{"title":"Erratum to: Superenhancers activate the autophagy-related genes Beclin1 and LC3B to drive metastasis and drug resistance in osteosarcoma.","authors":"Hongyi Wang, Zhuochao Liu, Jun Wang, Fangqiong Hu, Qi Zhou, Li Wei, Qiyuan Bao, Jizhuang Wang, Jing Liang, Zhihong Liu, Weibin Zhang","doi":"10.1007/s11684-026-1259-2","DOIUrl":"10.1007/s11684-026-1259-2","url":null,"abstract":"","PeriodicalId":521275,"journal":{"name":"MedScience","volume":" ","pages":"574"},"PeriodicalIF":0.0,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148582165","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
MedSciencePub Date : 2026-04-01Epub Date: 2026-04-20DOI: 10.1007/s11684-026-1211-5
Hongming Deng, Junyi Li, Lin-Rui Gao, Ning Huang, Chenxi Wang, Zefen Xiao, Xiaobing Wang, Liming Wang, Ting Xiao, Mei Liu
{"title":"Secretory leukocyte peptidase inhibitor as a dynamic radiotherapy response biomarker in esophageal squamous cell carcinoma.","authors":"Hongming Deng, Junyi Li, Lin-Rui Gao, Ning Huang, Chenxi Wang, Zefen Xiao, Xiaobing Wang, Liming Wang, Ting Xiao, Mei Liu","doi":"10.1007/s11684-026-1211-5","DOIUrl":"10.1007/s11684-026-1211-5","url":null,"abstract":"<p><p>Esophageal cancer is the seventh leading cause of cancer-related deaths, with most cases diagnosed at locally advanced stages. Chemoradiotherapy is one of the most effective treatments for these patients. However, high rates of recurrence persist, highlighting the need for more reliable prognostic biomarkers. In this study, we identified immune-related prognostic genes through bulk (n = 119) and single-cell (n = 60) transcriptomic analyses. We then used Western blotting, enzyme-linked immunosorbent assay (ELISA), and immunofluorescence to preliminarily investigate the potential biological functions of the candidate biomarker. The clinical prognostic utility of the candidate biomarker was validated in an independent cohort (n = 91) via ELISA of serum samples collected before and during chemoradiotherapy. The results showed that low expression of the secretory leukocyte peptidase inhibitor (SLPI) significantly correlated with tumor progression and poor prognosis. In epithelial cells, reduced SLPI expression was associated with decreased activation of differentiation-related pathways. Furthermore, SLPI expression levels were found to influence fibroblast phenotypes, with exogenous SLPI inhibiting the NF-κB pathway and restoring fibroblast quiescence. The results of ELISA showed that dynamic changes in serum SLPI levels during chemoradiotherapy serve as an independent prognostic factor. In conclusion, serum SLPI levels represent an easy-to-detect biomarker for dynamically monitoring the efficacy of chemoradiotherapy.</p>","PeriodicalId":521275,"journal":{"name":"MedScience","volume":" ","pages":"311-328"},"PeriodicalIF":0.0,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147731146","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
MedSciencePub Date : 2026-04-01Epub Date: 2026-05-16DOI: 10.1007/s11684-026-1216-0
Xin Xu, Chengnan Guo, Tingting Zhang, Yuqi Liang, Bingjie Tian, Ping Liu, Joanne W Y Chung, Liping Jiang
{"title":"Heavy drinking amplifies the risk of cardiometabolic multimorbidity attributed to adverse childhood experiences in middle-aged and older Chinese adults.","authors":"Xin Xu, Chengnan Guo, Tingting Zhang, Yuqi Liang, Bingjie Tian, Ping Liu, Joanne W Y Chung, Liping Jiang","doi":"10.1007/s11684-026-1216-0","DOIUrl":"10.1007/s11684-026-1216-0","url":null,"abstract":"<p><p>To examine longitudinal associations between adverse childhood experiences (ACEs) and cardiometabolic multimorbidity (CMM) and to assess whether unhealthy lifestyles modify these associations. This study utilized data from 5 waves of the China Health and Retirement Longitudinal Study (CHARLS). The study population comprised 11 200 participants aged 45 years or older, with available data on CMM and all 12 ACE indicators. The longitudinal associations between ACEs and CMM were assessed by generalized estimating equation (GEE) regression models. A mediation analysis examined the potential causal chain in which unhealthy lifestyle scores mediate the relationship between ACEs and CMM. A total of 11 200 participants were eligible for our analysis (mean (SD) age, 58.1 (8.8) years; 5839 (52.1%) were females), and 949 (8.47%) reported four or more ACEs. Compared with those without ACE exposure, participants who experienced four or more ACEs had an increased risk of CMM (odds ratio (OR), 1.40; 95% confidence interval (CI), 1.08-1.83). Drinking status significantly modified the associations between ACE groups and CMM (P for interaction = 0.034). Mediation analyses showed that unhealthy lifestyles partially explained 8.59% (95% CI, 0.56%-16.62%) of the relationship between ACEs and CMM. Childhood adverse events contribute to the development of CMM, and this effect is more significant in people who drink alcohol. Unhealthy lifestyles can aggravate the health inequity of ACEs on CMM.</p>","PeriodicalId":521275,"journal":{"name":"MedScience","volume":" ","pages":"358-366"},"PeriodicalIF":0.0,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147960671","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Targeting circSFPQ_008/SFPQ/BRCA1 axis for overcoming platinum resistance in ovarian cancer.","authors":"Yinan Jiang, Dongmei Zhou, Yan Liu, Baixue Li, Renci Liu, Jianqi Li, Xiujie Sheng","doi":"10.1007/s11684-026-1201-7","DOIUrl":"10.1007/s11684-026-1201-7","url":null,"abstract":"<p><p>Platinum resistance is the main cause of treatment failure in ovarian cancer. BRCA1/2-mediated DNA damage repairment is an important factor contributing to platinum resistance in ovarian cancer. Altering the expression levels of BRCA1/2 will affect the platinum sensitivity of ovarian cancer. We used proteomics to screen out SFPQ, which bound to BRCA1 with a high abundance. However, the role and potential mechanism of SFPQ in the progression of ovarian cancer remain unclear. Through immunohistochemical staining, we found that SFPQ was overexpressed in ovarian cancer tissues and associated with poor prognosis of patients. Functional analysis showed that SFPQ binds to BRCA1 and inhibits its ubiquitination and degradation, increases the expression level of BRCA1, and promotes platinum resistance of ovarian cancer. Exploration of the upstream mechanism revealed that hsa_circSFPQ_008, which was derived from the SFPQ parental gene, recruits HDAC1 to modify H3K27Ac of the SFPQ promoter and regulates its expression. This study reveals a novel regulatory mechanism by which SFPQ is involved in platinum resistance of ovarian cancer, providing a new theoretical basis for the individualized and precise treatment of ovarian cancer.</p>","PeriodicalId":521275,"journal":{"name":"MedScience","volume":" ","pages":"329-344"},"PeriodicalIF":0.0,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147597806","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
MedSciencePub Date : 2026-04-01Epub Date: 2026-04-20DOI: 10.1007/s11684-026-1222-2
Qian Liu, Yimin Chen, Hu Zhou
{"title":"Proteogenomics: decoding cancer in multiple dimensions.","authors":"Qian Liu, Yimin Chen, Hu Zhou","doi":"10.1007/s11684-026-1222-2","DOIUrl":"10.1007/s11684-026-1222-2","url":null,"abstract":"<p><p>A key challenge in cancer precision oncology is the limited ability of genomic analyses to accurately predict changes in protein expression or function, even though proteins serve as the main targets of numerous modern therapies. Bridging this gap necessitates precise quantification of proteins and their post-translational modifications (PTMs). Recent advances in mass spectrometry (MS)-based proteomics now enable large-scale, quantitative characterization of proteins and PTMs in tumor tissues. To link genomic aberrations to cancer phenotypes, the emerging field of proteogenomics integrates proteomic data, including PTMs, with genomic, epigenomic, and transcriptomic information. This comprehensive approach offers a deeper understanding of cancer biology at multiple levels. This review highlights recent advancements in MS-based proteomics, key discoveries in cancer proteogenomics, and the transformative potential of this field in decoding the complexities of cancer across diverse dimensions.</p>","PeriodicalId":521275,"journal":{"name":"MedScience","volume":" ","pages":"203-230"},"PeriodicalIF":0.0,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147731141","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
MedSciencePub Date : 2026-04-01Epub Date: 2026-05-08DOI: 10.1007/s11684-026-1215-1
Qingzhe Wu, Tingting Hou, Hai Song
{"title":"Unraveling the intricacies of small cell lung cancer: FAK splicing variants as a new feature and therapeutic vulnerability of small cell lung cancer.","authors":"Qingzhe Wu, Tingting Hou, Hai Song","doi":"10.1007/s11684-026-1215-1","DOIUrl":"10.1007/s11684-026-1215-1","url":null,"abstract":"","PeriodicalId":521275,"journal":{"name":"MedScience","volume":" ","pages":"387-391"},"PeriodicalIF":0.0,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147849390","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Association of sarcopenia with the long-term risk of overall infections and infectious diseases: a prospective cohort study of 458 332 participants.","authors":"Meng Gao, Bolong Liu, Hequn Chen, Zewu Zhu, Juliet Matsika, Minghui Liu, Jiao Hu, Xiaogen Kuang, Jinbo Chen","doi":"10.1007/s11684-026-1224-0","DOIUrl":"10.1007/s11684-026-1224-0","url":null,"abstract":"<p><p>Sarcopenia, characterized by the progressive loss of muscle strength and mass, is a condition linked to increased frailty and mortality. However, its role in heightening the susceptibility to infections and infectious diseases remains unclear. This study aimed to investigate the long-term associations between sarcopenia and the risk of overall infections and infectious diseases using data from a large prospective cohort of 465 592 adults. Participants were categorized into three groups: non-sarcopenia, probable sarcopenia, and confirmed sarcopenia. Over a median follow-up of 12.5 years, compared with participants without sarcopenia, those with probable sarcopenia had a hazard ratio (HR) of 1.18 (95% confidence interval (CI) 1.15-1.21), and those with confirmed sarcopenia had an HR of 1.34 (95% CI 1.21-1.48) for developing infections or infectious diseases. The study also found that handgrip strength and muscle mass were independently associated with an increased risk of infections. These findings indicate that sarcopenia and low muscle strength are important markers of increased infection risk in the general population and highlight the need for further research, particularly in younger adults with low muscle strength, to determine whether interventions to improve muscle strength and mass can reduce infection risk.</p>","PeriodicalId":521275,"journal":{"name":"MedScience","volume":" ","pages":"345-357"},"PeriodicalIF":0.0,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147960563","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Brain-body interactions in systemic diseases: a survey from an imaging perspective.","authors":"Fan Li, Shilun Zhao, Zhichao Liang, Zhuoting Xu, Shuwei Bai, Weilin Zhou, Qiankun Zheng, Wei Yan, Luoyu Wang, Kaicong Sun, Han Zhang, Dinggang Shen","doi":"10.1007/s11684-026-1229-8","DOIUrl":"10.1007/s11684-026-1229-8","url":null,"abstract":"<p><p>Many diseases are now recognized as systemic, involving extensive crosstalk between brain and body. Although existing reviews have elucidated the biochemical basis of these brain-body connections, their dynamic interactions remain largely unexplored by imaging approaches. To fill this gap, this review investigates brainbody axes from an imaging perspective across three research paradigms: (1) the impact of brain diseases on the body, including Alzheimer's disease, Parkinson's disease, psychiatric disorders, and cerebral small vessel disease; (2) the influence of body diseases on the brain, particularly those originating in the eye, heart, liver, and gut; and (3) the new frontier encompassing multi-organ data acquisition and integrative modeling methods for brain-body interactions. Spanning from biological hypotheses and inter-organ crosstalk to recent technical advances, this review not only summarizes the systemic manifestations of diseases across organs but also offers perspectives toward improved diagnostics and therapies. The integration of whole-body networks from an imaging perspective holds promise for advancing precision medicine and provides a new paradigm for investigating and diagnosing complex systemic diseases.</p>","PeriodicalId":521275,"journal":{"name":"MedScience","volume":" ","pages":"268-300"},"PeriodicalIF":0.0,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148039262","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}