Background: Multiple sclerosis (MS) and autoimmune diseases (AIDs) share immunological underpinnings, leading to frequent co-occurrence. This study investigated the prevalence of AIDs among Polish patients with MS (PwMSs) and its potential effects on disease characteristics. The aims were to compare clinical and demographic characteristics between PwMSs with and without coexisting AIDs. Methods: A retrospective analysis was conducted on data from 580 PwMSs who were treated at the Department of Neurology, University Clinical Center in Katowice, Poland, between February 2018 and August 2023. Variables analyzed included age, sex, MS type, disease duration, treatment, Expanded Disability Status Scale (EDSS) scores, thyroid-stimulating hormone (TSH), and vitamin D3 serum concentrations. Results: AID was identified in 16.9% of PwMSs (n = 98). Compared with PwMSs without AIDs, PwMSs with AIDs exhibited significantly higher mean age (44.61 ± 11.40 vs. 42.24 ± 12.27 years; p = 0.0151), longer disease duration (10.77 ± 6.72 vs. 9.56 ± 7.19 years; p = 0.0102), and higher EDSS scores (2.97 ± 1.43 vs. 2.89 ± 1.84; p = 0.0261). Among PwMSs, the prevalence of AIDs was significantly higher in females (20.24%) compared to males (8.13%; p = 0.0022), and strongly associated with the relapsing-remitting MS subtype (p = 0.0352). Autoimmune thyroid diseases were markedly the most prevalent in PwMSs (hypothyroidism 7.24%). Conclusions: PwMSs with AIDs exhibit distinct characteristics, including older age, increased disease duration, and greater disability. Thyroid disorders are notably the most prevalent AIDs among PwMSs. These findings underscore the intricate interplay between AIDs and MS and highlight the necessity for further research into their long-term impact.

Lung cancer remains one of the leading causes of cancer-related mortality worldwide and is strongly associated with tobacco smoke exposure. In recent years, electronic cigarettes have gained popularity as seemingly safer alternatives to conventional cigarettes; however, their impact on tumor biology remains controversial. A central process in lung cancer progression is the epithelial–mesenchymal transition (EMT), which promotes cellular invasion, migration, and therapy resistance. This review summarizes current evidence on how nicotine, polycyclic aromatic hydrocarbons (PAHs), carbonyl compounds, and reactive oxygen species (ROS) modulate EMT through key signaling pathways, including PI3K/AKT, MAPK/ERK, Wnt/β-catenin, Notch, and HIF-1α. Moreover, it discusses the role of thermal processes during tobacco combustion and e-liquid heating in generating carcinogenic by-products. Emerging data indicate that both traditional and electronic cigarettes release bioactive agents capable of inducing EMT, thereby contributing to lung cancer pathogenesis and revealing potential therapeutic targets.

Epithelial–mesenchymal plasticity encompasses a spectrum of epithelial and mesenchymal identity states that enable cells to adapt to changing biological contexts. While CD44 isoform usage and epithelial splicing regulators ESRP1/2 are well-characterized in cancer-associated epithelial–mesenchymal transition (EMT), their regulation across physiological, non-transformed identity states remains less well defined. Here, we employed a non-malignant human cellular system comprising primary dermal fibroblasts, induced pluripotent stem (iPS) cells, and iPS-derived mesenchymal stem cells (iPS-MSCs) to define discrete epithelial, intermediate epithelial/mesenchymal, and mesenchymal identity states positioned along an epithelial–mesenchymal identity axis. Morphological assessment, lineage marker profiling, and RT-qPCR analyses revealed reproducible population-level stratification of these states. CD44 expression and alternative splicing followed this hierarchy, with CD44s predominating in fibroblasts, broad variant exon inclusion in iPS cells, and intermediate patterns in iPS-MSCs. ESRP1 expression mirrored CD44 splicing architecture, and ESRP1 silencing in iPS cells induced a shift toward CD44s, confirming its functional contribution to epithelial-associated CD44 splicing. In contrast, Notch-related transcriptional readouts displayed distinct, context-dependent profiles across the examined identity states. Together, this study establishes a tractable non-transformed human model that captures selected molecular features associated with epithelial–mesenchymal plasticity beyond malignant contexts.