Previous reports have highlighted that inflammation and poor nutritional condition are closely related to a poor prognosis for hypertension. The hemoglobin, albumin, lymphocyte, and platelet (HALP) score is a promising index to reflect potential interaction and synergistic effects between inflammation and nutrition. Our research objective is to excavate the HALP score and specific mortality outcomes of hypertensive adults. This study was a linked-mortality cohort analysis based on participants from the National Health and Nutrition Examination Survey 1999 to 2018. The HALP score was calculated based on 4 blood parameters, and hypertension was determined by blood pressure measurement, questionnaire, and prescription. All-cause mortality, cardiovascular disease (CVD) mortality, and cancer mortality were defined as the primary outcomes of this study. Cox regression analyses were conducted to estimate the hazard ratio (HR) and 95% confidence interval (CI). Restricted cubic spline analysis and subgroup analyses were performed to assess the robustness of our findings. Our research enrolled 20,256 hypertensive adults (mean age = 53.78 ± 0.22 years), including 10,808 (53.36%) males and 9448 (46.64%) females. During 189,593 person-years of follow-up, 4432 all-cause deaths were documented, with 1227 attributed to CVD and 966 to cancer. When compared with hypertensive participants in the lowest quartile (Q1) of the HALP score, those in the highest quartile (Q4) exhibited a 30% reduced risk of all-cause mortality (HR = 0.70, 95% CI = 0.64-0.77, P trend < .001), a 39% lower risk of CVD mortality (HR = 0.61, 95% CI = 0.49-0.76, P trend < .001), and a 22% lower risk of cancer mortality (HR = 0.78, 95% CI = 0.63-0.96, P trend = .086), respectively. Restricted cubic spline analysis revealed an L-shaped association between the HALP score and each of these mortality outcomes. Higher HALP scores correlated with lower risks of mortality from all causes, CVD, and cancer among adults with hypertension. These findings implicate that the HALP score could be a promising and powerful marker to predict prognosis among hypertensive adults in clinical practice.

Financial toxicity (FT) is increasingly recognized as an important patient-centered burden in cancer care. However, the heterogeneity of FT and its associations with healthcare utilization and catastrophic health expenditure (CHE) among patients with primary liver cancer (PLC) remain insufficiently understood. This study aimed to identify latent profiles of FT among patients with PLC and to examine their associations with healthcare utilization and CHE. We conducted a retrospective cohort study of consecutive adult patients with PLC who received inpatient and/or outpatient care between December 2024 and December 2025 (N = 720). FT was assessed using the COmprehensive Score for FT and multidimensional hardship indicators, including material hardship, financial worry, and coping behaviors. Latent profile analysis was used to identify FT profiles. Healthcare utilization outcomes included annual counts of outpatient visits, inpatient admissions, and emergency department visits. CHE was defined as annual out-of-pocket spending exceeding 40% of household capacity to pay, with a 25% threshold used in sensitivity analyses. Associations between FT profiles and utilization were estimated using covariate-adjusted negative binomial regression, and associations with CHE were estimated using covariate-adjusted logistic regression. A 3-profile solution was identified, comprising low FT (45.0%, n = 324), moderate FT (37.5%, n = 270), and high FT (17.5%, n = 126). Overall, the mean COmprehensive Score for FT score was 25.0 (standard deviation 10.9), and CHE occurred in 27.0% of participants. Compared with the low FT profile, the moderate and high FT profiles were associated with lower outpatient visit rates but higher inpatient admission and emergency department visit rates. CHE prevalence increased stepwise across the low, moderate, and high FT profiles. In adjusted models, moderate FT and high FT were associated with higher odds of CHE compared with low FT. Findings were robust using the 25% capacity-to-pay threshold. Patients with PLC exhibit distinct FT profiles that are strongly associated with healthcare utilization patterns and CHE risk. Routine FT screening and profile-informed interventions may help improve care continuity and strengthen financial protection in PLC management.

Breast cancer treatments, including surgery and chemotherapy, may affect the musculoskeletal system even before the patient has received postoperative radiotherapy. This study aimed to investigate the viscoelastic properties of the pectoralis major (PM), upper trapezius (UT), and sternocleidomastoid (SCM) muscles in patients with breast cancer treated with neoadjuvant taxane-based chemotherapy and to examine their associations with surgery type, age, and body mass index (BMI). In this observational study, viscoelastic muscle properties of the PM, UT, and SCM muscles were assessed using the MyotonPRO (Myoton Ltd.) device in 50 patients with breast cancer who received taxane-based neoadjuvant chemotherapy followed by either total mastectomy or breast-conserving surgery. Linear mixed-effects model analyses were used to evaluate differences in muscle viscoelastic properties according to side and surgery type, with adjustment for age, BMI, time since surgery, and pain scores. PM muscle tone and stiffness were significantly higher on the affected side compared to the unaffected side (P < .05); however, surgery type was not significantly associated with the viscoelastic properties of any muscle. Age was significantly associated with the viscoelastic properties of all evaluated muscles (P < .05), except for PM and UT elasticity. BMI was significantly associated only with SCM elasticity (P < .05). Surgery type was not significantly associated with the viscoelastic properties of the cervicothoracic muscles in patients with breast cancer treated with taxane-based neoadjuvant chemotherapy. These findings suggest that patient-related factors, such as age and BMI, may be associated with variations in the mechanical properties of the cervicothoracic muscles in this population.

Hereditary breast and ovarian cancer (HBOC) syndromes, responsible for 5%-10% of all breast and ovarian cancers in the general population, are largely associated with pathogenic variants of the BRCA1 and BRCA2 genes. Yet, the role of other cancer susceptibility genes highlights the genetic etiology of HBOC as complex, thus requiring thorough investigation beyond these main mutations, highlighting a need for a comprehensive genetic assessment in disease management strategies.

In India, advances in genetic research and clinical management have significantly impacted the knowledge of HBOC. A definitive prevalence of BRCA1/2 mutations among Indian populations has catalyzed the adoption of genetic counseling for precision diagnosis and treatment strategies in recent times, with collateral support extended from communities among oncologists, geneticists, and reproductive medicine specialists. The integration of next-generation sequencing and multiplex gene panels creates a platform for identifying high-risk subjects, leading to individualized care pathways and enhanced disease management plans. These programs have increased access to essential services such as genetic counseling, multidisciplinary management, and fertility preservation to provide holistic care to HBOC patients.

Future efforts should explore further the genetic heterogeneity of HBOC in Indian populations. There needs to be wider access to genetic testing and counseling services, and the implementation of strong, ethical policy guidelines for equitable use of genetic information. Through the creation of innovative, collaborative methods, these measures have tremendous potential to improve patient care, early detection, and outcomes for individuals affected by HBOC in India.

The efficacy of neoadjuvant chemotherapy (NAC) for locally advanced gastric cancer (LAGC) remains heterogeneous. The real-world efficacy and comparison of triplet regimens against doublet regimens is unclear. Moreover, the immunological mechanisms underlying differential responses to NAC are poorly understood. This study aimed to compare the efficacy of doublet versus triplet NAC in a Chinese LAGC cohort, and characterize the post-treatment tumor immune microenvironment (TIME) to identify immune correlates of response and survival.

This retrospective study enrolled patients with locally advanced gastric cancer (GC) who received NAC followed by D2 gastrectomy. The clinical outcomes of patients treated with different NAC regimens were analyzed. The TIME was further characterized using fluorescent multiplex immunohistochemistry (mIHC) to analyze the density and spatial proximity of the immune cells the SOX regimen group.

A total of 141 GC patients with complete survival data were included in the final analysis. The overall efficacy of NAC was consistent with prior reports: 7.8% (11/141) achieved ypT0, 36.2% (51/141) achieved ypN0, and 6.4% (9/141) attained a pathological complete response (pCR). Triplet regimens did not provide a statistically significant survival and response advantage over doublet regimens. mIHC analysis showed longer DFS were consistently associated with higher densities of effector immune cells and lower densities of exhausted/immunosuppressive subsets. Favorable survival was also linked to a closer spatial proximity of CD68⁺ cells to tumor cells. In treatment response subgroups, responders exhibited distinct spatial patterns, including higher overall CD56⁺ cell density but fewer CD68⁺cells near tumors, alongside a shorter CD56⁺-to-tumor distance.

This study confirms the consistent anticancer efficacy of neoadjuvant chemotherapy in LAGC. To better inform individualized post-NAC treatment strategies, analysis of the TIME using multiplex mIHC on surgical specimens is recommended.

Fatigue affects up to 90% of patients with cancer during chemotherapy and persists in approximately 30% after treatment completion. This study examined the longitudinal associations between fatigue and 16 inflammatory markers in patients with colorectal cancer (CRC) up to 3 years after surgery.

Patients with Stage I-IV CRC who participated in the prospective ColoCare cohort study were included. Fatigue was measured using the 3-item fatigue subscale of the European Organization for Research and Treatment of Cancer Quality of Life Questionnaire (EORTC-QLQ-C30) at baseline and each subsequent time point (score range: 0-100). Inflammatory markers were measured using blood specimens from each time point (T0: baseline/surgery; T1: 3-9 months; T2: 10-19 months; T3: 20-36 months post-baseline). Linear mixed-effects models were used to examine associations between inflammatory markers and fatigue scores over time. Linear regression was used to analyze the relationships between T0/T1 markers and fatigue at T3.

There were 271 patients with Stage I-III CRC and 30 patients with Stage IV CRC. Among patients with Stage I-III CRC, mean fatigue peaked at T1 (36.9), with higher fatigue among women than men (44.8 vs. 30.9). In longitudinal mixed-effects models, twofold higher mean levels of IL-6 and IL-17A were associated with higher fatigue over time (3.51 (p = 0.01) and 3.91 (p = 0.01), respectively). IL-4, IL-17A, and TNF-α at T1 were nominally associated with higher levels of fatigue at T3.

Higher levels of selected inflammatory biomarkers were associated with fatigue up to 3 years after CRC diagnosis. These markers may help identify patients at risk for persistent fatigue and warrant further study as potential therapeutic targets.

High-grade serous ovarian cancer (HGSOC) ascites represents a highly immunosuppressive tumour microenvironment characterized by complex stromal-immune interactions. In this study, we aimed to delineate the cellular communication networks shaping immune dysfunction within HGSOC ascites, identify key regulatory signalling pathways, characterize the fibroblast-macrophage axis at single-cell resolution, and evaluate the therapeutic potential of IL-10 blockade in reversing macrophage-mediated immunosuppression.

Single-cell RNA sequencing data of eight ascites samples from six HGSOC patients (GSE146026) were analysed using Seurat for clustering and differential expression, followed by CellChat to infer ligand-receptor communication. Sub-clustering defined inflammatory CAFs (iCAF), myofibroblast CAFs (mCAF), and macrophage subtypes (M1/M2). GO/KEGG enrichment assessed functional pathways. Multiplex immunofluorescence validated spatial interactions of IL10+ iCAF and IL10RA+ macrophages in patient tissues. An immune-humanized patient-derived xenograft (PDX) mouse model was established to evaluate the therapeutic effect of IL-10 blockade.

Single-cell transcriptomic analysis of HGSOC ascites revealed macrophages and cancer-associated fibroblasts as dominant cell populations within the tumour microenvironment. Cell-cell communication analysis identified IL-10-IL-10RA signalling as a prominent interaction pathway linking inflammatory CAFs (iCAFs) with M2-like macrophages. iCAFs displayed elevated IL-10 expression, while M2 macrophages showed increased IL-10RA/IL-10RB expression and were associated with exhausted immune states. Multiplex immunofluorescence confirmed spatial proximity between IL-10⁺ iCAFs and IL-10RA⁺ M2 macrophages in tumour tissues. In immune-humanized PDX models, IL-10 blockade with MK-1966 significantly suppressed tumour growth and reduced expression of M2 macrophage markers and proliferation-associated proteins.

This study identifies an IL-10-dependent iCAF-M2 macrophage immunoregulatory circuit as a central mechanism driving immune suppression in HGSOC. Targeting the IL-10 pathway effectively reverses M2 polarization and suppresses tumour progression, highlighting IL-10 blockade as a promising therapeutic strategy in ovarian cancer.

Colorectal cancer (CRC) is a leading cause of cancer mortality worldwide, with liver metastasis representing the principal cause of death in CRC patients. Current primary treatment options for colorectal cancer liver metastases (CRLM) encompass chemotherapy, radiotherapy, targeted therapy, and immunotherapy. However, the survival rate for CRLM patients remains below 40%. The unique immune-tolerant microenvironment of the liver has recently been recognized as a central driver of metastatic colonization, immune evasion, and therapeutic resistance. This review examines the development of CRLM, with particular emphasis on recent therapeutic advances. It also explores promising research and emerging treatment strategies. A deeper understanding of CRLM pathogenesis and therapeutic progress will enable clinicians to optimize treatment approaches and improve patient outcomes.

Macrophages are highly plastic innate immune cells. Their functional states are dynamically shaped by inflammatory signals, metabolic stress, and disease-associated remodeling. In cancer and atherosclerosis, pathological macrophages contribute to immune suppression, plaque destabilization, and therapeutic resistance, making their reprogramming a critical translational goal. Recent advances in nanomedicine provide new opportunities to manipulate macrophage behavior by combining selective cellular entry with conditionally controlled intracellular release. This review focuses on scavenger receptor-guided and cathepsin B-triggered nanodelivery systems as a mechanism-aligned strategy for phenotypic remodeling. While scavenger receptors provide selective molecular gateways enriched in diseased macrophage populations, cathepsin B serves as an endogenous trigger for subsequent nanocarrier disassembly and payload release. We discuss how aligning targeted internalization and enzymatic release can reshape macrophage function. We also examine how these platforms engage intracellular vulnerability networks, highlighting signal transducer and activator of transcription 3 (STAT3) as a translationally relevant node that stabilizes pathological states rather than an exclusive mechanistic axis. Finally, we assess major translational challenges, including off-target sequestration, target heterogeneity, and functional bioavailability. This review aims to advance the translational development of macrophage-centered immunomodulatory therapies by linking nanodelivery design to macrophage biology and disease-relevant intracellular mechanisms.

Myasthenia gravis (MG) is a rare autoimmune disorder that affects the neuromuscular junction, with a global prevalence of approximately 30 cases per 100,000 individuals. Although dysphagia occurs as an initial symptom in 6%-15% of patients, isolated dysphagia as the sole presenting and predominant manifestation is exceedingly rare, posing a significant diagnostic challenge. Furthermore, a complex bidirectional relationship exists between dysphagia and psychiatric conditions such as anxiety and depression, which often leads to misdiagnosis. Approximately 20% of patients with MG are refractory to conventional immunosuppressive therapy. The novel FcRn antagonist efgartigimod rapidly and sustainably reduces pathogenic IgG levels, providing a new therapeutic option for refractory generalized MG.

A 33-year-old previously healthy woman presented with fluctuating dysphagia and a sensation of a pharyngeal foreign body, exhibiting diurnal variation characterized by improvement in the morning and worsening in the evening. Symptom onset coincided with a family quarrel and subsequently intensified after an upper respiratory tract infection. Multiple laryngoscopies, gastrointestinal endoscopies, and brain magnetic resonance imaging (MRI) revealed no abnormalities. Initially misdiagnosed with an anxiety-depressive disorder, she experienced only partial and transient improvement with citalopram. Two subsequent acute exacerbations triggered by infections led to a complete inability to swallow. Neurological examination indicated dysarthria, choking when drinking, and mild distal limb weakness, assessed at 4+/5 on the Medical Research Council scale. The neostigmine test yielded a strong positive result, and serum anti-acetylcholine receptor (AChR) antibodies were detected at a titer of 1:10, while repetitive nerve stimulation (RNS) remained normal. Chest computed tomography (CT) revealed no thymoma. The patient was diagnosed with moderate generalized MG characterized by AChR-antibody positivity and classified as MGFA class IIIb. Following the failure of initial immunosuppressive therapy, which included prednisone at 30 mg daily, pyridostigmine at 60 mg three times daily, and azathioprine at 25 mg daily, the patient underwent two cycles (totaling 8 infusions) of the FcRn antagonist efgartigimod. Marked improvement in dysphagia was observed, as evidenced by a decrease in the MG-Activities of Daily Living (MG-ADL) score from 8 to 2 and a reduction in the Quantitative Myasthenia Gravis (QMG) score from 10 to 1. At the 6-month follow-up, the patient achieved complete clinical remission, with both MG-ADL and QMG scores reaching 0, and attained minimal manifestation status, while prednisone was tapered to 5 mg daily.

This case indicates that isolated fluctuating dysphagia warrants consideration of MG, even in the presence of psychosocial stressors or partial response to psychiatric medications. A negative RNS does not exclude MG, especially in bulbar-onset cases. Clinicians should prioritize organic etiologies and perform neostigmine and anti-AChR testing to avoid delayed diagnosis. Furthermore, efgartigimod is effective for refractory bulbar MG, enabling rapid remission and corticosteroid tapering.