Guillain-Barre syndrome (GBS) is an immune-mediated acute inflammatory polyradiculoneuropathy, with intravenous immunoglobulin (IVIG) and plasma exchange (PLEX) established as standard first-line treatments. A subset of severe overlapping GBS patients carrying multiple pathogenic anti-ganglioside immunoglobulin G (IgG) antibodies typically exhibits poor therapeutic responses to IVIG. Efgartigimod, a neonatal Fc receptor (FcRn) antagonist, accelerates the clearance of circulating pathogenic IgG, conferring theoretical therapeutic value for IgG-driven autoimmune neurological disorders. Herein, we present a 51-year-old female patient with severe multi-antibody-positive overlapping GBS who failed full-course standard IVIG treatment; sequential salvage Efgartigimod administration induced progressive recovery of limb muscle strength. We further performed a systematic literature review pooling 15 previously published cases of efgartigimod-treated GBS to synthesize global clinical evidence. Our pooled analysis suggests that Efgartigimod could act as a salvage therapeutic candidate for IVIG-refractory severe GBS complicated by multiple anti-ganglioside antibody positivity. Nevertheless, the definitive efficacy and optimal timing of intervention remain to be validated by large‑sample randomized controlled trials.

Immune checkpoint inhibitors (ICIs) have radically changed the treatment landscape of non-small cell lung cancer (NSCLC) and significantly improved patients' prognosis in many settings of the disease. Nevertheless, clinical outcomes remain highly heterogeneous, and a substantial proportion of patients do not achieve meaningful and/or durable benefit from immunotherapy. This variability in treatment response has highlighted the need to identify more robust predictive biomarkers that integrate, beyond established biomarkers such as programmed cell death ligand 1 (PD-L1) expression, additional clinical, genomic, immunologic, and microenvironmental features to better identify the biological determinants underlying sensitivity and resistance to ICIs. In this review, we will analyze the current evidence supporting established predictive biomarkers, including PD-L1 expression, while highlighting their major limitations. We will also discuss and summarize emerging clinical and molecular biomarkers and integrative predictive approaches aimed at improving the stratification of patients with NSCLC, to identify those most likely to benefit from ICI therapy and ultimately refine personalized treatment strategies.

Cancer is a leading cause of death globally, and traditional therapies including chemotherapy and radiotherapy are often constrained by systemic toxicity and lack of specificity. Thus, targeted therapies are the need of the hour to revolutionize cancer treatment by enhancing specificity and selectivity, and minimizing off-target effects. The epidermal growth factor receptor (EGFR) and its deletion mutant EGFRvIII exhibit pivotal roles in tumorigenesis, making them attractive targets across multiple cancers. Various targeted therapies, including small-molecule inhibitors, therapeutic antibodies, antibody-drug conjugates, and immunotherapies, are developed to target EGFR, EGFRvIII, and other clinically relevant EGFR mutations, namely L858R, C797S, and T790M. U.S. FDA has approved many of these agents as monotherapies or in conjunction with chemotherapy for treating lung, head and neck, and colorectal cancers; however, there are challenges. In this review, we discuss the role of EGFRvIII in driving aggressive tumor growth and highlight how effective targeting of EGFRvIII, and overcoming resistance mutations will be crucial to improve EGFR- and EGFRvIII-based therapies. The ongoing evolution of these interventions holds promise for long-term responses, reduced toxicity, and enhanced patient survival. Literature related to EGFR- and EGFRvIII-based therapies was searched systematically in PubMed, MEDLINE, Scopus, ScienceDirect, and Google Scholar up to June 2026.

The emergence of in vivo CAR-T technologies has generated considerable excitement as a means of simplifying cellular immunotherapy. However, whether current in vivo CAR-T platforms are truly positioned to succeed in solid tumors remains unclear. We argue that the major limitations of CAR-T therapy in solid tumors arise from a complex interplay between biological barriers and engineering constraints. Although in vivo CAR-T platforms may simplify manufacturing, the delivery strategy itself directly influences which T-cell populations are engineered, the level and duration of CAR expression, cellular phenotype, persistence, and safety. Therefore, in vivo CAR-T therapies do not eliminate the biological barriers that restrict ex vivo CAR-T therapy, including poor trafficking, stromal exclusion, antigen heterogeneity, T-cell dysfunction, and immunosuppressive tumor microenvironment (TME). Consequently, in vivo CAR-T therapies inherit nearly all of the challenges that have restricted ex vivo CAR-T therapy while simultaneously introducing additional limitations related to CAR-T generation, persistence, and controllability. The encouraging results observed in hematologic malignancies and autoimmune diseases may therefore not predict success in solid tumors. Future advances will likely depend less on improving gene delivery and more on establishing mechanisms that support CAR-T infiltration, expansion, and persistence within tumors.

Autoimmune diseases are very common worldwide. The immune system becomes dysregulated in a pro-inflammatory direction. Bromodomains play a crucial role in the regulation of many inflammatory pathways, including mitogen-activated protein kinase, nuclear factor kappa B, and interleukins. Bromodomain inhibitors could allow for better autoimmune disease control and reduction of symptom severity than currently available treatment due to their direct integration into the epigenetic mechanism. This review focuses on drugs currently being tested and how their mechanisms of action are beneficial in treatment of rheumatoid arthritis, osteoarthritis, fibrosis, cirrhosis, lupus, inflammatory bowel disease. The aim of this review is show Bromodomain inhibitors as a new possible treatment strategy for a variety of autoimmune diseases. The study was conducted by selecting articles from the PubMed database published between 2011 and 2026; for some studies describing the basic pathophysiology of the diseases, this period was extended to 2002.

Cancer vaccines represent a promising class of immunotherapeutic agents with potential applications in cancer prevention and treatment. By eliciting tumor-specific immune responses, these vaccines may offer durable protection against tumor progression, recurrence, and metastasis while minimizing off-target toxicity associated with conventional therapies. In addition, activation of adaptive immunity and the induction of immunological memory may contribute to sustained anti-tumor surveillance. Despite these advantages, clinical translation has been limited by immunological complexity, antigen selection, delivery constraints, and tumor-mediated immune evasion. Recent advances in vaccine platforms, including mRNA, peptide-based, and whole-cell vaccines, together with improved delivery systems and immune-modulating strategies, have renewed interest in cancer vaccine development and provided new opportunities to improve efficacy. This review summarizes current progress in cancer vaccine research, discusses major translational challenges, and considers future directions for the development of effective vaccine-based cancer therapies.