Search Results (8,649)

Background and Clinical Significance: Pediatric autoimmune gastritis (AIG) is a rare and frequently underdiagnosed disorder characterized by chronic immune-mediated inflammation and atrophy of the gastric mucosa. In children, AIG typically presents with iron-deficiency anemia (IDA) refractory to oral iron supplementation, in contrast to the pernicious anemia more commonly observed in adults. Diagnosis relies on a combination of serological markers, such as anti-parietal cell antibodies, and histopathological confirmation, with gastric biopsies demonstrating oxyntic mucosal atrophy and lymphocytic infiltration. Early recognition is essential, particularly in patients with personal or familial autoimmune backgrounds, to prevent long-term complications including nutritional deficiencies and increased gastric neoplasia risk. Case Presentation: An 11-year-old boy was referred for evaluation of severe microcytic anemia. He was clinically asymptomatic, with normal growth and physical examination except for mucocutaneous pallor. Celiac disease, thyroid dysfunction, hemoglobinopathies, and infectious or inflammatory gastrointestinal causes were excluded. Despite six months of high-dose oral iron therapy, anemia persisted. Upper gastrointestinal endoscopy showed macroscopically normal mucosa; however, histopathological analysis of gastric body biopsies revealed chronic atrophic gastritis. Serological testing confirmed autoimmune etiology, with positive anti-parietal cell antibodies and hypergastrinemia. Since diagnosis, the patient has required two courses of intravenous iron supplementation, and remains under close follow-up for associated autoimmune and hematologic conditions. Conclusions: Refractory IDA may represent the sole clinical manifestation of AIG in pediatric patients, even in the absence of gastrointestinal symptoms. Histological assessment is crucial, as endoscopic findings may be normal. Early diagnostic suspicion allows timely management focused on correction of nutritional deficiencies and long-term surveillance to mitigate neoplastic risk. AIG should therefore be considered in children with anemia unresponsive to conventional iron therapy. Full article

Background: Alemtuzumab is a recombinant DNA-derived humanized monoclonal antibody directed against the 21–28 kd cell surface glycoprotein, CD52. Alemtuzumab is used as an organ anti-rejection therapy in transplant recipients. Neuro-ophthalmic adverse effects are rarely described, and, to our knowledge, accommodative spasm has not previously been reported in a transplant recipient. Case Description: A thirty-nine-year-old woman with genetically confirmed NPHP1-associated nephronophthisis, with stage F3 fibrosis, developed persistent bilateral blurred vision 72 h following alemtuzumab administration for a biopsy-proven acute cellular rejection, approximately six to seven weeks post-transplant. Initial attribution to hyperglycaemia and tacrolimus toxicity delayed recognition. Cycloplegic refraction confirmed a marked hyperopic shift (+2.75 D right eye, +2.50 D left eye) with significant improvement in visual acuity, consistent with accommodative spasm. Systemic evaluations excluded hyperglycaemia-related lens changes, calcineurin inhibitor neurotoxicity, and cytomegalovirus retinitis. MRI was not pursued in the absence of red flag neurological features, and because a definitive ophthalmic diagnosis had been made. Management and Outcome: The patient was managed expectantly, as cycloplegic refraction had already confirmed the diagnosis, and symptoms were improving. Therapeutic cycloplegia (e.g., atropine) was withheld to avoid impairing near vision and driving ability. Full resolution occurred within 4 to 6 weeks without intervention. Drug exposure to onset of symptoms was 72 h; onset of symptoms to diagnostic confirmation was 22 days; total symptom duration was 5.5 weeks, and recovery was 2 weeks after diagnosis. Conclusions: This case represents the first reported transplant case of alemtuzumab-associated accommodative spasm. Causality assessment supports a WHO-UMC classification of “Probable”, aligning with five Bradford–Hill considerations (temporality, biological plausibility, consistency, specificity, and analogy), but without statistical “strength of association” given that this is a single case report. Early cycloplegic refraction should be incorporated into the evaluation of post-alemtuzumab visual complaints, and clinicians should contribute to pharmacovigilance through structured reporting to capture these rare but important events. Full article

SLAMF7, also known as CD319, a SLAM (signaling lymphocytic activation molecule) family receptor, is relatively weakly expressed on chronic lymphocytic leukemia (CLL) B cells. This study evaluated the ability of elotuzumab (E), an anti-SLAMF7/CD319 antibody, to induce antibody-dependent cellular cytotoxicity (ADCC) against CLL cell lines (MEC-1, MEC-2, CI, HG-3, PGA-1, WA-OSEL). ADCC was assessed by flow cytometry using E (100 μg/mL), rituximab (R, 100 μg/mL), and their combination (E + R). CLL lines served as targets (T), while peripheral blood mononuclear cells (PBMCs) or NK cells from healthy donors served as effectors (E) at an 8:1 E:T ratio for 4 h. With PBMCs, E-induced ADCC ranged from 1.3 ± 1.2% (PGA-1) to 14.6 ± 8.1% (MEC-1); R-induced ADCC ranged from 9.2 ± 4.6% (PGA-1) to 16.6 ± 9.4% (WA-OSEL). With NK cells, E-induced ADCC ranged from 1.8 ± 3.7% (PGA-1) to 27.3 ± 4.7% (MEC-1); R-induced ADCC ranged from 5.1 ± 4.3% (PGA-1) to 27.5 ± 13.6% (CI). E outperformed R in MEC-1, while R was superior elsewhere. Cell lines with higher SLAMF7/CD319 expression displayed increased sensitivity to E. Cell lines with del17p showed higher SLAMF7/CD319 expression. The combination of E + R showed no significant synergy over monotherapies. In conclusion, elotuzumab induced significant ADCC in CLL cells, warranting further therapeutic evaluation. Full article

Background: Patients with primary brain tumors face profound disease- and treatment-related immunosuppression, placing them at high risk for severe infections. Their capacity to mount protective immune responses to vaccination, particularly to repeated antigen exposures such as COVID-19 boosters, remains critically under-defined, leading to uncertainty in clinical practice. Methods: In this prospective cohort study, we analyzed humoral responses to seasonal COVID-19 (mRNA-based) and influenza vaccination in 17 patients with primary brain tumors (recruited from an initial cohort of 37) who received a booster shot, and 19 healthy controls. Serum samples were collected before (T1) and 30 ± 2 days after (T2) vaccination to quantify SARS-CoV-2 anti-Spike (S) IgG and anti-Influenza IgG titers. Results: Despite ongoing chemotherapy in 47% of patients, baseline anti-S antibody titers were comparable between groups. Following the booster, median anti-S titers increased significantly and to a similar magnitude in both patients (from 5030 to 18,500 BAU/mL; IQR: 13,885–24,420) and controls (from 4429 to 20,200 BAU/mL; IQR: 11,075–26,680; p = 0.6137, Mann–Whitney U test). Only two heavily pre-treated patients showed no booster response. All participants showed sero-positivity to Anti-Influenza IgG at baseline. For the primary brain tumor cohort, a significant increase for anti-Influenza IgG at T2 was observed (p = 0.0002). Mean antibody titers did not differ between both cohorts. Conclusions: Our findings provide evidence that patients with primary brain tumors can mount robust recall immunity to mRNA vaccines, addressing clinical uncertainty about booster efficacy in this population. These data provide a strong rationale for prioritizing booster vaccinations in this vulnerable population and argue for the inclusion of these patients in future pivotal vaccine trials. Full article

Fabry disease (FD) is an X-linked systemic lysosomal storage disease caused by mutations in the galactosidase-α (GLA) gene, which encodes the α-galactosidase A (α-AGAL) enzyme. FD can lead to serious complications, including early death, if left untreated. For over 20 years, enzyme replacement therapy (ERT) based on the use of agalsidase-α and agalsidase-β has been the standard treatment for FD, alongside new molecules that have enriched the therapeutic armamentarium and others that are being tested to expand it further. Unfortunately, ERT can be associated with the formation of inhibiting antidrug antibodies (ADAs), which impact ERT clinical efficacy and have consequences affecting safety and therapeutic adherence. A group of FD specialists discussed the problem of immunogenicity in FD, analyzing the most recent literature and the strategies that are currently being used to address it. Once formed, fluctuating levels of ADAs persist and have an impact on the clinical picture and prognosis of the disease that is still the subject of lively scientific debate. The critical nature of ADAs is demonstrated by their ability to bind to the enzyme, increasing drug clearance while forming immune complexes that can build up in the tissues causing chronic inflammation that aggravates the progression of the disease and affects the onset of acute reactions after the infusion, impacting therapeutic adherence. Although similar in their therapeutic mechanism, agalsidase-α and agalsidase-β differ in their production process, with resulting differences from a pharmacokinetic and pharmacodynamic point of view and diverse immunological implications: despite showing rather overlapping efficacy outcomes, agalsidase-α demonstrates a better tolerability profile, with a lower frequency of ADAs, than agalsidase-β. Given the extreme variability of the clinical picture, it is crucial for optimal FD management that the most appropriate molecule is chosen by taking into account the unique immunological risk profile of each single patient, and particular attention should be paid to naïve subjects by periodic measurement of ADAs during therapy and cross-referencing data to correlate serological and clinical patterns. Full article

Background: Osteosarcoma remains largely refractory to immune checkpoint inhibitor (ICI) monotherapy, and strategies to modulate the tumor immune microenvironment are being actively explored. Mild hyperthermia has been reported to influence antitumor immune responses; however, its impact in combination with PD-1 blockade in osteosarcoma has not been well characterized. Methods: Murine LM8 osteosarcoma cells were subjected to mild thermal stimulation, and changes in PD-L1 expression were evaluated. LM8-bearing mice were treated with mild hyperthermia, anti-PD-1 antibody, or their combination. Tumor growth, lung metastasis, and survival were assessed. Tumor-infiltrating immune cells were profiled using single-cell RNA sequencing to descriptively characterize immune-associated transcriptional features under each treatment condition. Results: Mild thermal stimulation (42 °C, 30 min) increased PD-L1 expression in LM8 cells in vitro. In vivo, combination therapy significantly suppressed primary tumor growth compared with control (χ² = 29.75, p = 1.6 × 10⁻⁶) and reduced lung metastasis burden, with a significant decrease in metastatic nodules (p < 0.01). Kaplan–Meier analysis demonstrated a significant survival benefit in the combination group (log-rank p < 0.001). Single-cell RNA sequencing revealed an increased proportion of CD8⁺ T cells with reduced exhaustion-associated gene expression and a shift toward pro-inflammatory (M1-like) macrophage transcriptional profiles. Conclusions: PD-1 blockade combined with mild hyperthermia was associated with enhanced antitumor efficacy and immune-associated transcriptional remodeling in a murine osteosarcoma model, supporting further preclinical evaluation of this combination strategy. Full article

The blood–brain barrier (BBB) is a major obstacle to the development of brain-targeted drug delivery systems, restricting greater than 98% of small molecules (<500 Da) and virtually all large-molecule drugs from entering the brain tissues from the bloodstream, resulting in suboptimal drug doses and therapeutic failure in the treatment of Alzheimer’s disease (AD). However, the advent of nanotechnology has provided significant solutions to the BBB challenges, enabling particle size reduction, enhanced drug solubility, reduced premature drug degradation, extended and sustained drug release, enhanced drug transport across the BBB, increased drug target specificity and enhanced therapeutic efficacy. In corollary, a library of brain-targeted surface-functionalized nanotherapeutics has been widely reported in the current literature. These promising in vitro, in vivo and pre-clinical results from the existing literature provide quantitative evidence for the relative clinical utility of each of the techniques, indicating remarkable capacity for brain-targeted carrier systems; many of them are still being tested in human clinical trials. However, despite the recorded research successes in drug transport across the BBB, there are currently no clinically proven medications that can slow or reverse the progression of AD because most of the novel therapeutics have not been successful during the clinical trials. Therefore, the main option for the treatment of AD is symptomatic treatment using cholinesterase inhibitors and N-methyl-D-aspartate (NMDA) receptor antagonists. Although these therapies help to alleviate symptoms of AD and improve patients’ quality of life, they neither slow the progression of disease nor cure it. Thus, an effective disease-modifying therapy for the treatment of AD is an unmet clinical need. It is apparent that a deeper understanding of the structural complexity and controlling dynamic functions of the BBB in tandem with a comprehensive elucidation of AD pathogenesis are crucial to the development of novel nanocarriers for the effective treatment of AD. Therefore, this narrative review describes the contextual analysis of several promising strategies that enhance brain-targeted drug delivery across the BBB in AD treatment and recent research efforts on two major AD biomarkers that have revolutionized AD diagnosis, amyloid-beta plaques and phosphorylated tau protein tangle, as potential targets in AD drug development. This has led to the Food and Drug Administration (FDA)’s approval of two intravenous (IV) anti-amyloid monoclonal antibodies, Lecanemab (Leqembi^®) and Donanemab (Kisunla^®), which were developed based on the Aβ cascade hypothesis for the treatment of early AD. This review also discusses the recent shift in the Aβ cascade hypothesis to Aβ oligomer (conformer), a soluble intermediate of Aβ, which is the most toxic mediator of AD and could be the most potent drug target in the future for a more accurate and effective drug development model for the treatment of AD. Furthermore, various promising nanoparticle-based drug carriers (therapeutic nanoparticles) that were developed from intensive research are discussed, including their clinical utility, challenges and prospects in the treatment of AD. Overall, it suffices to state that the advent of nanotechnology provided several innovative techniques for overcoming the BBB and improving drug delivery to the brain; however, their long-term biosafety is a relevant concern. Full article

Background: Antiphospholipid syndrome (APS) is diagnosed by characteristic clinical manifestations supported by positivity for lupus anticoagulant, anticardiolipin, and anti-β2-glycoprotein I antibodies. However, a proportion of patients, especially those with systemic lupus erythematosus, remain seronegative despite high clinical suspicion. Anti-phosphatidylserine/prothrombin antibodies (aPS/PT) have emerged as potential biomarkers in this setting. We conducted an expert perception-based Health Technology Assessment (HTA) to evaluate the clinical, ethical, and organizational impact of implementing aPS/PT testing. Methods: A structured HTA was performed across five domains: safety, perceived efficacy, equity, ethics, and organizational implications. A survey was distributed to 110 APS specialists; 50 experts contributed responses (45.5% response rate; 66% clinicians, 18% laboratory personnel, 8% nurses, 8% administrative/other). For each domain, Z-scores were calculated to compare current diagnostic practice (AS IS) with a scenario integrating aPS/PT testing (TO BE). Correlation analyses explored relationships across domains. Results: Across all five domains, the TO BE scenario scored substantially higher than standard practice. The largest improvements were observed in perceived diagnostic efficacy (ΔZ = +2.65) and safety (ΔZ = +2.03), followed by equity (ΔZ = +2.25), ethical/social impact (ΔZ = +1.96), and organizational feasibility (ΔZ = +1.61). Perceived diagnostic effectiveness showed a strong positive correlation with both equity (r = 0.70, p < 0.001) and ethics (r = 0.67, p < 0.001). Participants consistently rated the assay as safe, clinically useful, equitable, and organizationally easy to introduce in routine laboratory workflows. Conclusions: Experts perceived the addition of aPS/PT testing as a meaningful enhancement to APS diagnostics, particularly for SLE patients who are seronegative on conventional assays. Its favorable profile across all HTA domains supports further evaluation in prospective cohorts and consideration for integration into future diagnostic algorithms. Full article

Background/Objectives: Histological examination constitutes a fundamental methodology for establishing the vitality of a lesion. In cases where the corpse is preserved for an extended duration of time prior to the post-mortem evaluation, particularly if the body has undergone freezing and thawing cycles, post-mortem changes may obscure or alter evidence of traumatic injuries. Consequently, the reliability of hematoxylin and eosin (H&E) staining for the reliable detection of intralesional erythrocytes in suspected traumatic fatalities is potentially severely compromised. The primary objective of this study is to rigorously underscore the detrimental influence of freeze–thaw processes on histologic examination and to advocate the indispensable incorporation of immunohistochemical analysis, specifically employing anti-human glycophorin A antibodies, to ascertain the presence of red blood cells. Methods: Skin samples from 10 autopsy cases were subjected to serial freeze–thaw cycles and analyzed using anti-human Glycophorin A (GPA) immunohistochemistry staining to evaluate skin lesion vitality in freeze–thawed tissues compared to fresh controls. Results: Results indicated that while H&E reliability was limited to fresh tissue, anti-GPA staining remained stable across all freeze–thaw cycles. Conclusions: Forensic pathologists must remain acutely cognizant of the potential artifacts produced by freeze–thaw cycles. In these cases, anti-GPA staining proved to be a reliable asset for evaluating the vitality of a lesion. Full article

Immune checkpoint proteins including PD-1, CTLA-4, LAG-3, TIM-3, and TIGIT regulate T-cell functions, which are essential for anti-tumor immunity. Over-expression of these immune checkpoint proteins leads to T-cell exhaustion and a significant impairment of anti-tumor immunity. Rejuvenation of effector T-cell function with immune checkpoint inhibitors (ICI) restores anti-tumor immunity, which translates into clinical efficacy in the frontline and salvage treatment of various hematological malignancies. Efficacy of ICIs is highest in classical Hodgkin lymphoma, primary mediastinal large B-cell lymphoma, and NK/T-cell lymphomas, and modest in immune-privileged-site lymphomas and cutaneous T-cell lymphoma. However, in myeloid malignancies and multiple myeloma, the efficacy of ICIs remains doubtful. In addition to being used as single agents, ICIs have also been combined with other ICIs; as well as chemotherapy, antibody drug conjugates, and epigenetic agents (histone deacetylase inhibitors and hypomethylating agents). More innovative strategies include the use of ICIs in the context of allogeneic haematopoietic stem cell transplantation and chimeric antigen receptor T-cell therapy. This review synthesizes current evidence for the use of ICI in different haematological malignancies, and highlights future directions toward biomarker-driven, rationally designed therapeutic combinations. Full article

Background: Endocrine disturbances are increasingly recognized as components of long COVID, yet long-term data remain limited. This study evaluated the prevalence of dysglycemia and thyroid autoimmunity four years after SARS-CoV-2 infection in adults without previously known endocrine disease. Methods: We conducted a retrospective longitudinal 4-year evaluation of adults hospitalized for COVID-19 between 2020 and 2021. Of 1009 eligible patients without prior diabetes or thyroid disease, 96 completed a standardized 4-year post-infection evaluation. Acute-phase data included COVID-19 severity, admission glucose, inflammatory markers, imaging findings, and treatments. The 4-year evaluation comprised fasting plasma glucose, thyroid function tests, anti-thyroid antibodies (anti-TPO, anti-Tg), and thyroid ultrasonography. Baseline HbA1c, thyroid autoantibodies, and thyroid imaging were not available. Results: At four years post-infection, 27.1% of patients exhibited dysglycemia compatible with type 2 diabetes mellitus, 41.6% showed thyroid autoimmunity, and 15.6% presented with both conditions. Overall, 47.9% developed at least one endocrine alteration. Admission hyperglycemia strongly predicted long-term dysglycemia (OR 6.67; 95% CI: 1.45–30.58), and diabetes prevalence increased with acute disease severity. Thyroid autoimmunity was frequent but not associated with initial COVID-19 severity. Conclusions: Four years after SARS-CoV-2 infection, a substantial proportion of patients exhibited persistent metabolic and autoimmune alterations, supporting a long COVID immunometabolic phenotype. In the absence of baseline endocrine data, the reported findings reflect long-term endocrine alterations identified at the 4-year evaluation, with a potential role of SARS-CoV-2 infection. These findings highlight the importance of baseline metabolic and thyroid assessment—including HbA1c and thyroid autoantibodies—in hospitalized COVID-19 patients and underscore the need for structured long-term endocrine monitoring. Full article

Background: Thyroid hormones regulate energy homeostasis, lipid/glucose metabolism, and protein turnover. Chronic Hepatitis C Virus (HCV) infection is highly associated with autoimmune hypothyroidism, which may have profound metabolic implications. This study evaluates thyroid dysfunction and anti-thyroid peroxidase (anti-TPO) autoimmunity in HCV patients and explores its potential metabolic implications in a high-prevalence region. Methods: In this comparative cross-sectional study adhering to STROBE guidelines, we enrolled 100 PCR-confirmed chronic HCV patients and 100 age/gender-matched controls from District Peshawar, Pakistan. Serum TSH, fT3, fT4, and anti-TPO antibodies were quantified. Multivariable logistic regression, adjusted for age, gender, and viral load, was used to compute adjusted odds ratios (aOR) with 95% confidence intervals (CI). Results: Thyroid dysfunction affected 41% of HCV patients vs. 12% of controls (aOR 5.2, 95% CI 2.8–9.6, p < 0.001), predominantly hypothyroidism (29% overall; 18% overt, 11% subclinical). Anti-TPO positivity was 38% in HCV vs. 8% in controls (aOR 6.7, 95% CI 3.1–14.5, p < 0.001). Anti-TPO titers correlated positively with TSH (r = +0.62, p < 0.001) and inversely with fT3/fT4. Subgroup analysis showed higher dysfunction in patients aged ≥40 years (52% vs. 28%, p = 0.012) and viral load ≥ 10⁶ IU/mL (48% vs. 32%, p = 0.041). We hypothesize that these findings may have significant metabolic implications, including impaired mitochondrial β-oxidation and insulin resistance. Conclusions: HCV infection is strongly associated with autoimmune hypothyroidism, which may amplify cardiometabolic risk. The paper has not explicitly identified metabolic parameters, including lipid profiles, indices of insulin resistance, and metabolomic signatures, and, therefore, any metabolic inferences are speculative and based on established thyroid and HCV pathophysiology. Routine thyroid screening pre- and post-DAA therapy is recommended, alongside metabolomic profiling to validate these proposed metabolic pathways. Full article

Background: Experimental autoimmune thyroiditis is an important animal model for studying Hashimoto’s thyroiditis. Our aim was to develop the model using CBA/J-DR3 mice expressing human HLA-DR3, which is associated with autoimmune thyroiditis in humans, to better simulate human autoimmune thyroiditis. Such a humanized model can be used to test specific antigen therapies for autoimmune thyroiditis. Methods: CBA/J-DR3 mice were produced by back-crossing B6-DR3 mice to the CBA/J background. Female CBA/J-DR3 mice were immunized with human thyroglobulin (Tg) in complete Freund’s adjuvant on days 0 and 7. On day 21, mice were sacrificed, blood collected, spleen and thyroid harvested for analysis. Splenocytes were analyzed for T cell responses to Tg and its major T-cell epitope in human autoimmune thyroiditis, Tg.2098. Serum anti-thyroglobulin antibodies were measured by ELISA, and thyroid-stimulating hormone was measured using the Luminex assay. Thyroid histology and immunohistochemistry were examined. Results: Immunized CBA/J-DR3 mice showed significant T cell proliferation in response to Tg (stimulation index 3.4 ± 4.5) and Tg.2098 (1.5 ± 0.7). Anti-thyroglobulin antibody levels were elevated in immunized mice when compared to control mice (2.05 ± 0.75 vs. 0.15 ± 0.06, p < 0.0001). T cells demonstrated higher reactivity to thyroid antigens by enhanced production of pro-inflammatory cytokines. Thyroid immunohistochemistry revealed mild CD3-positive T-cell infiltration. Conclusions: This novel humanized CBA/J-DR3 mouse model of Hashimoto’s thyroiditis demonstrates key features of human autoimmune thyroiditis. The HLA-DR3 background and the immune response to Tg and Tg.2098 enhance translational relevance, making this a valuable model for studying thyroid disease pathogenesis and testing targeted immune-modifying therapies. Full article

Chronic arthritis following arthritogenic alphavirus infections presents symptoms resembling autoimmune rheumatic diseases, raising questions about the underlying mechanisms, including molecular mimicry and autoantibody production. This systematic review evaluated evidence supporting molecular mimicry and the potential role of autoantibodies as predictive biomarkers in alphavirus-induced chronic arthritis. A comprehensive search of PubMed, Scopus and Web of Science was conducted following PRISMA 2020 guidelines and PECO framework. Thirteen studies met the inclusion criteria: four computational studies assessing peptide homology between viral and human proteins, and nine clinical studies evaluating autoantibodies in chronic post-alphavirus arthritis. Computational analyses identified conserved alphavirus peptides with sequence and structural similarity to human proteins implicated in autoimmunity, supporting the hypothesis of molecular mimicry. However, most lacked experimental validation. Clinical studies showed variable detection of autoantibodies, rheumatoid factors, anti-cyclic citrullinated peptide, and antinuclear antibodies in chronic patients, though seropositivity rates were inconsistent and generally low. Only one study reported a significant association between autoantibody levels and disease chronicity. The findings suggest a potential autoimmune component in post-alphavirus arthritis driven by molecular mimicry, though current evidence remains inconclusive due to methodological heterogeneity and limited validation. Autoantibodies may contribute to pathogenesis but are not reliable predictors of chronicity. Future longitudinal studies with standardized assays and validation of computational findings in human models are needed. Full article

We report a novel dual-receptor lateral flow biosensor (LFB) for the rapid, sensitive, and visual detection of MCF-7 breast cancer cells as a model for circulating tumor cells (CTCs). The biosensor employs a MUC1-specific aptamer conjugated to colloidal gold nanoparticles as the detection probe and an anti-MUC1 antibody immobilized at the test line as the capture probe, forming a unique “aptamer–cell–antibody” sandwich complex upon target recognition. This design enables instrument-free, visual readout within minutes, achieving a detection limit of 675 cells. The assay also demonstrates robust performance in spiked human blood samples, highlighting its potential as a simple, cost-effective dual-mode point-of-care testing (POCT) platform. This platform supports both rapid visual screening and optional strip-reader-based quantification, making it suitable for early detection and monitoring of breast cancer CTCs. Full article