J Hazard Mater. 2025 Jun 23;495:139049. doi: 10.1016/j.jhazmat.2025.139049. Online ahead of print.ABSTRACTBACKGROUND: Chronic arsenic exposure is a global health concern linked to pulmonary diseases like fibrosis. However, its precise molecular mechanisms remain unclear. This study explored the effects of chronic arsenic exposure on a murine model (via diet) and BEAS-2B cells, focusing on oxidative stress, lipid peroxidation, mitochondrial dysfunction, and ferroptosis-mediated cell death.METHODS
J Hazard Mater. 2025 Jun 23;495:139049. doi: 10.1016/j.jhazmat.2025.139049. Online ahead of print.
ABSTRACT
BACKGROUND: Chronic arsenic exposure is a global health concern linked to pulmonary diseases like fibrosis. However, its precise molecular mechanisms remain unclear. This study explored the effects of chronic arsenic exposure on a murine model (via diet) and BEAS-2B cells, focusing on oxidative stress, lipid peroxidation, mitochondrial dysfunction, and ferroptosis-mediated cell death.
METHODS: BEAS-2B cells were exposed to 1 μmol/L NaAsO₂ for 30 passages. Oxidative stress was assessed via ROS quantification, GSH depletion, and T-SOD activity. Lipid peroxidation was measured using BODIPY fluorescence and MDA levels. Mitochondrial dysfunction was determined by mtROS imaging and JC-1 staining. Ferroptosis was analyzed through GPX4 expression and TEM-based mitochondrial integrity. A 14-month murine model evaluated histopathology, metabolomic dysregulation, and gut-lung axis crosstalk.
RESULTS: Arsenic exposure significantly increased ROS, depleted GSH, and reduced T-SOD activity. Lipid peroxidation and mitochondrial dysfunction were evident, with more than 60 % decline in GPX4. Murine lung histology showed alveolar thickening, inflammatory infiltration, and elevated IL-6, TNF-α, and VEGF. Metabolomic analysis revealed disrupted lipid metabolism, correlating with ferroptosis markers (Acetyl-carnitine, L-Acetylcarnitine).
CONCLUSIONS: This was the first study to demonstrate ferroptosis as a key mechanism in arsenic-induced lung epithelial damage using a 14-month murine model and a 30-passage cellular model. We further demonstrated that ferroptosis induced by chronic exposure becomes functionally irreversible, as ferroptosis inhibition by Ferrostatin-1 failed to rescue GPX4 expression, unlike prior acute exposure models.
Ann Surg Oncol. 2025 Jul 3. doi: 10.1245/s10434-025-17738-3. Online ahead of print.ABSTRACTBACKGROUND: This study aimed to identify the most effective drug therapeutics for patients with the mesenchymal subtype of advanced gastric cancer (AGC). Extensive research employing diverse omics methodologies has unveiled a varied landscape of AGC. Recent progress in next-generation sequencing and other genomic technologies has facilitated a more intricate exploration of AGC at the molecular level. Nonet
Ann Surg Oncol. 2025 Jul 3. doi: 10.1245/s10434-025-17738-3. Online ahead of print.
ABSTRACT
BACKGROUND: This study aimed to identify the most effective drug therapeutics for patients with the mesenchymal subtype of advanced gastric cancer (AGC). Extensive research employing diverse omics methodologies has unveiled a varied landscape of AGC. Recent progress in next-generation sequencing and other genomic technologies has facilitated a more intricate exploration of AGC at the molecular level. Nonetheless, the optimal treatment for patients with the mesenchymal subtype of gastric cancer remains elusive. Lei's molecular classification of AGC is based on gene expression profiles named "mesenchymal," "immunogenic," "classical," and "metabolic."
PATIENTS AND METHODS: Based on RNA-seq transcriptome, 234 patients were divided into four molecular subtypes: mesenchymal (n = 96), immunogenic (n = 37), metabolic (n = 61), and classic (n = 40).
RESULTS: Among those with mesenchymal-subtype AGC, compared with non-Apatinib group, the Apatinib treatment group demonstrated a significant increase in objective response rate (ORR 89.3% versus 69.3%, p = 0.038; odds ratio (OR) 0.269, 95% confidence interval (CI) (0.073-0.989)); overall survival (OS) 89.3% versus 60.2%, p = 0.010; hazard ratio (HR) 0.241, 95% CI (0.073-0.796)) and disease-free survival (DFS 78.6% versus 52.9%, p = 0.031; HR 0.400, 95% CI (0.167-0.956)). Furthermore, Apatinib significantly reduced the risk of death and recurrence in patients with mesenchymal subtype (OS: HR 0.129, 95% CI (0.030-0.563), p = 0.006; DFS: HR 0.340, 95% CI (0.138-0.833), p = 0.018). However, no significant differences were observed in the ORR, OS, or DFS between patients with metabolic and classical subtypes who underwent combination chemotherapy with additional Apatinib or camrelizumab.
CONCLUSIONS: Our analysis has revealed that, for neoadjuvant therapy in AGC, the mesenchymal subtype stands out as the ideal patient population benefiting from Apatinib.
Nature, Published online: 02 July 2025; doi:10.1038/s41586-025-09096-7The Somatic Mosaicism across Human Tissues Network aims to create a reference catalogue of somatic mosaicism across different tissues and cells within individuals.
The Somatic Mosaicism across Human Tissues Network aims to create a reference catalogue of somatic mosaicism across different tissues and cells within individuals.
Sci Rep. 2025 Jul 1;15(1):21173. doi: 10.1038/s41598-025-08986-0.ABSTRACTEffective clinical management of patients with cancer requires highly accurate diagnosis, precise therapy selection, and highly sensitive monitoring of disease burden. Caris Assure is a multifunctional blood-based assay that couples whole exome and whole transcriptome sequencing on plasma and leukocytes with advanced machine learning techniques to satisfy all three clinical testing needs on one platform. Caris Assure for th
Effective clinical management of patients with cancer requires highly accurate diagnosis, precise therapy selection, and highly sensitive monitoring of disease burden. Caris Assure is a multifunctional blood-based assay that couples whole exome and whole transcriptome sequencing on plasma and leukocytes with advanced machine learning techniques to satisfy all three clinical testing needs on one platform. Caris Assure for therapy selection was CLIA validated using 1,910 samples. 376,197 tissue profiles along with 7,061 paired blood and tissue profiles were used to engineer features for three machine learning models. The MCED model was trained on 1,013 patients and validated on an independent set of 2,675 patients. The tissue of origin for MCED model was trained on 1,166 samples and validated using 5-fold cross validation. The MRD & Monitoring model was trained on 3,439 patients and validated on two independent sets of 86 patients for MRD and 101 patients for monitoring. For early detection, sensitivities for stages I-IV cancers (n = 284, 129, 90, 23 respectively) were 83.1%, 86.0%, 84.4%, and 95.7%, all at 99.6% specificity (n = 2149). The diagnostic first-line procedure for tissue of origin was determined for 8 categories with a top-3 accuracy of 85% for stage I and II cancers. Detection of driver mutations for therapy selection from blood collected within 30 days of matched tumor tissue, demonstrated high concordance (PPA of 93.8%, PPV of 96.8%) using CHIP subtraction. For MRD and recurrence monitoring, the disease-free survival of patients whose cancers were predicted to have an event was significantly shorter than those predicted not to have an event using a tumor naïve approach (HR = 33.4, p < 0.005, HR = 4.39, p = 0.008, respectively). The data presented here demonstrate a unified liquid biopsy platform that uses blood-based whole-exome and transcriptome sequencing coupled with artificial intelligence to address the important clinical needs in multi-cancer early detection, monitoring of MRD and recurrent cancers, and precision selection of molecularly targeted therapies.
J Am Soc Mass Spectrom. 2025 Aug 6;36(8):1598-1608. doi: 10.1021/jasms.4c00505. Epub 2025 Jul 2.ABSTRACTGastric signet ring cell carcinoma (GSRC) is an aggressive subtype of gastric cancer (GC) with a poor prognosis. The lack of a systematic molecular and metabolic heterogeneity overview has led to slow progress in clinical practice. This study used mass spectrometry imaging (MSI) to investigate the metabolic landscape of GSRC in GC tissue with various differentiation grades. Our comprehensive s
J Am Soc Mass Spectrom. 2025 Aug 6;36(8):1598-1608. doi: 10.1021/jasms.4c00505. Epub 2025 Jul 2.
ABSTRACT
Gastric signet ring cell carcinoma (GSRC) is an aggressive subtype of gastric cancer (GC) with a poor prognosis. The lack of a systematic molecular and metabolic heterogeneity overview has led to slow progress in clinical practice. This study used mass spectrometry imaging (MSI) to investigate the metabolic landscape of GSRC in GC tissue with various differentiation grades. Our comprehensive spatial profiling of metabolites and lipids unveiled distinct metabolic signatures across different tissue subregions. A substantial number of lipidomic biomarkers associated with GSRC were identified, including phosphatidylethanolamine N-methyl (PE-NMe), phosphatidylethanolamine (PE), sphingomyelin (SM), diacylglycerol (DG), phosphatidic acid (PA), and phosphatidylcholine (PC), which may provide insights into its pathogenesis and potential therapeutic targets. Furthermore, multi-omics network analysis revealed intricate metabolic pathways involved in GSRC progression. Our findings highlight the importance of understanding the metabolic heterogeneity of GSRC and pave the way for future studies exploring its clinical implications and therapeutic strategies.
Nature, Published online: 01 July 2025; doi:10.1038/d41586-025-02016-9The decades-old limit on how long human embryos can be grown in culture is under debate. A new road map outlines how to extend the length of culture responsibly.
The decades-old limit on how long human embryos can be grown in culture is under debate. A new road map outlines how to extend the length of culture responsibly.
Nature, Published online: 30 June 2025; doi:10.1038/d41586-025-02034-7After a quarter of a century, the website remains an essential tool for navigating the genome and understanding its structure, function and clinical impact.
After a quarter of a century, the website remains an essential tool for navigating the genome and understanding its structure, function and clinical impact.
Eur J Trauma Emerg Surg. 2025 Jun 27;51(1):238. doi: 10.1007/s00068-025-02922-7.ABSTRACTPURPOSE: Obesity is a prevalent disease, but its influence on post-injury biology remains unclear. In this study, we aimed to characterize the independent effect of obesity on the proteomic and metabolomic signatures of trauma.METHODS: Plasma was obtained on arrival from injured patients at a Level 1 Trauma Center and analyzed with modern mass spectrometry-based proteomics and metabolomics. Samples obtained a
Eur J Trauma Emerg Surg. 2025 Jun 27;51(1):238. doi: 10.1007/s00068-025-02922-7.
ABSTRACT
PURPOSE: Obesity is a prevalent disease, but its influence on post-injury biology remains unclear. In this study, we aimed to characterize the independent effect of obesity on the proteomic and metabolomic signatures of trauma.
METHODS: Plasma was obtained on arrival from injured patients at a Level 1 Trauma Center and analyzed with modern mass spectrometry-based proteomics and metabolomics. Samples obtained after start of transfusion were excluded. Patients were stratified by "obesity" (body mass index [BMI]≥30 kg/m2) vs. "no obesity" (BMI < 30 kg/m2). In sub-group analyses, patients were sub-stratified by Low Injury/Low Shock (ISS < 15, base excess [BE]≥-6mEq/L) and High Injury/High Shock (ISS≥15, BE<-6). Multiple regression was used to adjust the omics data for significant covariates prior to performing ome-wide analyses.
RESULTS: There were 183 patients included (48 [26%] with obesity and 135 [74%] without). After covariate-adjustment, multiple proteins and metabolites were correlated with ISS and/or BE and were significantly different from Low Injury/Low Shock to High Injury/High Shock only in patients with obesity. This obesity-specific omics response to injury was characterized by increased inflammation, hypercoagulability, altered nitrogen metabolism, and mitochondrial dysfunction. Patients with obesity also exhibited excessive injury-provoked tissue destruction and organ damage compared to patients without obesity. In injury severity-adjusted analyses, the obesity signature consistently displayed markers of hemolysis, likely reflecting a pre-injury hemolytic propensity.
CONCLUSION: Obesity is independently associated with altered post-injury biology, which likely underlies unique pathology in trauma patients with obesity. Identifying this aberrant response to injury is the first step in developing personalized therapies for this patient population.
JCI Insight. 2025 Jun 26:e191595. doi: 10.1172/jci.insight.191595. Online ahead of print.ABSTRACTPancreatic ductal adenocarcinoma (PDAC) has a poor survival rate due to late detection. PDAC arises from precursor microscopic lesions, termed pancreatic intraepithelial neoplasia (PanIN), that develop at least a decade before overt disease--this provides an opportunity to intercept PanIN-to-PDAC progression. However, immune interception strategies require full understanding of PanIN and PDAC cellula
JCI Insight. 2025 Jun 26:e191595. doi: 10.1172/jci.insight.191595. Online ahead of print.
ABSTRACT
Pancreatic ductal adenocarcinoma (PDAC) has a poor survival rate due to late detection. PDAC arises from precursor microscopic lesions, termed pancreatic intraepithelial neoplasia (PanIN), that develop at least a decade before overt disease--this provides an opportunity to intercept PanIN-to-PDAC progression. However, immune interception strategies require full understanding of PanIN and PDAC cellular architecture. Surgical specimens containing PanIN and PDAC lesions from a unique cohort of five treatment-naïve patients with PDAC were surveyed using spatial-omics (proteomic and transcriptomic). Findings were corroborated by spatial proteomics of PanIN and PDAC from tamoxifen-inducible KPC (tiKPC) mice. We uncovered the organization of lymphoid cells into tertiary lymphoid structures (TLSs) adjacent to PanIN lesions. These TLSs lacked CD21+CD23+ B cells compared to more mature TLSs near the PDAC border. PanINs harbored mostly CD4+ T cells with fewer Tregs and exhausted T cells than PDAC. Peri-tumoral space was enriched with naïve CD4+ and central memory T cells. These observations highlight the opportunity to modulate the immune microenvironment in PanINs before immune exclusion and immunosuppression emerge during progression into PDAC.
This study demonstrates that extrachromosomal DNA (ecDNA) replication induces DNA double-strand breaks and activates the DNA damage response (DDR). The DDR pathways, such as alt-NHEJ, are critical for ecDNA maintenance in tumor cells. Mechanistic insights into ecDNA replication and maintenance unveil a therapeutic approach for treating tumors harboring ecDNA.
This study demonstrates that extrachromosomal DNA (ecDNA) replication induces DNA double-strand breaks and activates the DNA damage response (DDR). The DDR pathways, such as alt-NHEJ, are critical for ecDNA maintenance in tumor cells. Mechanistic insights into ecDNA replication and maintenance unveil a therapeutic approach for treating tumors harboring ecDNA.
Nature, Published online: 25 June 2025; doi:10.1038/s41586-025-09202-9Disruption of dendritic cell (DC) interstitial motility in the tumour microenvironment promotes immune evasion, and enhancement of DC interstitial motility offers a route for DC-centric immunotherapy.
Disruption of dendritic cell (DC) interstitial motility in the tumour microenvironment promotes immune evasion, and enhancement of DC interstitial motility offers a route for DC-centric immunotherapy.
Trends Mol Med. 2025 Jun 23:S1471-4914(25)00118-2. doi: 10.1016/j.molmed.2025.05.007. Online ahead of print.ABSTRACTGastric cancer (GC) remains a deadly disease because of late detection and limited treatment options at advanced stages. Treatment of patients with metastatic disease is based on chemotherapy, complemented by antibodies targeting HER2, VEGFR2, and more recently PD-1 or claudin 18.2. Further targets, such as FGFR2b, as well as novel drug classes including antibody-drug conjugates (A
Trends Mol Med. 2025 Jun 23:S1471-4914(25)00118-2. doi: 10.1016/j.molmed.2025.05.007. Online ahead of print.
ABSTRACT
Gastric cancer (GC) remains a deadly disease because of late detection and limited treatment options at advanced stages. Treatment of patients with metastatic disease is based on chemotherapy, complemented by antibodies targeting HER2, VEGFR2, and more recently PD-1 or claudin 18.2. Further targets, such as FGFR2b, as well as novel drug classes including antibody-drug conjugates (ADCs) and bispecific antibodies, are promising developments in GC treatment. Despite the failure of several targeted agents, the landscape of GC therapy is evolving rapidly, facilitated by umbrella or platform precision medicine trials. The integration of next-generation sequencing and other omics techniques into molecular tumor boards, as well as functional drug testing on patient-derived models, might bring us closer to personalized oncology and ultimately improve patient survival.
Front Immunol. 2025 Jun 6;16:1606125. doi: 10.3389/fimmu.2025.1606125. eCollection 2025.ABSTRACTBACKGROUND: Lung adenocarcinoma (LUAD) is characterized by metabolic and immune heterogeneity, driving tumor progression and therapy resistance. While G protein-coupled receptors (GPCR) signaling is known to regulate metabolism and immunity in cancers, its role in LUAD remains poorly defined. This study explores the influence of GPCR signaling on LUAD metabolism and immune landscape.METHODS: We perfor
Front Immunol. 2025 Jun 6;16:1606125. doi: 10.3389/fimmu.2025.1606125. eCollection 2025.
ABSTRACT
BACKGROUND: Lung adenocarcinoma (LUAD) is characterized by metabolic and immune heterogeneity, driving tumor progression and therapy resistance. While G protein-coupled receptors (GPCR) signaling is known to regulate metabolism and immunity in cancers, its role in LUAD remains poorly defined. This study explores the influence of GPCR signaling on LUAD metabolism and immune landscape.
METHODS: We performed non-negative matrix factorization (NMF) clustering of GPCR signaling genes in TCGA-LUAD cohort to identify distinct molecular subgroups. A prognostic model was developed based on GPCR signaling genes using least absolute shrinkage and selection operator (LASSO) analysis and Cox regression. Differentially expressed genes were analyzed for metabolic pathway enrichment and immune infiltration. In addition, key genes within GPCR signaling were identified and validated through functional assays.
RESULTS: NMF clustering based on GPCR signaling identified three subgroups in LUAD, with cluster 3 exhibiting poorer overall survival and significant enrichment in multiple prognostic associated metabolism pathways including purine, pyrimidine, glyoxylate and dicarboxylate metabolism. Then, we developed a GPCRscore prognostic model and validated across multiple cohorts, which effectively stratified LUAD patients into distinct risk groups. High-risk LUAD patients had an immunosuppressive microenvironment and activated metabolic reprogramming. ADM was identified as a key gene in the high-risk group, correlating with tumor stage, immune suppression, and resistance to immunotherapy. Clinically, ADM was highly expressed in tumor tissues and shows elevated concentrations in the peripheral blood of patients with advanced-stage LUAD. Subsequently, we demonstrated that knock-down of ADM in LUAD cells impaired their proliferation, migration, and invasion, while also reducing the angiogenic potential of endothelial cells in vitro. Adrenomedullin promoted LUAD progression in a murine metastasis model. Further, adrenomedullin inhibited CD8+ T cells proliferation, induced exhaustion, and impaired cytotoxic function. Finally, drug sensitivity and cell viability analysis showed LUAD patients with high levels of ADM exhibited sensitivity to the treatment of Staurosporine and Dasatinib.
CONCLUSIONS: In summary, this study reveals the pivotal role of GPCR signaling particularly mediated by ADM in orchestrating metabolic reprogramming and immune modulation in LUAD. ADM emerges as a potential predictive biomarker and therapeutic target, offering valuable implications for optimizing strategies.
When testing an AI model, it’s hard to tell if it is reasoning or just regurgitating answers from its training data. Xbench, a new benchmark developed by the Chinese venture capital firm HSG, or HongShan Capital Group, might help to sidestep that issue. That’s thanks to the way it evaluates models not only on the ability to pass arbitrary tests, like most other benchmarks, but also on the ability to execute real-world tasks, which is more unusual. It will be updated on a regular basis to try to
When testing an AI model, it’s hard to tell if it is reasoning or just regurgitating answers from its training data. Xbench, a new benchmark developed by the Chinese venture capital firm HSG, or HongShan Capital Group, might help to sidestep that issue. That’s thanks to the way it evaluates models not only on the ability to pass arbitrary tests, like most other benchmarks, but also on the ability to execute real-world tasks, which is more unusual. It will be updated on a regular basis to try to keep it evergreen.
This week the company is making part of its question set open-source and letting anyone use for free. The team has also released a leaderboard comparing how mainstream AI models stack up when tested on Xbench. (ChatGPT o3 ranked first across all categories, though ByteDance’s Doubao, Gemini 2.5 Pro, and Grok all still did pretty well, as did Claude Sonnet.)
Development of the benchmark at HongShan began in 2022, following ChatGPT’s breakout success, as an internal tool for assessing which models are worth investing in. Since then, led by partner Gong Yuan, the team has steadily expanded the system, bringing in outside researchers and professionals to help refine it. As the project grew more sophisticated, they decided to release it to the public.
Xbench approached the problem with two different systems. One is similar to traditional benchmarking: an academic test that gauges a model’s aptitude on various subjects. The other is more like a technical interview round for a job, assessing how much real-world economic value a model might deliver.
Xbench’s methods for assessing raw intelligence currently include two components: Xbench-ScienceQA and Xbench-DeepResearch. ScienceQA isn’t a radical departure from existing postgraduate-level STEM benchmarks like GPQA and SuperGPQA. It includes questions spanning fields from biochemistry to orbital mechanics, drafted by graduate students and double-checked by professors. Scoring rewards not only the right answer but also the reasoning chain that leads to it.
DeepResearch, by contrast, focuses on a model’s ability to navigate the Chinese-language web. Ten subject-matter experts created 100 questions in music, history, finance, and literature—questions that can’t just be googled but require significant research to answer. Scoring favors breadth of sources, factual consistency, and a model’s willingness to admit when there isn’t enough data. A question in the publicized collection is “How many Chinese cities in the three northwestern provinces border a foreign country?” (It’s 12, and only 33% of models tested got it right, if you are wondering.)
On the company’s website, the researchers said they want to add more dimensions to the test—for example, aspects like how creative a model is in its problem solving, how collaborative it is when working with other models, and how reliable it is.
The team has committed to updating the test questions once a quarter and to maintain a half-public, half-private data set.
To assess models’ real-world readiness, the team worked with experts to develop tasks modeled on actual workflows, initially in recruitment and marketing. For example, one task asks a model to source five qualified battery engineer candidates and justify each pick. Another asks it to match advertisers with appropriate short-video creators from a pool of over 800 influencers.
The website also teases upcoming categories, including finance, legal, accounting, and design. The question sets for these categories have not yet been open-sourced.
ChatGPT-o3 again ranks first in both of the current professional categories. For recruiting, Perplexity Search and Claude 3.5 Sonnet take second and third place, respectively. For marketing, Claude, Grok, and Gemini all perform well.
“It is really difficult for benchmarks to include things that are so hard to quantify,” says Zihan Zheng, the lead researcher on a new benchmark called LiveCodeBench Pro and a student at NYU. “But Xbench represents a promising start.”
Around the world, countries are facing the challenges of aging populations, growing rates of chronic disease, and workforce shortages, leading to a growing burden on health care systems. From diagnosis to treatment, AI and other digital solutions can enhance the efficiency and effectiveness of health care, easing the burden on straining systems. According to the World Health Organization (WHO), spending an additional $0.24 per patient per year on digital health interventions could save more than
Around the world, countries are facing the challenges of aging populations, growing rates of chronic disease, and workforce shortages, leading to a growing burden on health care systems. From diagnosis to treatment, AI and other digital solutions can enhance the efficiency and effectiveness of health care, easing the burden on straining systems. According to the World Health Organization (WHO), spending an additional $0.24 per patient per year on digital health interventions could save more than two million lives from non-communicable diseases over the next decade.
To work most effectively, digital solutions need to be scaled and embedded in an ecosystem that ensures a high degree of interoperability, data security, and governance. If not, the proliferation of point solutions— where specialized software or tools focus on just one specific area or function—could lead to silos and digital canyons, complicating rather than easing the workloads of health care professionals, and potentially impacting patient treatment. Importantly, technologies that enhance workforce productivity should keep humans in the loop, aiming to augment their capabilities, rather than replace them.
Through a survey of 300 health care executives and a program of interviews with industry experts, startup leaders, and academic researchers, this report explores the best practices for success when implementing integrated digital solutions into health care, and how these can support decision-makers in a range of settings, including laboratories and hospitals.
Health care is primed for digital adoption. The global pandemic underscored the benefits of value-based care and accelerated the adoption of digital and AI-powered technologies in health care. Overwhelmingly, 96% of the survey respondents say they are “ready and resourced” to use digital health, while one in four say they are “very ready.” However, 91% of executives agree interoperability is a challenge, with a majority (59%) saying it will be “tough” to solve. Two in five leaders say balancing security with usability is the biggest challenge for digital health. With the adoption of cloud solutions, organizations can enjoy the benefits of modernized IT infrastructure: 36% of the survey respondents believe scalability is the main benefit, followed by improved security (28%).
Digital health care can help health care institutions transform patient outcomes—if built on the right foundations. Solutions like AI-powered diagnostics, telemedicine, and remote monitoring can offer measurable impact across the patient journey, from improving early disease detection to reducing hospital readmission rates. However, these technologies can only support fully connected health care when scaled up and embedded in ecosystems with robust data governance, interoperability, and security.
Health care data has immense potential—but fragmentation and poor interoperability hinder impact. Health care systems generate vast quantities of data, yet much of it remains siloed or unusable due to inconsistent formats and incompatible IT systems, limiting scalability.
Digital tools must augment, not overload, the workforce. With global health care workforce shortages worsening, digital solutions like clinical decision support tools, patient prediction, and remote monitoring can be seen as essential aids rather than threats to the workforce. Successful deployment depends on usability, clinician engagement, and training.
Regulatory evolution, open data policies, and economic sustainability are key to scaling digital health. Even the best digital tools struggle to scale without reimbursement frameworks, regulatory support, and viable business models. Open data ecosystems are needed to unleash the clinical and economic value of innovation. Regulatory and reimbursement innovation is also critical to transitioning from pilot projects to high-impact, system-wide adoption.
This content was produced by Insights, the custom content arm of MIT Technology Review. It was not written by MIT Technology Review’s editorial staff.
This content was researched, designed, and written entirely by human writers, editors, analysts, and illustrators. This includes the writing of surveys and collection of data for surveys. AI tools that may have been used were limited to secondary production processes that passed thorough human review.
Early-stage founders, listen up! You will want a front row seat at the Builders Stage on October 27 at 1:00 p.m. PT. This session at TechCrunch Disrupt 2025 brings together Nina Achadjian, partner, Index Ventures; Jerry Chen, general partner, Greylock; and Viviana Faga, general partner, Felicis, all of whom will share their 2026 investment priorities […]
Early-stage founders, listen up! You will want a front row seat at the Builders Stage on October 27 at 1:00 p.m. PT. This session at TechCrunch Disrupt 2025 brings together Nina Achadjian, partner, Index Ventures; Jerry Chen, general partner, Greylock; and Viviana Faga, general partner, Felicis, all of whom will share their 2026 investment priorities […]
iScience. 2025 May 15;28(6):112681. doi: 10.1016/j.isci.2025.112681. eCollection 2025 Jun 20.ABSTRACTMetabolic reprogramming is a defining feature of pancreatic cancer, influencing tumor progression and the tumor microenvironment. By integrating single-cell transcriptomics, spatial transcriptomics, and spatial metabolomics, this study visualized the spatial co-localization of metabolites and gene expression within tumor samples, uncovering metabolic heterogeneity and intercellular interactions.
iScience. 2025 May 15;28(6):112681. doi: 10.1016/j.isci.2025.112681. eCollection 2025 Jun 20.
ABSTRACT
Metabolic reprogramming is a defining feature of pancreatic cancer, influencing tumor progression and the tumor microenvironment. By integrating single-cell transcriptomics, spatial transcriptomics, and spatial metabolomics, this study visualized the spatial co-localization of metabolites and gene expression within tumor samples, uncovering metabolic heterogeneity and intercellular interactions. Spatial transcriptomics identified distinct pathological regions, which were further characterized using single-cell transcriptomic data and pathologist annotations. Pseudotime trajectory analysis revealed metabolic shifts along the malignant progression, while single-cell Metabolism (scMetabolism) delineated metabolic differences between pathological regions, classifying them as hypermetabolic or hypometabolic. Notably, aberrant cell communication between cancer cells, macrophages, and fibroblasts was observed, with key receptor-ligand pairs significantly co-expressed in malignant regions and correlated with poor prognosis. Spatial metabolomics imaging identified signature metabolites, highlighting metabolic alterations in amino acid metabolism, polyamine metabolism, fatty acid synthesis, and phospholipid metabolism. This integrated analysis provides critical insights into pancreatic cancer metabolism, offering potential avenues for targeted therapeutic interventions.
Cancer Treat Rev. 2025 Jun 14;139:102979. doi: 10.1016/j.ctrv.2025.102979. Online ahead of print.ABSTRACTBreast cancer is characterized by significant molecular heterogeneity; therefore, there are distinct clinical features, treatment modalities, and prognostic outcomes across its various molecular subtypes. In the era of precision medicine, liquid biopsy has emerged as a convenient and minimally invasive technique capable of dynamically representing the comprehensive tumor gene spectrum. This r
Cancer Treat Rev. 2025 Jun 14;139:102979. doi: 10.1016/j.ctrv.2025.102979. Online ahead of print.
ABSTRACT
Breast cancer is characterized by significant molecular heterogeneity; therefore, there are distinct clinical features, treatment modalities, and prognostic outcomes across its various molecular subtypes. In the era of precision medicine, liquid biopsy has emerged as a convenient and minimally invasive technique capable of dynamically representing the comprehensive tumor gene spectrum. This review systematically elaborates the clinical value of liquid biopsy as a breakthrough tool for precision diagnosis and treatment in breast cancer through dynamic detection of key biomarkers, including circulating tumor DNA (ctDNA), circulating tumor cells (CTCs), exosomes, and non-coding RNA (ncRNA). Specific genetic mutations and methylation signatures in ctDNA can be applied to early breast cancer screening, minimal residual disease monitoring, and tracking drug resistance mechanisms. CTCs enumeration (≥1/7.5 mL in early-stage cancer or ≥ 5/7.5 mL in metastatic cancer) and PD-L1 expression levels demonstrate direct correlations with prognostic stratification and the efficacy of immunotherapy. As the specificity and sensitivity of liquid biopsy continue to improve, personalized treatment strategies, informed by biomarker analysis and targeted precision therapies, have unveiled new avenues of hope for patients with breast cancer. However, several challenges persist in the practical application of liquid biopsy. Despite persistent challenges, such as insufficient standardization and difficulties in resolving low-abundance variants, future advancements should focus on multi-omics integration and AI-driven technological breakthroughs to overcome bottlenecks in clinical translation. This review summarizes cutting-edge liquid biopsy technologies for identifying clinically significant molecular biomarkers, focusing on discussing critical challenges in the strategies to advance precision oncology applications for optimized treatment guidance and disease surveillance in breast cancer.
Cell Signal. 2025 Jun 18;134:111950. doi: 10.1016/j.cellsig.2025.111950. Online ahead of print.ABSTRACTFAAP100 plays an essential role in DNA damage repair, with dysregulation associated with elevated cancer susceptibility. Nevertheless, comprehensive pan-cancer analyses examining FAAP100 prognostic significance, immune correlations, and epigenetic regulation remains unexplored. This study systematically characterized FAAP100 across 33 cancer types utilizing multi-omics data from TCGA, UALCAN, c
Cell Signal. 2025 Jun 18;134:111950. doi: 10.1016/j.cellsig.2025.111950. Online ahead of print.
ABSTRACT
FAAP100 plays an essential role in DNA damage repair, with dysregulation associated with elevated cancer susceptibility. Nevertheless, comprehensive pan-cancer analyses examining FAAP100 prognostic significance, immune correlations, and epigenetic regulation remains unexplored. This study systematically characterized FAAP100 across 33 cancer types utilizing multi-omics data from TCGA, UALCAN, cBioPortal, TIMER2.0, and CPTAC. Analytical assessments included expression profiles, prognostic significance, and diagnostic utility, alongside associations with DNA methylation, immune cell infiltration, immune checkpoint gene expression, tumor mutational load (TMB), microsatellite instability (MSI), and drug resistance. Findings revealed significant FAAP100 upregulation across multiple cancer types, exhibiting inverse correlations to patient survival. Genomic characterization identified associations between FAAP100 overexpression and both copy number amplification and promoter hypomethylation. Immune profiling demonstrated robust correlations with immune cell infiltration levels and checkpoint molecule activity. Functional assays utilizing PC9 and H1299 cells indicated that FAAP100 enhances cellular proliferation and migration while inhibiting apoptosis processes. In vivo studies confirmed tumor growth suppression upon FAAP100 knockdown. Collectively, this multi-omics investigation identifies FAAP100 as a pan-cancer oncogene driver, highlighting its potential as both a prognostic biomarker and therapeutic target. The integrated analysis of expression patterns, epigenetic modifications, immune characteristics, and genomic alterations elucidates the mechanistic involvement of FAAP100 in tumor progression, providing a foundation for clinical application in precision oncology approaches..
J Gastrointest Cancer. 2025 Jun 19;56(1):139. doi: 10.1007/s12029-025-01249-1.ABSTRACTBACKGROUND: Hepatocellular carcinoma (HCC) is the most common primary malignant liver tumor, with rising incidence and mortality rates posing a significant threat to global public health. Accurate prediction of liver cancer occurrence and progression is essential for improving patient prognosis. This study uses bibliometric methods to analyze the current state and future trends in liver cancer prediction resear
J Gastrointest Cancer. 2025 Jun 19;56(1):139. doi: 10.1007/s12029-025-01249-1.
ABSTRACT
BACKGROUND: Hepatocellular carcinoma (HCC) is the most common primary malignant liver tumor, with rising incidence and mortality rates posing a significant threat to global public health. Accurate prediction of liver cancer occurrence and progression is essential for improving patient prognosis. This study uses bibliometric methods to analyze the current state and future trends in liver cancer prediction research.
METHODS: A search was conducted in the Web of Science (WOS) database on October 22, 2023, identifying 1092 articles on liver cancer prediction. These articles were quantitatively analyzed using CiteSpace 6.2 software, with a focus on research hotspots, authors, countries, and keywords.
RESULTS: The study involved 114 countries, 4254 institutions, and 280 journals, with 48,788 citations. China (826 papers) and the USA (96 papers) dominate the field. Leading institutions include Sun Yat-sen University, Fudan University, Zhejiang University, and Yonsei University. The most cited journals were Hepatology (2209 citations) and Journal of Hepatology (946 citations). Frontiers in Oncology had the highest H-index (14). Key authors include Kim Seung Up (23 papers) and Ahn Sang Hoon (H-index = 14). Early research focused on risk factors and staging, while recent studies emphasize DNA methylation, immune microenvironments, and tumor metastasis. Future research will focus on multi-omics data integration and AI-driven predictive model optimization.
CONCLUSION: This study provides a comprehensive overview of liver cancer prediction research, highlighting key trends and the potential of multi-omics data and machine learning to enhance predictive models and clinical outcomes.
Login
