Cancer registration in North Rhine-Westphalia began in 1974 and celebrated its 50th anniversary in 2024. The aim of this paper is to describe the development phases of cancer registration in North Rhine-Westphalia between 1974 and 2025.Following an international symposium in Düsseldorf in 1973 and with the support of the Society for the Fight Against Cancer (later: Cancer Society of North Rhine-Westphalia), a cancer registry was established in 1974 under the leadership of Prof. Ekkehard Grundmann, initially focusing on oncological aftercare in Münster. Pathologists who had no contact with patients were not able to report to the registry. Federal political debates between 1978 and 1981 promoted the establishment of cancer centers and cancer registries. The Cancer Registry Act of North Rhine-Westphalia of 1985 created the legal basis for epidemiological cancer registration in the administrative district of Münster. Pathologists were still unable to report to the registry. It was not until the establishment of an electronic procedure for transmitting pathology reports using control numbers in the early 2000s that pathologists were able to report directly to the registry. Only then was it possible to achieve the required completeness of registration of 95%.In 2005, an amendment to the law led to the comprehensive expansion of cancer registration in North Rhine-Westphalia. Since then, reports could only be submitted electronically. The Cancer Early Detection and Registration Act (KFRG) of 2013 led to the amendment of the Cancer Registry Act in North Rhine-Westphalia in 2016. Since then, the cancer registry has been an epidemiological and clinical cancer registry. The cancer registry currently covers a population of 18 million people and registers 173,000 new cases of cancer per year (including non-melanotic skin cancer).

Oxidative stress plays a significant regulatory role in tumor immune responses and can influence the efficacy of immunotherapy. Accordingly, therapeutic interventions targeting oxidative stress-related mechanisms, whether alone or in combination with other modalities, represent a compelling strategy to enhance cancer therapy. In this study, we first profiled the landscape of oxidative stress responses within the tumor microenvironment by integrating pan-cancer single-cell RNA sequencing datasets, which revealed that cancer-associated fibroblasts (CAFs) possessed the highest oxidative stress response score. Based on this finding, we developed a fibroblast-derived oxidative stress-related signature (FOSR.Sig) by screening for genes most correlated with oxidative stress responses in CAFs. Furthermore, with a machine learning framework, our model achieved exceptional accuracy in predicting ICI response, and its robustness was subsequently validated. Importantly, a prognostic model incorporating the FOSR.Sig was developed using TCGA pan-cancer datasets and LASSO regression analysis, which provides novel prognostic biomarkers applicable across diverse cancer types. Mechanistic investigation of TFG, the top risk score gene, revealed its critical role in the tumor microenvironment through comprehensive in vitro and in vivo experiments and RNA-seq assays. Our study highlights the therapeutic potential of targeting oxidative stress in cancer-associated fibroblasts as a novel strategy to empower antitumor immunity and prevent immune escape. And provide a promising powerful tool for predicting responses to tumor immunotherapy and patient outcomes.

Ferroptosis is a form of regulated cell death driven by labile iron-dependent lipid peroxidation and is closely integrated with cellular energy metabolism and redox homeostasis. Once viewed primarily as the terminal product of glycolysis, lactate is now recognized as a central metabolic intermediate, signaling molecule, and epigenetic substrate that reshapes intracellular and microenvironmental redox networks and thereby influences cell fate. Emerging evidence suggests that lactate exerts a context-dependent and bidirectional influence on the ferroptosis machinery. This regulation is mediated through four closely interconnected dimensions: lactate flux and concentration gradients, extracellular acidosis within the microenvironment, monocarboxylate transporter (MCT)-dependent transmembrane metabolic exchange, and site-specific histone and non-histone lactylation. This review systematically examines how lactate regulates ferroptosis in a context-dependent manner across different cell types, subcellular compartments, and disease microenvironments. In many tumors and stromal niches, lactate can act as a metabolic barrier that supports immunosuppression and ferroptosis resistance. By contrast, under specific stress conditions, dysregulated lactate flux may promote metabolic imbalance, epigenetic reprogramming, and increased ferroptotic vulnerability. We further summarize recent translational advances targeting the lactate-ferroptosis axis, including compartment-specific pharmacological strategies, emerging nanomedicine-based delivery platforms, and physical approaches for modulating the microenvironment. Although this framework provides a useful basis for therapeutic exploration, most current evidence remains preclinical. Rigorous validation in human tissues, patient-derived models, and early-phase clinical studies will be required before lactate-targeted ferroptosis strategies can be advanced toward precision therapy.

The investigation aimed to determine whether there has been an increase in the amount of stem cells discarded due to patient mortality resulting from COVID-19 infection in our apheresis unit. Records were reviewed to investigate whether there were any differences in stem cell discards before and after the COVID-19 pandemic period following 2015.

In both periods, products retrieved from patients with myeloma and non-Hodgkin lymphoma constituted the majority of discarded stem cells. The process of discarding 230 hematopoietic stem cell products that were discarded after 2015 involved a period of five years prior to the COVID-19 pandemic, during which half of the products were discarded, and the other half were discarded in the last 2.5 years of the pandemic. Over 90% of the discarded products were autologous stem cell products. Additionally, 43 patients had their products discarded due to mortality associated with COVID-19 infection. This number does not include those who passed away at home for unknown reasons or in cases where COVID-19 infection could not be confirmed. The disposal of a single hematopoietic stem cell product, including the cost of the collection bag and DMSO freezing, was approximately 5,000 Turkish Lira during that period. In our country, which has around 50 hematopoietic stem cell transplantation centers, if we assume an average of about 40 stem cell disposals per center, this would result in a total loss of approximately 10 million Turkish Lira (calculated as 5,000 TL x 40 x 50 centers = 10,000,000 TL). This figure does not account for personnel labor costs.

Furthermore, this review suggests that, similar to previous observations, preserving stem cells for second transplants in patients with non-Hodgkin lymphoma and certain elderly myeloma patients may be unnecessary.

Despite the clinical success of cancer immunotherapies, their efficacy is often compromised by antigen-related problems, including downregulation, loss, and off-tumour toxicity.

To overcome these limitations that challenge the current immunotherapies dependent on native antigens, we here describe a new cancer immunotherapy strategy that artificially and specifically expresses a clinically validated antigen on variant tumours and thus repurposes clinical antibody drugs to treat cancers not belonging to their indications. To authenticate the strategy, we delivered a CD20 gene under the control of an NF-κB-specific promoter to tumours by adeno-associated virus and then treated them with a CD20 antibody, rituximab.

We found that CD20 was selectively expressed in tumours, and subsequent rituximab treatment engaged multiple antibody-dependent effector mechanisms, including NK-cell-mediated ADCC and macrophage-mediated ADCP. We demonstrated that this strategy is effective not only in variant-cultivated cancer cells, HCT116 spheroids, and patient-derived organoids of human colorectal cancer, but also in a humanized mouse with an HCT116 xenograft and immunocompetent mouse with an MC38 transplant. The strategy showed high cancer cell specificity in both in vitro and in vivo models, resulting in high therapeutic efficacy.

This strategy thus creates a new modality of cancer immune-redirection therapy by repurposing both the clinically validated antigen and antibody.

TRAP enables tumour-selective ectopic expression of the clinically validated antigen CD20, overcoming antigen limitations in solid tumour immunotherapy. TRAP repurposes anti-CD20 antibodies to engage diverse immune effector mechanisms, including ADCC, ADCP, and CDC. TRAP demonstrates antitumour efficacy across cellular, 3D tumour spheroid, patient-derived organoid, and in vivo solid tumour models.

No abstract available.

Myxopapillary ependymomas are a subset of spinal ependymomas that arise almost exclusively in the conus medullaris and filum terminale, and most commonly affect young adults. However, multifocality has been described, originating in the cervicothoracic spinal cord, the lateral ventricle, the fourth ventricle, and the brain. Spinal myxopapillary ependymomas are associated with a favourable prognosis in children and adults, with 10-year overall survival rates > 90%. Many patients, however, live with persistent disease and require repeated operations and adjuvant therapy, because myxopapillary ependymomas often resist complete removal owing to locally advanced growth and/or cerebrospinal fluid-borne seeding of the thecal sac or more rostral neuraxis.

We present a case of a 27-year-old woman who underwent gross-total resection and adjuvant radiotherapy for an L2-L3 spinal tumour, which was diagnosed histologically as ependymoma, but developed a recurrent tumour of myxopapillary ependymoma after a long-term symptom-free period. The recurrent tumour is larger, multifocal, heterogeneously enhancing and extending from the lumbar into the sacrum, resulting in local effects on the bones. Previously, the diagnosis of ependymoma was based solely on histomorphology, with no molecular confirmation of DNA methylation profiling.

This case highlights the importance of diagnostic accuracy when molecular testing is limited, emphasising the crucial role of clinical and histopathological correlation. Hence, a histo-molecular classification is vital for risk stratification and tailored surveillance.

Recent clinical trials have shown the usefulness of anti-HER2 (Human epidermal growth factor receptor 2) treatment in the newly described "HER2-low" subset of breast carcinoma, offering added treatment option to the once considered non-responders. This study aimed to identify this important new subset's demographic and pathological features in a Malaysian cohort.

All newly and recurrent histopathologically-diagnosed invasive breast carcinomas encountered at the University of Malaya Medical Centre (UMMC) between January 2018 to December 2023 that satisfied inclusion criteria were enrolled. Patient demographics were retrieved from the histopathological requests. All haematoxylin and eosin (H&E) stained, immunohistochemically (IHC) stained HER2, oestrogen receptor (ER) and progesterone receptor (PR) together with HER2 amplification assayed by dual-colour dual-hapten in situ hybridisation (DDISH) sections for all cases were reviewed for histological type, histological grade, pathological stage, hormone receptors (HR encompassing ER and PR) and HER2 status.

710 invasive breast carcinomas were finally included. HER2-low was noted in 48.2% (n = 342) of the carcinomas, while 191 (26.9%) were in the conventional HER2 positive category. HER2-low carcinomas demonstrated significantly lower (Grade 1 and 2) histological grade and were more commonly hormone status positive compared with both HER2 positive and negative groups.

HER2-low constituted a significant number of breast carcinomas and appears to have its own unique features. The recognition of this category has expanded anti-HER2 treatment options to an additional 48% of breast carcinomas.

Esophageal cancer (OC) is currently the eighth most common form of cancer worldwide with a 5-year survival rate of 10%-20%, with the primary risk factor of esophageal adenocarcinoma (OAC) being the development of Barrett's Esophagus (BO). Despite its clinical significance, the molecular pathogenesis underlying both BO and OC is not well understood. In recent years, epigenetic dysregulation, particularly aberrant DNA methylation, has emerged as a critical area of investigation, given its potential utility in the identification of diagnostic, prognostic, and therapeutic biomarkers. This review examines the evolving epigenetic landscape of esophageal cancer, including a focus on its origins in BO with a particular emphasis on DNA methylation, the most extensively researched epigenetic mechanism. Key DNA methylation-associated alterations involved in OAC and OSCC initiation and progression are discussed, alongside their potential clinical application as biomarkers for early detection, prognosis, and risk stratification in BO populations. Furthermore, the role of these epigenetically regulated genes in the disruption of Wnt signaling and cell cycle control pathways implicated in esophageal carcinogenesis is explored. The review concludes by outlining future research directions, current challenges, and the promise of epigenetic studies in advancing our understanding of OC pathogenesis and improving patient outcomes.

The cyclic GMP-AMP synthase (cGAS)-stimulator of interferon genes (STING) signaling pathway, as a key DNA sensor, plays a significant role in the regulation of innate immune responses. This pathway can be activated by sensing abnormal DNA, and is of great significance for resisting the invasion of pathogenic microorganisms and maintaining tissue homeostasis. In addition, the cGAS-STING pathway plays a dual role in cancer, and oncogenic viruses can cause cell carcinogenesis in the body through multiple mechanisms, thereby affecting human health. This manuscript reviews the vital role of cGAS-STING in the immune process, as well as the fact that viruses causing human tumor lesions can activate cGAS-STING, leading to virus inhibition and further preventing the occurrence and development of related cancers, and the paradoxically promoted progression of related cancers by viruses through cGAS-STING. And summarize the agonists and inhibitors that act in different ways based on the activation mechanism of cGAS-STING.