsinki University Hospital (Helsinki, Finland). Demographic and medical data were retrieved. Sixty-nine patients were included. Median age was 74 years (range, 7–93 years). The most common operative indication for exenteration was a malignant tumour (99%). Histopathological types that were most frequently encountered were uveal melanoma in 10 (14%), basal cell carcinoma in 9, (13%) and cutaneous squamous cell carcinoma in 8 (12%) patients. Orbital exenteration could have been avoided in 32 (46%) patients if the primary surgery had been performed with sufficient margins and without delay. The median follow-up time was 16 months (range, 0–169 months). At the end of follow-up, 34 (49%) patients had no evidence of disease, 12 (17%) were alive with disease and 23 (33%) had died of the disease. Kaplan–Meier analysis revealed 1- and 2-year DFS of 74% and 67%, respectively. One- and 2-year OS were 77% and 69%, respectively. Selected periorbital malignancies, especially those with insufficient primary treatment or with treatment delay, may warrant exenteration. Given the diverse origins of malignancies, a multidisciplinary approach, including ophthalmological consultation, appears to be the optimal strategy for these patients. © 2025 The Authors

关键词： Conjunctival tumour Malignancy Multidisciplinary tumour board Orbital surgery Survival Uveal melanoma

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Invitation and welcome to the 2025 ISTH Congress

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Journal of Thrombosis and Haemostasis 2025年第5期23卷 1461-1463页

作者： Young, Guy Lassila, Riitta Wolberg, Alisa S. Department of Pediatric Hematology Children's Hospital Los Angeles University of Southern California Keck School of Medicine Los Angeles United States HUS Helsinki University Hospital Coagulation Disorders Unit Department of Hematology Comprehensive Cancer Center and University of Helsinki Research Program Unit in Systems Oncology Helsinki Finland Department of Pathology and Laboratory Medicine and University of North Carolina Blood Research Center University of North Carolina at Chapel Hill Chapel Hill United States

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Novel Genetic Risk Variants Associated with Oral Tongue Squamous Cell Carcinoma

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Head and Neck Pathology 2025年第1期19卷 45-45页

作者： Nikkilä, Rayan Mäkitie, Antti Joensuu, Heikki Markkanen, Saara Elenius, Klaus Monni, Outi Palotie, Aarno Saarentaus, Elmo Salo, Tuula Bizaki-Vallaskangas, Argyro Department of Otorhinolaryngology - Head and Neck Surgery University of Helsinki and HUS Helsinki University Hospital Helsinki Finland Finnish Cancer Registry Institute for Statistical and Epidemiological Cancer and Research Helsinki Finland Research Program in Systems Oncology Faculty of Medicine University of Helsinki Helsinki Finland Department of Oncology HUS Helsinki University Hospital and University of Helsinki Helsinki Finland Department of Otolaryngology Faculty of Medicine and Health Technology Tampere University Tampere Finland The Wellbeing Services County of Pirkanmaa Tampere Finland Institute of Biomedicine and MediCity Research Laboratory University of Turku Turku Finland Turku Bioscience Centre University of Turku and Åbo Akademi University Turku Finland Department of Oncology Turku University Hospital Turku Finland iCAN Digital Precision Cancer Medicine Flagship University of Helsinki Helsinki Finland Applied Tumor Genomics Research Program Faculty of Medicine University of Helsinki Helsinki Finland Institute for Molecular Medicine Finland and the Helsinki Institute of Life Science University of Helsinki Helsinki Finland The Stanley Center for Psychiatric Research and Program in Medical and Population Genetics The Broad Institute of MIT and Harvard Cambridge MA United States Analytic and Translational Genetics Unit Department of Medicine Department of Neurology and Department of Psychiatry Massachusetts General Hospital Boston MA United States Department of Oral and Maxillofacial Diseases University of Helsinki Helsinki Finland Translational Immunology Research Program Faculty of Medicine University of Helsinki Helsinki Finland Department of Pathology HUS Helsinki University Hospital Helsinki Finland Research Unit of Population Health Faculty of Medicine University of Oulu Oulu Finland Medical Research Center Oulu University Hospital Oulu Finland

Purpose: Limited data from genome-wide association studies (GWAS) focusing on oral tongue squamous cell carcinoma (OTSCC) are available. The present study was conducted to explore genetic associations for OTSCC. Methods: A GWAS on 376 cases of OTSCC was conducted using the FinnGen Data Freeze-12 dataset. The case-cohort included 205 males and 171 females. Cases with malignancies involving the base of the tongue or lingual tonsil were excluded from the case-cohort. Individuals with no recorded history of malignancy were used as controls (n = 407,067). A Phenome-wide association study (PheWAS) was performed for the lead variants to assess their co-associations with other cancers. Results: GWAS analysis identified three genome-wide significant loci associated with OTSCC (p < 5 × 10–8), located at 5p15.33 (rs27067 near gene LINC01511), 10q24 (rs1007771191 near RPS3AP36), and 20p12.3 (rs1438070080 near PLCB1), respectively. PheWAS showed associations of rs27067 mainly with prostate cancer (OR = 1.06, p = 5.41 × 10^–7), and seborrheic keratosis (OR = 1.11, p = 1.51 × 10^–11). A co-directional effect with melanoma was also observed (OR = 0.93, p = 6.24 × 10^–5). Conclusion: The GWAS detected two novel genetic associations with OTSCC. Further research is needed to identify the genes at these loci that contribute to the molecular pathogenesis of OTSCC. © The Author(s) 2025.

关键词： FinnGen Genetic variant Genome-wide association Single nucleotide polymorphism Tongue cancer

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SynergyFinder Plus:Toward Better Interpretation and Annotation of Drug Combination Screening Datasets

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Genomics, Proteomics & Bioinformatics 2022年第3期20卷 587-596页

作者： Shuyu Zheng Wenyu Wang Jehad Aldahdooh Alina Malyutina Tolou Shadbahr Ziaurrehman Tanoli Alberto Pessia Jing Tang Research Program in Systems Oncology Faculty of MedicineUniversity of HelsinkiHelsinki 00290Finland

Combinatorial therapies have been recently proposed to improve the efficacy of anticancer treatment. The Synergy Finder R package is a software used to analyze pre-clinical drug combination datasets. Here, we report the major updates to the Synergy Finder R package for improved interpretation and annotation of drug combination screening results. Unlike the existing implementations, the updated Synergy Finder R package includes five main innovations. 1) We extend the mathematical models to higher-order drug combination data analysis and implement dimension reduction techniques for visualizing the synergy landscape. 2) We provide a statistical analysis of drug combination synergy and sensitivity with confidence intervals and P values. 3)We incorporate a synergy barometer to harmonize multiple synergy scoring methods to provide a consensus metric for synergy. 4) We evaluate drug combination synergy and sensitivity to provide an unbiased interpretation of the clinical potential. 5) We enable fast annotation of drugs and cell lines, including their chemical and target information. These annotations will improve the interpretation of the mechanisms of action of drug combinations. To facilitate the use of the R package within the drug discovery community, we also provide a web server at www.s *** as a user-friendly interface to enable a more fexible and versatile analysis of drug combination data.

关键词： SynergyFinder Drug combination Synergy modeling Drug discovery Drug combination sensitivity analysis

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Antiplatelet-anticoagulant, APAC, a mimic of endogenous heparin, is an antithrombotic with von Willebrand factor-mediated characteristics

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Thrombosis research 2025年 250卷 109318-109318页

作者： Jouppila, Annukka Nevola, Ilja Lemponen, Marja Mattila, Tomi Lassila, Riitta Clinical Research institute HUCH Helsinki Finland Research Program Unit in Systems Oncology Medical Faculty University of Helsinki Helsinki Finland HUS Diagnostic Center Department of Clinical Chemistry and Hematology University of Helsinki and Helsinki University Hospital Helsinki Finland Coagulation Disorders Unit Departments of Hematology and Clinical Chemistry (HUSLAB Laboratory Services) Comprehensive Cancer Center Helsinki University Hospital Helsinki Finland Aplagon Ltd. Helsinki Finland

Background: We have conjugated selected number of unfractionated heparin (UFH) chains to human albumin core to mimic mast-cell heparin proteoglycans (HEP-PG). Indeed, APAC, dual antiplatelet and anticoagulant, as HEP-PG, has inhibited collagen- (CIPA) and thrombin-induced platelet aggregation, being simultaneously an anticoagulant. In several animal models of arterial thrombosis, APAC has provided vascular-injury-associated local antithrombotic properties mediated by von Willebrand factor (VWF). Aims: We compared the structure-function effects of APAC with those of UFH in vitro, and when supplemented in blood studied platelet and VWF-dependency and anticoagulation. Methods: We assessed the total thrombosis formation analysis system (T-TAS) and coagulation (rotational thromboelastometry, ROTEM) in blood, and thrombin generation and aggregation in platelet-rich plasma. We studied aggregation responses of APAC to collagen, ristocetin, ADP, and potential synergism with cangrelor, P2Y12 receptor antagonist. Finally, heparin-neutralizing role of platelet factor 4 (PF4) on antiplatelet and anticoagulant functions of APAC was investigated. Results: APAC concentration-dependently exceeded the anticoagulant and antithrombotic action of UFH in ROTEM, and platelet thrombus formation under arterial blood flow over collagen/tissue factor. APAC uniquely inhibited CIPA. While ADP- and ristocetin-induced aggregation were unaffected by APAC, we detected synergism with cangrelor for CIPA. Disruption of the tertiary structure of APAC reverted its mode of action to anticoagulation only, alike UFH. PF4 neutralized antithrombotic actions of APAC. Conclusion: The structure-function of APAC conveys dual and unique antiplatelet and anticoagulant actions in flowing blood over collagen and beyond. Our studies confirmed the inhibitory role of APAC on VWF functions and fibrin formation. © 2025 The Authors

关键词： Antithrombotic APAC Platelet Unfractionated heparin von Willebrand factor

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Methylation-based biological age and cardiotoxicity risk in breast cancer patients treated with trastuzumab

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Cardio-oncology (London, England) 2025年第1期11卷 44页

作者： Jamila Mammadova Alicia Richards Adriana Gonzalez-Torriente Evan R Adler Rachel J Cruz Stefanie Palfi Dae Hyun Lee Christine Sam Mohammed Al-Jumayli Anders Berglund Jong Y Park Mohammed Alomar Jacob K Kresovich Department of Internal Medicine Vanderbilt University Medical Center Nashville TN USA. Department of Cancer Epidemiology H. Lee Moffitt Cancer Center and Research Institute Tampa FL USA. Department of Pediatrics University of Miami/Jackson Health Systems Miami FL USA. Department of Internal Medicine University of Virginia Charlottesville VA USA. Division of Cardiovascular Sciences Morsani College of Medicine University of South Florida Tampa USA. Department of Cardio-Oncology H. Lee Moffitt Cancer Center and Research Institute Tampa FL USA. Department of Individualized Cancer Management/Senior Adult Oncology Program H. Lee Moffitt Cancer Center and Research Institute Tampa FL USA. Department of Oncological Sciences Morsani College of Medicine University of South Florida Tampa FL USA. Department of Quantitative Health Sciences Division of Computational Biology Mayo Clinic Jacksonville FL USA. Department of Cancer Epidemiology H. Lee Moffitt Cancer Center and Research Institute Tampa FL USA. jacob.kresovich@***. Department of Breast Oncology H. Lee Moffitt Cancer Center and Research Institute Tampa FL USA. jacob.kresovich@***.

BACKGROUND:Trastuzumab is an effective treatment for HER2-positive cancers that has known cardiotoxic properties. Discovering biomarkers that assess cardiotoxicity risk before trastuzumab therapy is essential for protecting the cardiovascular health of cancer patients. OBJECTIVE:To examine the associations between pre-treatment epigenetic age acceleration, circulating leukocyte composition, and candidate single nucleotide polymorphisms (SNPs) with cardiotoxicity risk in breast cancer patients receiving trastuzumab. METHODS:Among a retrospective cohort of HER2-positive breast cancer patients treated with trastuzumab at Moffitt Cancer Center, we profiled blood DNA methylation and genetic profiles. Epigenetic clocks and circulating leukocyte subsets were derived from MethylationEPIC BeadChip data, and candidate SNPs were measured using the Global Screening Array. Cardiotoxicity events (i.e., reductions in left ventricular ejection fraction, symptomatic heart failure), were identified in medical records. Logistic regression models, adjusted for traditional risk factors, estimated odds ratios (ORs) for biomarker associations with cardiotoxicity risk. RESULTS:Among 157 patients selected for this study, 39 (25%) experienced cardiotoxicities within one year of treatment initiation. rs776746 was inversely associated with cardiotoxicity risk (OR: 0.38, 95% CI: 0.14, 1.00, P = 0.05). After adjusting for traditional risk factors and leukocyte composition, the Hannum AgeAccel, Horvath AgeAccel, and Horvath Skin and Blood AgeAccel metrics were significantly positively associated with cardiotoxicity risk (ORs ranging between 1.62 and 1.89). Adding Horvath Skin and Blood AgeAccel to traditional cardiotoxicity risk factors significantly improved cardiotoxicity risk prediction (AUC: 0.75 vs. 0.79; P-diff = 0.04). CONCLUSIONS:Pre-treatment epigenetic age acceleration appears to be a novel biomarker for cardiotoxicity risk that improves cardiotoxicity risk prediction.

关键词： Biological age Breast cancer Cardiotoxicity Epigenetic clocks Trastuzumab

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Deconstructing the ISTH hemophilia guidelines for the clinician

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Journal of Thrombosis and Haemostasis 2025年第5期23卷 1483-1495页

作者： Guy Young Riitta Lassila Jane Mason Saskia Prasca Cancer and Blood Disorders Institute Children’s Hospital Los Angeles University of Southern California Keck School of Medicine Los Angeles California USA HUS Helsinki University Hospital Coagulation Disorders Unit Dept Hematology Comprehensive Cancer Center Helsinki Finland University of Helsinki Research Program Unit in Systems Oncology Helsinki Finland Queensland Haemophilia Centre Cancer Care Services Royal Brisbane and Women’s Hospital Brisbane Australia University of Queensland School of Medicine and Department of Haematology and Haemophilia QLD Children’s Hospital Brisbane Australia Medicarte IPS National Comprehensive Hemophilia Treatment Center Medellin Colombia

Recently, the International Society on Thrombosis and Haemostasis (ISTH) Hemophilia Guidelines were published in this journal. The authors of these guidelines should be commended for a herculean task that took years to complete, and while this is no doubt a welcome addition to the literature, it does leave many questions for the clinician. This is primarily because 11 of the 13 recommendations are conditional, essentially meaning “that clinicians and patients need to consider individual preferences as well as the specific circumstances in which the decision is being made for implementation of the recommendation.” So, in essence, most of the recommendations allow the clinician to decide whether to use them or not. In our view, most clinicians are seeking more concrete recommendations when they search for a guidelines paper. Unfortunately, numerous conditional recommendations have been developed because hemophilia is a rare disease and the ISTH Guidelines rely upon the Grading of Recommendations, Assessment, Development, and Evaluation methodology. We endeavored to “deconstruct” the ISTH recommendations and offer clinicians a more concrete path forward based in part on the guidelines but supplemented with more recent literature and our own extensive experience and perspective managing hemophilia patients of all ages from 4 continents.

关键词： emicizumab guidelines hemophilia therapy

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Reply to Letter to the Editor: "Deconstructing the ISTH Hemophilia Guidelines for the Clinician": comment from Mancuso-ME et al

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Journal of thrombosis and haemostasis : JTH 2025年第5期23卷 1737-1738页

作者： Guy Young Riitta Lassila Jane Mason Saskia Prasca Children's Hospital Los Angeles University of Southern California Keck School of Medicine Los Angeles California USA. Electronic address: gyoung@chla.usc.edu. HUS Helsinki University Hospital Coagulation Disorders Unit Department of Hematology Comprehensive Cancer Center and University of Helsinki Research Program Unit in Systems Oncology Helsinki Finland. Queensland Haemophilia Centre Cancer Care Services Royal Brisbane and Women's Hospital the University of Queensland School of Medicine and Department of Haematology and Haemophilia QLD Children's Hospital Brisbane Australia. Medicarte IPS National Comprehensive Hemophilia Treatment Center Medellin Colombia.

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Identification and external validation of tumor DNA methylation panel for the recurrence risk stratification of stage II colon cancer

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Translational oncology 2025年 57卷 102405-102405页

作者： Yuan, Tanwei Edelmann, Dominic Moreno, Víctor Georgii, Elisabeth de Andrade e Sousa, Lisa Barros Pelin, Helena Jiang, Xiaofeng Kather, Jakob Nikolas Tagscherer, Katrin E. Roth, Wilfried Bewerunge-Hudler, Melanie Brobeil, Alexander Kloor, Matthias Bläker, Hendrik Brenner, Hermann Hoffmeister, Michael Division of Clinical Epidemiology and Aging Research German Cancer Research Center (DKFZ) Heidelberg Germany Medical Faculty Heidelberg Heidelberg University Heidelberg Germany Division of Biostatistics German Cancer Research Center (DKFZ) Heidelberg Germany Oncology Data Analytics Program Catalan Institute of Oncology (ICO). Hospitalet de Llobregat Barcelona Spain Colorectal Cancer Group ONCOBELL Bellvitge Biomedical Research Institute (IDIBELL). Hospitalet de Llobregat Barcelona Spain Biomedical Research Centre Network for Epidemiology and Public Health (CIBERESP) Madrid Spain Department of Clinical Sciences Faculty of Medicine and health Sciences and Universitat de Barcelona Institute of Complex Systems (UBICS) University of Barcelona Barcelona Spain Helmholtz AI Helmholtz Munich Munich Germany Else Kroener Fresenius Center for Digital Health Technical University Dresden Dresden Germany Institute of Pathology University Medical Center Mainz Mainz Germany Institute of Pathology Heidelberg University Hospital Heidelberg Germany Microarray Core Facility German Cancer Research Center (DKFZ) Heidelberg Germany Institute of Pathology University of Leipzig Medical Center Leipzig Germany German Cancer Consortium (DKTK) German Cancer Research Center (DKFZ) Heidelberg Germany

Background: Tailoring surveillance and treatment strategies for stage II colon cancer (CC) after curative surgery remains challenging, and personalized approaches are lacking. We aimed to identify a gene methylation panel capable of stratifying high-risk stage II CC patients for recurrence beyond traditional clinical variables. Methods: Genome-wide tumor tissue DNA methylation data were analyzed from 562 stage II CC patients who underwent surgery in Germany (DACHS study). The cohort was divided into a training set (N = 395) and an internal validation set (N = 131), with external validation performed on 97 stage II CC patients from Spain. DNA methylation markers were primarily selected using the Elastic Net Cox model. The resulting prognostic index (PI), a combination of clinical factors and selected methylation markers, was compared to baseline models using clinical variables or microsatellite instability (MSI), with discrimination and prediction accuracy assessed through time-dependent receiver operating characteristic curves (AUC) and Brier scores. Results: The final PI incorporated age, sex, tumor stage, location, and 27 DNA methylation markers. The PI consistently outperformed the baseline model including age, sex, and tumor stage in time-dependent AUC across validation cohorts (e.g., 1-year AUC and 95 % confidence interval: internal validation set, PI: 0.66, baseline model: 0.52;external validation set, PI: 0.72, baseline model: 0.64). In internal validation, the PI also showed a consistently improved time-dependent AUC compared with a combination of MSI and tumor stage only. Nevertheless, the PI did not improve the prediction accuracy of CC recurrence compared to the baseline model. Conclusions: This study identified 27 tumor tissue DNA methylation biomarkers that improved the discriminative power in classifying recurrence risk among stage II colon cancer patients. While this methylation panel alone lacks sufficient prediction accuracy for clinical application

关键词： Colon cancer DNA methylation panel Prognostic index Recurrence risk

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The Genomic Landscape of Wilms' Tumor 1 (WT1) Mutant Acute Myeloid Leukemia

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BLOOD 2020年第Sup1期136卷 28-28页

作者： Awada, Hassan Durmaz, Arda Gurnari, Carmelo Zawit, Misam Kongkiatkamon, Sunisa Pagliuca, Simona Kerr, Cassandra M. Carraway, Hetty E. Nazha, Aziz Sekeres, Mikkael A. Maciejewski, Jaroslaw P. Visconte, Valeria Department of Translational Hematology and Oncology Research Taussig Cancer Institute Cleveland Clinic Foundation Cleveland OH Department of Systems biology and Bioinformatics CWRU cleveland Department of Translational Hematology and Oncology Taussig Cancer Institute Cleveland OH Department of Translational Hematology and Oncology Research Taussig Cancer Institute Cleveland Clinic Cleveland OH Department of Hematology and Medical Oncology Leukemia Program Taussig Cancer Institute Cleveland Clinic Foundation Cleveland OH Leukemia Program Department of Hematology and Medical Oncology Taussig Cancer Institute Cleveland Clinic Cleveland OH Leukemia Program Department of Hematology and Medical Oncology Cleveland Clinic Taussig Cancer Institute Cleveland OH

Mutations in tumor suppressor genes and oncogenes are both potentially therapeutically actionable in acute myeloid leukemia (AML). The Wilms' Tumor 1 (WT1 ) gene is located on 11p13 and encodes a zinc finger transcription factor which has been found to be overexpressed and mutated in AML. In normal development, WT1 is only expressed in a small subset of hematopoietic stem cells. While its overexpression suggests an oncogenic role, the invariable presence of mutations in the cysteine-histidine zinc finger domains indicates a tumor suppressor function, similar to that in WAGR syndrome/11p deletion syndrome in which it was first discovered. Like its unknown function in AML, the clinical significance and genetic associations of WT1 mutations have been also controversial. Although studies of WT1 mutations in AML have been conducted, the lack of solid clinical and molecular characterization of large WT1 -mutant (WT1 MT ) AML cohort has hampered its definition. In this study, we took advantage of a compendia of genomic results from Cleveland Clinic and publicly available data of 2188 AML patients (primary (p)AML, n= 1636; secondary (s)AML, n= 433; therapy-related (t)AML, n= 119, excluding cases with acute promyelocytic leukemia, MLL- rearrangement, and core-binding factor AML). While several reports only focused on cytogenetic normal AML (CN-AML), which represented 61% of our cohort, we additionally included all other cytogenetic risk groups. In total, WT1 mutations were detected in 5% (114/2188) of patients. WT1 mutations were enriched in pAML (85%) compared to sAML (11%) and tAML (4%). Thirty-nine patients (13%) carried more than 1 WT1 mutation. WT1 MT were younger [59 vs 64 years, P =0.0002] and more often females (55% vs 45%, P =0.03) as compared to WT1 wild type (WT1 WT ) patients. Univariate analyses of baseline parameters showed that WT1 MT AML had a more proliferative phenotype with a higher WBC [15.1 vs 9.5 x109 /L, P =0.03] and bone marrow blast percentages [73 v

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