To systematically compare the effects of Baduanjin exercise, bedside cycle ergometer training, and balloon-blowing training on pulmonary function recovery in patients undergoing thoracoscopic radical resection for lung cancer.

This study is a prospective randomized controlled trial. From January, 2021 to June, 2022, 334 patients undergoing thoracoscopic radical resection for lung cancer were enrolled and randomly assigned to Baduanjin group (108 cases), bedside cycle ergometer training group (109 cases), and balloon-blowing training group (117 cases). All the patients received 12 weeks of assigned intervention. Systematic assessments of lung function, exercise tolerance, dyspnea level, pain intensity, immune function, aerobic capacity, quality of life, and patient engagement were conducted at postoperative day 1 (baseline), 4 weeks, 12 weeks, 6 months, and 1 year postoperatively.

At 12 weeks postoperatively, all observed indicators in the 3 groups showed significant improvement compared to the baseline levels (P<0.05). Baduanjin exercise resulted in the most pronounced improvements in immune function indicators (CD4⁺/CD8⁺ ratio, IgA, and IgG levels), pain intensity, dyspnea score, quality of life score, and treatment engagement, outperforming the other two trainings (P<0.05). The patients in bedside cycle ergometer group showed significantly more obvious improvements in forced expiratory volume in one second (FEV1), 6-min walking distance, and peak oxygen uptake (VO₂peak) than those in balloon-blowing training group (P<0.05), but these improvements did not differ significantly from those observed in Baduanjin group (P>0.05). Balloon-blowing training resulted in only limited overall improvements of the measured indicators.

Baduanjin, bedside cycle ergometer training and balloon-blowing training are all effective rehabilitation methods after video-assisted thoracoscopic radical resection for lung cancer. Personalized rehabilitation choices can be provided for patients based on their rehabilitation needs.

To investigate the effects of remimazolam administered during anesthesia induction on hemodynamics and postoperative renal function in patients undergoing laparoscopic partial nephrectomy (LPN).

Clinical data of 265 renal tumor patients undergoing LPN between January, 2022 and December, 2024 were collected. The patients were divided into control group and remimazolam group (0.2 mg/kg for induction), and after propensity score matching (PSM), 65 patients in each group were included. Mean arterial pressure (MAP) and heart rate (HR) were recorded before induction (T₀), immediately after induction (T₁), immediately after intubation (T₂), and 10 min after intubation (T₃). Renal function indicators at 24 h postoperatively and incidences of acute kidney injury (AKI) were recorded. Estimated glomerular filtration rates (eGFRsCr, eGFRCys-C, and eGFRdiff) were calculated using serum creatinine (sCr) and cystatin C (Cys-C). From 36 patients in control group and 41 patients in remimazolam group followed up for 3-12 months, eGFRsCr data were collected to evaluate the incidence of chronic kidney disease (CKD) and analyze its correlation with AKI.

After PSM and covariate adjustment, remimazolam group showed significantly smaller changes than control group in ΔMAP at T3 (-20.11±11.65 vs -13.54±12.75 mmHg, P<0.05), ΔHR at T2 (-3.78±11.18 vs 2.82±10.79 min^-1, P<0.05), and ΔHR at T3 (-10.85±15.54 vs -3.35±11.67 min^-1, P<0.05). The remimazolam group showed significantly higher postoperative Cys-C level than the control group [0.96 (0.96, 1.03) vs 0.91 (0.77, 1.01), P<0.05] but lower eGFRCys-C at 24 h (83.65±9.84 vs 94.83±20.92, P<0.05). eGFRdiff showed a significant negative shift in remimazolam group (18.55±17.06 vs 8.52±15.85, P<0.05). Other indicators did not differ significantly between the two groups. AKI showed a significant correlation with CKD following LPN (P<0.05).

Compared with propofol, remimazolam induction improves hemodynamic stability during anesthesia induction but does not reduce the incidences of postoperative AKI or CKD after LPN.

People with cancer are at increased cardiovascular risk due to treatment-related cardiotoxicity and shared risk factors. Exercise-based cardiac rehabilitation (exCR) may mitigate these risks, but access to center-based programs is limited. This systematic review and meta-analysis evaluated the effectiveness, safety, and adherence of home-based exCR in oncology populations.

Six databases were searched in January 2025 for randomized controlled trials (RCTs) of home-based exCR in adults with cancer. Eligible interventions included structured aerobic and/or resistance exercise consistent with established CR guidelines. Primary outcomes were cardiorespiratory fitness (CRF), health-related quality of life (HRQoL), adherence, and safety. Random-effects meta-analyses used standardized mean differences (SMDs).

Nine RCTs (632 participants) were included. Home-based exCR improved CRF (SMD 0.42; 95% CI 0.09-0.75; I²=62%) and HRQoL (SMD 0.63; 95% CI 0.05-1.22; I²=84%). TESTEX scores indicated generally good methodological and reporting quality (mean 10/15; range 7-13). Adherence exceeded 75% in most studies reporting this outcome, and dropout was 15.2%. Adverse-event reporting was inconsistent; no clear safety signal emerged, but evidence was insufficient for firm conclusions. Strength and fatigue findings were inconsistent.

Home-based exCR appears feasible and may improve CRF and HRQoL in people with cancer, offering an accessible alternative or complement to center-based rehabilitation. Incomplete adverse-event reporting limits safety conclusions. Future studies should evaluate full, multi-component CR models in oncology.

Quality of life (QoL) is important for patients with metastatic breast cancer (MBC). We examined QoL in daily life among patients with MBC using ecological momentary assessment (EMA).

From 2023 to 2024, patients with MBC were recruited from 5 Mid-Atlantic sites. Eligible patients were English- or Spanish-speaking, with a life expectancy > 6 months and access to a smartphone. Participants were invited to complete 12 EMAs over 4 weeks. EMAs assessed global QoL, symptom severity (depression, anxiety, pain, fatigue, slowed cognition, appetite loss, nausea, gastrointestinal distress, decreased libido), and positive affect (social connection, peace, joy). Multilevel mixed-effects models analyzed the relationships between QoL and between-person and within-person variations in symptom severity and positive affect. We also explored associations between QoL and years since MBC diagnosis at the time of study entry.

Participants (N = 108; Mean age 57.8 years) were a mean of 4.4 years post-diagnosis (range = 0.06-20.65 years). Between-person effects indicated QoL was worse among individuals reporting more nausea (β = -0.109, p = 0.035) and less joy (β = 0.593, p < 0.001). Within-person effects indicated individuals' QoL was lower at times when they had more depression (β = -0.177, p < 0.001), anxiety (β = -0.049, p = 0.023), fatigue (β = -0.052, p = 0.009), appetite loss (β = -0.053, p = 0.028), and decreased libido (β = -0.058, p = 0.036) and less social connectedness (β = 0.091, p = 0.001), joy (β = 0.055, p = 0.047), and peace (β = 0.107, p < 0.001) than their personal average. QoL was not associated with years since MBC diagnosis (β = 0.106, p = 0.956). Age (β = 0.482, p = 0.013) and being partnered (β = 13.356, p = 0.005) at baseline were positively associated with estimated QoL at MBC diagnosis. Changes in QoL per year since MBC diagnosis were positively associated with being employed at baseline (β = 2.453, p < 0.001) and negatively associated with HR positive disease (β = -1.334, p = 0.001).

Both within-person and between-person variations in symptom severity and positive affect are associated with QoL, highlighting the need for adaptive, targeted intervention strategies to optimize QoL for all patients.

The optimal chemotherapy strategy after progression on cyclin-dependent kinase 4/6 inhibitors (CDK4/6i) in hormone receptor-positive/human epidermal growth factor receptor 2-negative (HR+/HER2-) metastatic breast cancer remains a matter of controversy. This study evaluated the efficacy of metronomic chemotherapy compared with other post-CDK4/6i treatment strategies in a real-world setting.

This retrospective multicenter study included patients with HR+/HER2- metastatic breast cancer progressing on CDK4/6i plus endocrine therapy and subsequently treated with systemic therapy. Progression-free survival (PFS) was the primary endpoint. Secondary endpoints included overall survival (OS), objective response rate (ORR), clinical benefit rate (CBR), and safety. Propensity score matching (1:2) was performed to reduce selection bias.

A total of 177 patients were included, of whom 52 (29.4%) received metronomic chemotherapy. Among treatment strategies, metronomic chemotherapy achieved the longest median PFS (9 months; 95% CI: 5.46-12.53; p = 0.003). In multivariable analysis, metronomic chemotherapy was independently associated with prolonged PFS (HR 0.46, 95% CI: 0.30-0.69; p < 0.001). Median OS did not significantly differ across treatment groups. ORR was 48.0%, and CBR was 60.0% with metronomic chemotherapy. After propensity score matching, metronomic chemotherapy maintained a significant association with improved PFS (HR 0.49, 95% CI: 0.31-0.78; p = 0.003). Toxicities were predominantly Grade 1-2, with no severe adverse events reported in the metronomic cohort.

In this real-world study, metronomic chemotherapy was associated with improved disease control and a favorable safety profile in patients with HR+/HER2- metastatic breast cancer progressing after CDK4/6i-based therapy.

Protocol Number 0037558/23.

Estrogen receptor (ER)-positive/HER2-positive breast cancer demonstrates significantly lower rates of pathological complete response (pCR) to neoadjuvant HER2-targeted therapies compared to ER-negative/HER2-positive disease. However, the optimal ER positivity cutoff for clinically meaningful patient stratification remains undefined.

We analyzed a retrospective cohort of 741 HER2-positive breast cancer patients treated with neoadjuvant chemotherapy plus dual HER2 blockade (trastuzumab and pertuzumab) at Sun Yat-sen University Cancer Center. The optimal ER cutoff for predicting pCR was determined by ROC analysis with Youden index and validated by bootstrap resampling (1000 iterations). Transcriptomic data from TCGA and SCAN-B cohorts were analyzed to characterize biological differences between ER subgroups. Drug response was predicted using the oncoPredict algorithm, and cancer dependency was assessed using DepMap CRISPR screening data.

ER ≥ 50% positivity was identified as the optimal predictive cutoff (bootstrap 95% CI: 25.0%-77.5%) and was an independent predictor of significantly lower pCR rates in multivariate analysis (OR = 0.27; 95% CI: 0.19-0.40; p < 0.001). Transcriptomic analysis revealed that ER ≥ 50% tumors are characterized by activated estrogen response signaling, downregulated cell cycle and immune pathways. Predicted resistance to trastuzumab, T-DM1, and T-DXd was consistently enriched in this subgroup, consistent with lower HER2 and CD16A expression observed in ER ≥ 50% tumors. CCND1, a canonical transcriptional target of ESR1, was significantly upregulated in ER ≥ 50% tumors across both cohorts, and ER + /HER2 + cell lines exhibited significantly higher CCND1 and CDK4 dependency scores in DepMap CRISPR screening (p < 0.05), supporting activation of the ESR1-CCND1-CDK4/6 axis in this subgroup.

ER ≥ 50% positivity defines a clinically and biologically distinct HER2-positive subgroup with poor response to standard neoadjuvant therapy and predicted resistance to ADCs, consistent with lower HER2 and CD16A expression in this subgroup. The convergent transcriptomic and functional evidence for ESR1-CCND1 axis activation provides mechanistic support for combining CDK4/6 inhibitors with endocrine and anti-HER2 therapies to improve outcomes in this resistant subgroup.

CD169+ cells represent a distinct subset of macrophages with potential immunomodulatory roles, but their function in colorectal cancer (CRC) progression remains unclear. This study focuses on the spatial profiling and prognostic significance of CD169+ macrophages in adjacent nontumor mucosa (NM), primary CRC (pCRC), and synchronous or metachronous liver metastases (LM).

We enrolled into this retrospective cohort study patients who underwent resection of both pCRC with adjacent NM and synchronous LM (N = 55) or metachronous LM (N = 44). We applied immunohistochemical staining and computer-assisted image analysis to quantify CD169+ cell density in the NM, pCRC, synchronous, and metachronous LM. Correlations between CD169+ macrophages and T cells were evaluated. Associations between CD169+ cell density and overall survival (OS) of the patients were assessed.

CD169+ cell density was greater in NM than in the tumor center (TC) of pCRC and in the peritumor (PT) region of LM compared to pCRC. The synchronous group exhibited a higher density of CD169+ cells than the metachronous group in the inner margin (IM) of pCRC, the TC, and the outer margin (OM) of LM. CD169+ cells were more abundant in the exterior than in the interior tumor areas in both pCRC and LM. Positive correlations were observed between densities of CD169+ macrophages with CD3+ and CD8+ lymphocytes. In the synchronous group, a high density of CD169+ macrophages in the TC of pCRC was associated with longer OS, whereas a high density in the PT of LM was associated with shorter OS. High density of CD169+ macrophages in the OM of metachronous LM was associated with poor survival.

Our study highlights context-dependent prognostic associations of CD169+ macrophages in CRC. While high CD169+ macrophage density in the TC of pCRC was linked to favorable survival in the synchronous group, increased density in both synchronous and metachronous LM was associated with adverse outcomes. Further prospective studies and functional investigations are needed to validate these observations.

Head and neck cancer (HNC) trials have demonstrated pathological complete response (pCR) in patients receiving neoadjuvant treatment prior to surgery; however, systematic reviews have reported marked variation in pCR rates. This scoping review was designed to determine the definition, criteria, and assessment methodologies for pCR in interventional neoadjuvant HNC clinical trials. The review was conducted in accordance with the JBI Manual for Evidence Synthesis and the protocol prospectively registered. Medical databases, trial registries, and grey literature were systematically searched, and eligibility criteria applied. Study characteristics and pCR assessment methodologies were extracted and described. A total of 4,931 sources were identified, and screening identified 114 trials. Only 22 studies had publicly accessible protocols for assessment. Trials were initiated between 1989 and 2025, and the majority were phase II investigating chemotherapy + immunotherapy regimens (51%). pCR was most frequently classified as a secondary endpoint (55%), and reported pCR rates ranged from 0% to 100%. There was heterogeneity and incomplete documentation in both specimen preparation and pCR assessment. Where specified, most included assessment at both primary tumour and lymph nodes (50 of 69; 72%), and quantitative assessment calculating percentage residual viable tumour was common. While no formal guidelines for pCR assessment in HNC were identified, one trial outlined an immune-related pathological response criteria for oral squamous cell carcinoma, and another included a detailed 'pathological response assessment' proforma. Citation of methodologies used in other cancers, for example, lung and breast cancer, was a recurring theme. Based on these findings, we propose pragmatic definitions, assessment considerations, and a structured reporting proforma to support increased transparency and reproducibility in pCR reporting. While these proposed elements are not consensus based, they provide a foundation for harmonisation efforts and highlight priorities for development of international consensus guidelines to enable meaningful comparison of interventions and determine the validity of pCR as a surrogate endpoint in HNC.

Cellular senescence and regulated cell death represent two fundamental but intricately connected biological programs that govern tumor cell fate. Cellular senescence can suppress tumor growth by inducing stable cell-cycle arrest and promoting immune clearance, but persistent senescent cells may also drive tumor progression through the senescence-associated secretory phenotype (SASP). Concurrently, multiple modalities of regulated cell death-including apoptosis, ferroptosis, cuproptosis, necroptosis, pyroptosis, parthanatos, and autophagy-dependent cell death-have emerged as critical determinants of therapeutic response. The crosstalk between senescence and cell death is orchestrated by key molecular hubs including p53, mitochondria, autophagy machinery, and epigenetic regulators. In this review, we summarize the hallmarks and classification of cellular senescence in cancer, outline major cell death modalities, discuss the cross-regulatory networks linking senescence and death, and highlight emerging therapeutic strategies that target these interconnected processes for cancer treatment.

Cancer-associated fibroblasts (CAFs) act as key drivers of cancer progression and therapeutic resistance within the tumor microenvironment, but their diverse and context-dependent functions complicate therapeutic targeting. The limited clinical efficacy of CAF-targeting therapeutics has prompted a critical reassessment of CAF biology, therapeutic development, and emerging CAF-directed strategies. Unlike prior reviews that predominantly focused on CAF heterogeneity or isolated therapeutic modalities, this review systematically compares pharmacological and biologic CAF-targeting therapeutics, multifunctional nanomedicines, and biologically inspired and living platforms in terms of their underlying mechanisms of action and translational bottlenecks. Drawing on clinical evidence from CAF-targeting therapeutics, we identify several interconnected barriers to successful translation, including CAF heterogeneity and plasticity, patient-selection and biomarker limitations, preclinical-clinical mismatch and combination-treatment dependency, insufficient tumor penetration and systemic toxicity, and signaling redundancy and pathway compensation. Importantly, lessons from unsuccessful clinical trials are used to critically reassess whether current CAF-targeting nanomedicines and platforms adequately address these barriers. In parallel, we evaluate platform-specific translational challenges, particularly those related to biosafety and manufacturing feasibility. These analyses highlight the persistent gaps between the evolving understanding of CAF functional states, existing design rationales for nanomedicine and platforms, and real-world clinical practice. Future directions should therefore prioritize the identification of functionally defined CAF states, the optimization of clinically relevant models of advanced disease, and the development of therapeutic platforms tailored to clearly defined clinical needs. Finally, we propose an iterative translational roadmap and a hypothesis-generating sequential cancer cell/CAF dual-targeting framework to guide the development of clinically translatable CAF-directed therapies.