Background/Objectives: Patients with chronic lymphocytic leukemia (CLL) are susceptible to infections that can affect their clinical outcomes. Aims: The aims of this study were to assess the following: (1) the incidence of pneumonia in CLL patients treated with venetoclax-based regimens in a real-world setting, (2) the risk factors for event-free survival (EFS), and (3) overall survival (OS). Methods: This multicenter study included 322 patients from eight centers. Univariable and multivariable analyses (MVA) were performed, with the development of pneumonia during venetoclax-based treatment and OS as outcomes. Results: The most common complication was neutropenia (59%). During treatment with venetoclax-based regimens, 66 (20%) patients developed pneumonia—50 (23%) patients in the rituximab-plus-venetoclax (R-VEN) group and 13 (16%) patients in the obinutuzumab-plus-venetoclax (O-VEN) group (p = 0.15). Chronic obstructive pulmonary disease (COPD)/asthma, splenomegaly, elevated creatinine, and anemia < 8 g/dL were the risk factors for EFS in MVA (HR = 2.08, 95%CI 1.16–3.74, p = 0.014; HR 1.73, 95%CI 1.08–2.78, p = 0.02; HR 2.13, 95%CI 1.10–4.11, p = 0.03, HR 3.58, 95%CI 2.18–5.89, p < 0.001, respectively). Relapsed/refractory (R/R) CLL patients treated with R-VEN with pneumonia had worse OS than those without (p < 0.001). In patients treated with O-VEN, median OS did not differ between patients with and without pneumonia (p = 0.45). Conclusions: Our real-world study showed that pneumonia during venetoclax treatment occurs more frequently than reported in registration trials and has a negative impact on OS, especially in patients with R/R CLL who are treated with R-VEN. Neutropenia is not a risk factor for pneumonia.

Introduction: Rheumatoid arthritis (RA) is a chronic systemic autoimmune disease in which pain remains the most prominent and burdensome symptom from the patient’s perspective. Despite effective control of peripheral inflammation with biological and targeted synthetic disease-modifying antirheumatic drugs, an estimated 20–30% of patients continue to experience persistent moderate-to-severe pain after achieving clinical remission. This therapeutic gap reflects the evolution of pain mechanisms from peripheral nociception towards central sensitisation and nociplastic pain, creating a need for integrative approaches to patient stratification. The Rheumatoid Arthritis Pain Artificial Intelligence (RA-PAIN-AI) study aims to identify and characterise clinical, neurophysiological and multiomic signatures associated with chronic pain in patients with RA using integrative artificial intelligence (AI)-based analytical methods. Methods and analysis: RA-PAIN-AI is a prospective, observational, single-centre case–control study integrating clinical laboratory neurophysiological and multiomic data. Two groups of adult patients with RA will be enrolled: patients with active RA qualifying for biological therapy under the Polish national drug programme B.33 and patients receiving biological therapy who are in sustained clinical remission for at least 1.5 years without clinically significant chronic pain. All participants will undergo clinical assessment, validated patient-reported outcome measures and peripheral blood collection at baseline, followed by repeat questionnaires and peripheral blood collection at 3–6 months. The exact interval between visits will be recorded and included in longitudinal analyses where appropriate. Electroencephalography will be performed only in an exploratory subset according to predefined feasibility, safety and eligibility criteria. Biological samples will be analysed using whole genome sequencing (genomics), messenger RNA expression profiling (transcriptomics) and measurement of circulating proteins (secretomics). A minimum of 50 participants per group will be recruited. Because the study is exploratory and high-dimensional, AI and machine-learning analyses will use prespecified feature filtering, dimensionality reduction, regularisation and internal validation procedures, and all predictive models will require external validation in future cohorts. Ethics and dissemination: The protocol received a favourable opinion from the Bioethics Committee at the Hirszfeld Institute of Immunology and Experimental Therapy, Polish Academy of Sciences, Wroclaw, Poland (Opinion No. KB-17/2025, dated 25 September 2025). Written informed consent will be obtained from all participants before any study-related procedure. The results will be disseminated through peer-reviewed publications, conference presentations and communication with relevant scientific, clinical and patient communities. Trial registration number: NCT07769619 .

The Cancers journal retracts the article titled “Pneumonia in Patients with Chronic Lymphocytic Leukemia Treated with Venetoclax-Based Regimens: A Real-World Analysis of the Polish Adult Leukemia Group (PALG)”

Atherosclerotic stenosis of the internal carotid artery (ICA-S) is among the significant causes of ischemic stroke. Current noninvasive imaging techniques

Kidney transplantation is the optimal treatment for end-stage renal disease, yet long-term graft survival remains limited by allograft rejection. While T and B cells and donor-specific antibodies (DSA) have been the main focus, accumulating evidence indicates that natural killer (NK) cells play a significant dual role in both graft injury and immune adaptation, including in DSA-negative rejection. This narrative review summarizes current knowledge on the dual role of NK cells in kidney transplantation, with emphasis on antibody-independent mechanisms, adaptive NK-cell subsets, and their potential as biomarkers of graft outcome. NK cells are highly heterogeneous, consisting of CD56 ^bright and CD56 ^dim CD16 subsets. Cytomegalovirus infection promotes expansion of adaptive NKG2C ⁺ CD57 ⁺ cells with memory-like features. In rejection, NK cells act through both antibody-dependent cellular cytotoxicity and antibody-inde-pendent pathways, such as “missing-self” recognition via killer immunoglobulin-like receptors (KIR)/human leukocyte antigen (HLA) mismatch and release of the killer-specific secretory protein of 37 kDa (Ksp37). Specific NK subsets are associated with microvascular inflammation and graft loss even in the absence of DSA. In contrast, NK cells support tolerance by killing donor dendritic cells and activated T cells, producing interleukin (IL)-10 and transforming growth factor-β (TGF-β), and undergoing reeducation, gradually shifting from a cytotoxic to a regulatory phenotype. NK cells exert a dual, often opposing role in kidney transplantation, mediating both allograft injury and immune tolerance. Better understanding of their plasticity may enable new biomarkers and NK-targeted therapies to improve long-term graft survival.

Introduction: Access to oncology care in Poland remains uneven, with rural residents limited to specialist availability. We analyzed geographic factors that may worsen cancer outcomes and deepen health disparities in Poland between rural and urban inhabitants. Objectives: This study aims to evaluate the impact of geographic and demographic factors on cancer diagnosis in central Poland, focusing on disparities between urban and rural populations. Methods: A retrospective cohort analysis was conducted on 4,771 patients suspected of having cancer at the Nikolay Pirogov Specialized District Hospital in Łódź between 2020 and 2024. Clinical records and public health datasets were analyzed. Logistic regression was used to assess associations between cancer diagnosis and variables such as distance to the nearest hospital, residence type (urban vs. rural), age, and sex. Models were adjusted for potential confounders. Results: Of the 4,771 patients evaluated, 2,996 (62.8%) received a cancer diagnosis and 1,775 (37.2%) did not. In multivariable models, living 5–10 km from the hospital (vs. 10 km and urban/rural status did not demonstrate independent effects after adjustment. These findings are hypothesis-generating and should be interpreted as indicators of potential access pathways among hospital-admitted patients, rather than causal effects. Targeted interventions (e.g., mobile diagnostics, transportation support, and optimized referral pathways) warrant evaluation.