The complex metabolic network in the tumor microenvironment (TME) plays a key role in controlling the growth and spread of malignant tumor cells, and it is closely linked to the function of infiltrating immune cells. Through metabolic reprogramming, tumor cells remodel the TME, leading to low oxygen, local acidity, nutrient depletion, and buildup of metabolic waste. This metabolic imbalance directly weakens the metabolic capacity and effector functions of infiltrating immune cells. In turn, the metabolic remodeling of immune cells further strengthens the immunosuppressive state of the TME, promoting tumor immune escape. Additionally, TME metabolites systematically reshape the genome through epigenetic modifications, speeding up T cell exhaustion and reinforcing the immunosuppressive features of the TME. Targeting metabolic pathways to provide metabolic intervention strategies for clinical anti-cancer therapy is currently under exploration. However, the high heterogeneity of tumors and the diversity of metabolic pathways present major challenges for translating these therapies into clinical practice. This review systematically outlines the molecular mechanisms by which metabolic reprogramming in the TME drives immune escape, summarizes the metabolic-epigenetic immune regulatory network, and provides a comprehensive overview of current metabolism-targeted therapeutic approaches, aiming to provide a reference for developing new anti-tumor immunometabolic strategies.

The Whole Person One Health medical model is an outcome of advanced human social development, serving as both a reflection on and a supplement to existing medical models. Its innovation lies in incorporating spiritual health into the scope of holistic health and the medical model, while also integrating environmental friendliness, the health of other species, and intergenerational development ethics. This model establishes four key intervention entry points—diet, sleep, activity, and medical care—and standardizes the principles of health grading and stepped care. It specifies evaluation indicators across three levels (outcomes, processes, and resources), emphasizes multisectoral linkage and cross-sector collaboration, enhances clinical operability, and forms a collaborative mechanism to address global health challenges. The goal of the "Whole Person One Health medical model" is to shift the focus of medical practice from a "disease-centered" approach to a "health-centered" approach, and ultimately to a "symbiosis-centered" approach centered on ecological integrity and life dignity. This transformation will establish "healthy environment → healthy land → healthy food → healthy body" as the fundamental logic of medicine. Adhering to and implementing the holistic medical model is conducive to the sustainable, high-quality development of both humanity and nature, ultimately benefiting all of humanity.

Esophageal stent placement is a minimally invasive and effective intervention for the management of benign and malignant esophageal strictures and esophageal fistulas, facilitating the rapid restoration of oral intake. Among the available devices, self-expanding metal stents are the most widely used. However, stent migration remains one of the most common complications, significantly compromising therapeutic efficacy and patient outcomes. Migration may result in recurrent dysphagia, fistula reopening, gastrointestinal obstruction, and even tissue injury. This review summarizes the risk factors associated with esophageal stent migration and recent advances in anti-migration strategies. Current evidence indicates that migration is influenced by multiple factors, including stent structural characteristics, covering type, diameter and length, deployment location, severity of stricture, esophageal motility, and chemoradiotherapy. In particular, fully covered stents, smaller stent diameters, placement across the gastroesophageal junction, and tumor regression following chemoradiotherapy are associated with an increased risk of migration. To reduce migration, various anti-migration stent designs have been developed, including stents with fins, circumferential protuberances, double-layer mesh structures, segmented stents, patient-specific three-dimensional (3D)-printed stents, and bioadhesive coatings. These approaches aim to improve stent stability through enhanced mechanical anchorage, better tissue conformity, or increased interface friction. In addition, fixation techniques such as external traction fixation, endoscopic suturing, over-the-scope clips, and through-the-scope clips have been employed to reduce migration in high-risk patients. Nevertheless, these methods remain limited by procedural complexity, cost, and variable long-term efficacy. Although current anti-migration strategies can reduce the incidence of stent migration to some extent, complete prevention remains challenging. Future developments should integrate advances in materials science, bioengineering, 3D printing, and intelligent manufacturing to develop esophageal stents with improved biocompatibility, individualized adaptability, and long-term stability. Furthermore, high-quality prospective clinical studies are required to validate their safety and efficacy and to optimize the clinical benefits of esophageal stent therapy.

The metabolic remodeling represents a critical hallmark of cancer. Numerous studies have revealed that methionine metabolism reprogramming promotes tumor progression. Methionine, the only sulfur-containing amino acid among essential amino acids, is essential for protein synthesis, redox balance and metabolic regulation, also participating in the transfer of methyl groups in the body. Dietary methionine restriction has been proven to inhibit tumor growth and improve response to various anti-cancer therapies. There are other cellular components in the tumor microenvironment, including T cells as a major driver of anti-tumor immunity. T cell-targeted immunotherapy has become the cornerstone of cancer treatments in recent years. Methionine is also essential for T cells, and its dual effects on cancer cells and immune cells have raised concerns about dietary methionine restriction for cancer treatment. In addition, methionine restriction may cause side effects on nutritional status and gut microbiota, even increasing the risk of cachexia of cancer patients. Here, this review summarizes the methionine metabolism in cancer biology, and highlights the research progress on targeting methionine metabolism for cancer immunotherapy.

Lipid metabolism reprogramming participates in the initiation, progression, metastasis, and drug resistance of colorectal cancer (CRC), and represents an important link between tumor biology and nutritional metabolic disorders. This review summarizes key processes including lipid uptake and transport, de novo fatty acid synthesis, lipid droplet storage and mobilization, fatty acid β-oxidation, and cholesterol homeostasis, with emphasis on their regulation by Wnt/β-catenin, PI3K/AKT/mTOR, and SREBP-related pathways. We further discuss how abnormal lipid metabolism affects adipose tissue function, the immune microenvironment, gut microbiota, and systemic nutritional status, contributing to malnutrition, cancer cachexia, sarcopenia, and myosteatosis. Current evidence suggests that lipid metabolism-related molecules, circulating lipid profiles, and CT-derived body composition parameters may support risk stratification and prognostic assessment in CRC, while metabolic targeting, nutritional therapy, and exercise intervention show potential for clinical translation.

Obesity is associated with an increased risk of cancer. Fat accumulation and dysfunction of adipose tissue trigger inflammatory responses and abnormal hormone secretion, leading to a reduction in gut probiotic species and an overgrowth of bacterial communities linked to cancer development. These changes inhibit immune-mediated tumor cell clearance and promote cancer progression through genomic instability induced by oxidative stress and DNA damage, potentially adversely affecting treatment outcomes and survival rates in cancer patients. Achieving a healthy body weight can be achieved through a balanced diet, increased physical activity, maintaining a regular lifestyle, as well as pharmacological and surgical interventions. Weight loss therapy reduces cancer risk by mitigating the adverse effects of obesity; however, a weight loss over 10% is typically required to achieve significant cancer risk reduction. This article discusses the correlation between obesity and cancer pathogenesis, as well as weight loss strategies from a scientific anticancer perspective.

Tumor drug resistance remains one of the most prevalent and clinically challenging causes of treatment failure across chemotherapy, radiotherapy, targeted therapy, and immunotherapy. The role of lipid metabolic reprogramming in driving this resistance has attracted considerable attention in recent years. This review examines the lipid metabolic alterations characteristic of drug-resistant tumor cells, focusing on three interconnected aspects: enhanced exogenous lipid uptake, remodeling of plasma membrane lipid composition, and intracellular lipid droplet accumulation. The molecular mechanisms through which these alterations contribute to resistance against distinct therapeutic modalities are subsequently discussed. Regarding intervention strategies, we analyze existing approaches targeting lipid synthesis enzymes, the cholesterol biosynthetic pathway, antioxidant defense nodes, and rate-limiting steps of fatty acid oxidation, along with their early-stage clinical translation. Given the substantial intratumoral heterogeneity of lipid metabolism and the compensatory limitations inherent to single-target interventions, we propose that future efforts should prioritize integrating single-cell lipidomics with spatial metabolomics to map metabolic vulnerabilities with greater precision, while leveraging emerging technologies such as nano-delivery systems and PROTACs to enhance targeting selectivity and exploring combination strategies built on complementary lethality mechanisms — avenues that hold real promise for overcoming the clinical challenge of drug resistance.

Objective To explore the correlations among nutritional knowledge, attitude, practice (KAP), nutritional status and quality of life in gastric cancer patients, and analyze the independent risk factors affecting quality of life, so as to provide evidence-based basis for clinical nutritional management and intervention. Method A total of 350 gastric cancer patients who underwent radical gastrectomy in Huai'an First People's Hospital from February 2022 to February 2025 were selected by convenience sampling. General information questionnaire, digestive system tumor nutrition KAP scale, Patient-Generated Subjective Global Assessment (PG-SGA) and the Global Health Status/Quality of Life (GHS/QoL) dimension of EORTC QLQ-C30 were used for investigation. Spearman correlation analysis was used to explore the correlations between variables, and multiple linear regression was used to analyze the independent influencing factors of quality of life. Result Place of residence of the family, main caregiver, average monthly family income, and TNM stage had significant effects on the nutritional knowledge, attitude, and practice level of patients with gastric cancer (P<0.05); the TNM stage affected the nutritional status of patients (P<0.05); the univariate analysis of the TNM stage indicated that it had an impact on the quality of life (P<0.05).Spearman correlation analysis showed that the KAP score was negatively correlated with the PG-SGA score (r =-0.202, P<0.01), and the GHS/QoL score was negatively correlated with the PG-SGA score (r=-0.964, P<0.001), and the KAP score was positively correlated with the GHS/QoL score (r=0.215, P<0.001). After controlling for potential confounding variables, the multivariate linear regression results showed that the PG-SGA score had a significant independent negative impact on the GHS/QoL score of patients (β=-2.744, 95%CI: -3.176 to -2.313, P<0.001); the KAP score had a significant independent positive impact on the GHS/QoL score of patients (β=0.171, 95%CI:0.061 to 0.281, P=0.003). The confounding variables such as age, gender, place of residence of the family, main caregiver, marital status, average monthly family income, TNM stage, surgical type, and medical insurance status did not significantly affect the quality of life in the multivariate analysis (all P>0.05). Conclusion Nutritional status is negatively correlated with quality of life scores, while nutritional knowledge, attitude, and practice (KAP) scores are positively correlated with quality of life scores. Nutritional status is a key independent factor influencing quality of life, and improving nutritional status can significantly enhance patients' quality of life.

Objective To investigate the postoperative malnutrition status in elderly patients with gastric cancer, and to analyze the relationship between postoperative malnutrition status and prognosis. Method A retrospective analysis was conducted on case data of 120 elderly patients with gastric cancer admitted to the hospital from May 2019 to May 2020, and the patients were divided into group A and group B according to the postoperative nutritional status. Patients with malnutrition were included in group A, and patients with normal nutritional status were included in group B. The prognostic nutritional index (PNI) was compared between the two groups, and the risk factors affecting postoperative malnutrition in elderly patients with gastric cancer were analyzed by univariate and multivariate Logistic regression analyses, and the survival curve was drawn by Kaplan-Meier method for prognosis analysis. Result Among 120 elderly patients with gastric cancer, 85 cases had postoperative malnutrition, with the incidence rate of postoperative malnutrition of 70.83%. Univariate analysis showed that there were significant differences in tumor differentiation degree, tumor diameter, depth of tumor invasion, total cholesterol, PNI, presence or absence of adjuvant chemotherapy, anemia, lymph node metastasis and hypoproteinemia between group A and group B (P<0.05). After multivariate Logistic regression analysis, it was found that low tumor differentiation, lymph node metastasis, tumor invasion depth T3+T4a, low PNI and hypoproteinemia were independent risk factors for postoperative malnutrition in elderly patients with gastric cancer. The 5-year overall survival rate of patients in group A was 38.82% and that in group B was 54.29%. The 5-year overall survival rate in group A was significantly lower than that in group B (χ²=4.266, P=0.039). Conclusion The incidence rate of postoperative malnutrition is high in elderly patients with gastric cancer. The 5-year overall survival rate of patients with postoperative malnutrition is reduced, and the prognosis is poor. It is necessary to pay clinical attention to nutritional support therapy for high-risk population with postoperative malnutrition among elderly patients with gastric cancer.

Objective To analyze the developmental trajectory of nutritional risk and disease perception among postoperative patients with cervical cancer, and to explore the predictive relationship between these two factors, thereby providing a theoretical basis for reducing disease perception and alleviating symptoms in patients with cervical cancer. Method A total of 132 patients diagnosed with cervical cancer were selected as research subjects using convenient sampling. Their nutritional risk and disease perception were tracked and investigated at three distinct time points: T1 (immediately following surgery), T2 (one month post-surgery), and T3 (two months post-surgery). Result A total of 118 valid questionnaires were retrieved in this study, (yielding a recovery rate of 89.39%. The cross-lag model indicates that at the initial stage, nutritional risk and disease perception can positively predict each other (β=0.423, P < 0.001). Specifically, nutritional risk significantly and positively predicted illness perception at the subsequent time point (T1→T2: β=0.440, P=0.012; T2→T3: β=0.430, P=0.004). Similarly, the average disease perception level significantly and positively predicts the nutritional risk level at the next time point (T1→T2: β=0.378, P=0.007; T2→T3: β=0.392, P=0.003). The latent variable growth model reveals that the initial level of nutritional risk positively predicts the initial level of disease perception (β=0.336, P=0.007) and can also positively predict the rate of development of disease perception (β=0.430, P=0.008). Furthermore, the rate of development of nutritional risk can positively predict the rate of development of disease perception (β=0.469, P < 0.001).Conclusion Medical staff should concentrate on monitoring the nutritional status and changes in disease perception among patients within two months following cervical cancer surgery. Early nutritional intervention, including personalized dietary support and enteral nutrition supplementation, can not only mitigate the body's nutritional risk but also indirectly alleviate symptoms and disease perception by reducing the rate of nutritional decline. Consequently, this can improve patient prognosis and enhance their quality of life.

Objective This study aims to screen nutritional status indicators with predictive value for the prognosis of lung cancer patients through Cox proportional hazards regression analysis and nomogram modeling, and construct a comprehensive predictive model. The nutrition-inflammation-immune axis indicators reflecting the overall condition of patients will be incorporated into the evaluation system. Method This study included 177 patients with non-small cell lung cancer (NSCLC) who underwent surgical treatment and were admitted to Xingtai People's Hospital from January 2019 to January 2022. They were divided into the death group (n=63) and the survival group (n=114) based on their 3-year survival status after surgery. The clinical data and nutritional status indicators [body mass index (BMI), musculoskeletal mass index (SMI), prealbumin (PA), transferrin (TRF), hemoglobin - albumin - lymphocyte - platelet composite index (HALP), prognostic nutritional index (PNI), and controlled nutritional status score (CONUT)] of the two groups of patients were collected. The differences in the above indicators between the death group and the survival group were compared. Cox proportional hazards regression was used to analyze the independent risk factors affecting prognosis, and a nomogram prediction model was constructed based on the screened key variables. The model discrimination was evaluated by the ROC curve, the prediction accuracy was tested by the calibration curve, and the clinical benefits were analyzed by the decision curve. Result The single-factor analysis showed that the patients in the death group had a higher proportion of TNM stage (stage Ⅲ/Ⅳ) and lower degree of malignancy, and the levels of SMI and HALP were significantly lower than those in the survival group (P < 0.05). The Cox regression results indicated that the degree of tumor differentiation and HALP were the influencing factors for poor prognosis in NSCLC patients (P < 0.05). The model efficacy analysis revealed that the AUC of a single indicator (degree of differentiation, HALP) for prediction was 0.591 and 0.767 respectively, and the AUC of the comprehensive prediction model reached 0.776. The calibration curve showed that the predicted values of the model were highly consistent with the actual observations (the Bias-corrected curve was close to the Ideal line). The decision curve indicated that the clinical net benefit of this model was > 0, which was superior to relying solely on TNM stage or nutritional indicators. Conclusion This study, through Cox regression analysis, clearly confirmed that HALP is an independent nutritional predictor for the prognosis of NSCLC patients. On this basis, by integrating the key clinical pathological feature of tumor differentiation degree, a comprehensive nomogram prediction model was successfully constructed.

Objective To construct a nomogram model for predicting the 3-year tumor-specific mortality risk of patients with stage II-III gastric cancer after radical resection based on nutritional inflammation metabolism-related indicators, and to explore its potential clinical value, in order to provide evidence-based basis for individualized prognosis assessment and management of gastric cancer patients. Method A total of 363 patients with stage II-III gastric cancer who underwent radical resection at Beijing Friendship Hospital, Capital Medical University from January 2018 to December 2022 were retrospectively selected as the research subjects. They were randomly divided into a training set (254 cases) and a validation set (109 cases) at a ratio of 7:3. The training set was divided into a death group (91 cases) and a survival group (163 cases) based on the prognosis outcome. Clinical baseline data and nutritional, inflammatory, and metabolic-related laboratory indicators of the patients were collected. Cox proportional hazards regression analysis was used to screen the independent influencing factors of tumor-specific death in gastric cancer patients. Based on the screening results, a prognostic nomogram model was constructed. The discrimination, goodness-of-fit, and clinical application value of the model were verified through consistency index (C-index), time-dependent ROC curve, Gronnesby-Borgan test, Bootstrap self-repeated sampling, and decision curve analysis (DCA). Result Cox proportional hazards regression analysis showed that Eastern Cooperative Oncology Group performance status (ECOG-PS)of 2-3 (HR=2.074, 95%CI=1.351-3.186,P=0.001), neutrophil-to-lymphocyte ratio (NLR)≥2.66 (HR=1.753,95%CI=1.132-2.714,P=0.012), platelet-to-lymphocyte ratio (PLR) ≥ 151.72 (HR=2.258,95%CI=1.456-3.502,P<0.001), albumin-bilirubin (ALBI) grade 2 (HR=2.057, 95%CI=1.342-3.152,P=0.001), and prognostic immune-inflammation-nutrition index (PIIN) ≥ 31.49 (HR=2.120, 95%CI=1.366-3.291, P=0.001) were independent risk factors for tumor-specific death in gastric cancer patients; albumin/globulin ratio (AGR) ≥ 1.46 (HR=0.415,95%CI=0.263-0.654,P<0.001), and prognostic nutrition index (PNI) ≥ 45 (HR=0.571, 95%CI=0.357-0.912, P=0.019) were independent protective factors for tumor-specific death in gastric cancer patients. The C-index of the prognostic nomogram model based on the above indicators for predicting tumor-specific death in gastric cancer patients was 0.850 (95%CI=0.799-0.901); the AUC of 1-year, 2-year, and 3-year survival in the training set was 0.729, 0.783, and 0.829, respectively, and in the validation set were 0.590, 0.839, and 0.829; the Gronnesby-Borgan test showed that the fitting goodness of the training set (χ²=8.762,P=0.271) and the validation set (χ²=9.125,P=0.244) was good; the internal validation and decision curve of the Bootstrap method showed that the net benefit interval of the model for predicting tumor-specific death in gastric cancer patients was large, which was helpful for clinical decision-making. Conclusion The prognostic nomogram model constructed based on multiple-dimensional indicators of nutrition, inflammation, and metabolism in gastric cancer patients has good predictive efficacy and clinical practicability, can stratify the prognosis risk of gastric cancer patients, and provides scientific basis for the formulation of individualized intervention strategies such as perioperative nutritional support, anti-inflammation, and metabolic regulation for gastric cancer patients.

Objective To investigate the expression of nuclear factor erythroid 2-related factor 1 (NFE2L1) and tripartite motif-containing protein 26 (TRIM26) in gastric cancer tissues and their correlation with patient prognosis. Method A total of 80 patients with gastric cancer admitted between March 2022 and March 2024 were enrolled from the electronic medical record system of our hospital. Patients were divided into the poor prognosis group and the good prognosis group according to the occurrence of death, tumor progression or severe complications within 1 year of follow-up. The mRNA expression levels of NFE2L1 and TRIM26 in gastric cancer tissues and adjacent normal tissues were detected by real-time fluorescent quantitative PCR (qPCR). The protein expressions of NFE2L1 and TRIM26 were determined by immunohistochemistry. Kaplan-Meier method was used for survival analysis. Multivariate Logistic regression analysis was performed to screen prognostic risk factors. Receiver operating characteristic (ROC) curve and decision curve analysis (DCA) were adopted to evaluate the prognostic predictive efficiency of NFE2L1 and TRIM26 mRNA. Result The mRNA expressions and positive protein rates of NFE2L1 and TRIM26 were significantly higher in gastric cancer tissues than in adjacent normal tissues (P＜0.05), and their expressions were correlated with TNM stage (P＜0.05). Kaplan-Meier survival analysis revealed that the 1-year survival rates of patients with positive NFE2L1 and TRIM26 expression were 75.44% and 73.58%, which were markedly lower than those of patients with negative expression (95.65% and 96.30%, log-rank χ²=4.243, 5.972; P=0.039, 0.015). The mRNA levels of NFE2L1 and TRIM26 in the poor prognosis group were significantly higher than those in the good prognosis group (P＜0.05). Multivariate Logistic regression analysis identified TNM stage, NFE2L1 and TRIM26 as independent risk factors for poor prognosis (P＜0.05). The area under the curve (AUC) of combined NFE2L1 and TRIM26 mRNA for predicting poor prognosis was 0.944 (95%CI=0.890-0.999), which was significantly higher than the AUC of NFE2L1 alone (0.815, 95%CI=0.710-0.920, Z=2.152, P=0.031) and TRIM26 alone (0.837, 95%CI=0.747-0.927, Z=2.007, P=0.037). DCA demonstrated that the combined detection yielded a higher net clinical benefit within the high-risk threshold range of 0.10 to 0.99. Conclusion The expression levels of NFE2L1 and TRIM26 are upregulated in gastric cancer tissues, and their combined detection exhibits high efficiency in predicting the prognosis of patients with gastric cancer.

Objective To investigate the temporal, geographic, and population distribution characteristics of folate deficiency and its associated factors among elderly individuals with chronic diseases in Rongcheng, Shandong Province. Method This study was based on data from the 2024 Rongcheng City Precision Nutrition Intervention for Chronic Diseases: Real-World Study (R-RWS). A total of 15,604 participants were included. Baseline information, including demographic characteristics, lifestyle factors, and folic acid supplementation status, was collected, and serum folate concentrations were measured. Differences in folate status across temporal, geographic, and population characteristics were assessed using chi-square tests and analysis of variance. Multivariable logistic regression models were applied to identify factors associated with folate deficiency.Result The overall prevalence of folate deficiency was 16.5%. Regarding temporal distribution, the prevalence of folate deficiency was higher in summer than in spring (18.8% vs. 16.0%), with the highest proportion of deficient individuals observed during April and May. In terms of geographic distribution, participants residing in inland townships exhibited a higher prevalence of folate deficiency than those living in coastal townships (17.5% vs. 15.9%). Regarding population distribution, folate deficiency was more prevalent among males than females (23.0% vs. 12.9%), among individuals aged ≥70 years than those aged <70 years (18.1% vs. 14.5%), among participants without folic acid supplementation than those receiving supplementation (24.7% vs. 7.9%), and among current smokers than former smokers and never smokers (26.4% vs. 20.5% vs. 13.9%, respectively) (all P < 0.05). Conclusion Folate deficiency was common among elderly individuals with chronic diseases in Rongcheng, China, and exhibited marked temporal and population-level variations. Males, individuals aged ≥70 years, current smokers, and those not receiving folic acid supplementation were identified as key high-risk groups. Targeted public health strategies, including strengthened nutritional surveillance, health education, promotion of healthy lifestyles, and appropriate folic acid supplementation, should be implemented according to seasonal and population-specific characteristics to reduce the burden of folate deficiency and support comprehensive chronic disease prevention and management.

The Warburg effect, proposed by Otto Warburg in 1924, describes the preferential glycolysis occurring in cancer cells even under aerobic conditions. His original hypothesis attributed this phenomenon to irreversible impairment of cellular respiration and regarded such respiratory damage as the driving force of carcinogenesis, yet this theory failed to gain widespread academic recognition because certain cancer cells retain robust mitochondrial respiratory activity. This review systematically sorts out and resolves the apparent contradiction between the coexistence of the Warburg effect and functional mitochondrial respiration in cancer cells. It proposes that irreversible damage to Complex I of the mitochondrial respiratory chain triggers a positive feedback loop of lipid synthesis, which constitutes the core mechanism underlying cell carcinogenesis, whereas lipid metabolism in normal cells is precisely regulated by negative feedback pathways. Lipid synthesis in cancer cells is highly dependent on glutamine rather than glucose, and lipid biosynthesis is an essential prerequisite for the proliferation and division of tumor cells. Based on this metabolic characteristic, developing specific inhibitors targeting glutaminase, glutamate dehydrogenase, alanine transaminase and aspartate transaminase is expected to become a novel strategy for cancer treatment.

Early diagnosis of lung cancer is of paramount importance. The recommended screening strategy is annual low-dose spiral computed tomography for high risk populations; however, it has limitations including low specificity and a high false positive rate. Serological tumor marker tests may also indicate the development and progression of lung cancer, but their sensitivity and specificity are both low, and they are not routinely recommended for lung cancer screening. Breath analysis (BA), as an emerging noninvasive diagnostic method for pulmonary malignancies, is based on the detection of volatile organic compounds (VOCs) in exhaled breath that are associated with malignant diseases. Its advantages include convenience, accuracy, and noninvasiveness, making it a potential new approach to improve early diagnosis of lung cancer. Currently, gas analysis technologies targeting major chemical classes such as alcohols, aliphatic hydrocarbons, aldehydes, esters, ketones and aromatic compounds have become increasingly mature. The sensitivity of diagnostic models constructed on these VOC panels is generally above 80%. With further technological advancements, more detection techniques will be introduced into clinical practice, gradually addressing current challenges such as the lack of standardized detection protocols and limited availability of detection equipment. It is believed that breath analysis will become one of the key technologies for early diagnosis of lung cancer in the future.

CRC is one of the most common and highly lethal malignancies worldwide. Epidemiological studies consistently demonstrate an inverse association between dietary calcium intake and CRC risk; however, several RCTs have failed to confirm a protective effect of calcium supplementation, giving rise to a “clinical paradox.” Taking this paradox as a starting point, this article proposes a “four-level cascade” framework linking low calcium intake to CRC pathogenesis: at the luminal level, low calcium weakens the chelation and detoxification of bile acids and free fatty acids, leading to damage to the intestinal mucosal barrier; at the molecular level, low calcium inactivates the CaSR, relieving its dual negative regulation of the Wnt/β-catenin pathway; at the synergistic level, the vitamin D-VDR axis and CaSR form a bidirectional positive feedback loop, and low calcium and low vitamin D create a “bidirectional lock” effect that amplifies the loss of tumor suppressor signals; at the microbiota level, gut dysbiosis and its metabolic byproducts reciprocally exacerbate the damage to the previous three layers, forming a vicious cycle. Based on this integrative framework, this article systematically examines how three sources of heterogeneity—vitamin D status, CaSR genotype, and microbial metabolic load—modify calcium signaling, thereby providing a plausible explanation for the inconsistent results of RCTs. Finally, we distill four testable hypotheses, offering an integrated theoretical foundation and verifiable directions for the precision prevention of CRC.

Branched-chain amino acid (BCAA) metabolism is a critical component of metabolic reprogramming in cancer. BCAA, including valine, leucine, and isoleucine, are transported into cancer cells via LAT1 and catabolized by BCAT1/2 to produce branched-chain α-keto acids, which are further metabolized by the BCKDH complex to fuel the tricarboxylic acid cycle. Dysregulated BCAA metabolism activates oncogenic signaling pathways such as mTORC1, ERK, and PI3K/Akt, thereby promoting proliferation, stemness, metastasis, and immune evasion. Notably, BCAA metabolism exhibits cancer-type-specific heterogeneity across lung, breast, colorectal, liver, pancreatic cancers, and leukemia. Emerging therapeutic strategies targeting LAT1, BCAT1, BCAT2, and BCKDH with small-molecule inhibitors (e.g., JPH203, Eupalinolide B, BT2) have shown preclinical antitumor efficacy. This review summarizes the functional heterogeneity, molecular mechanisms, and therapeutic advances of BCAA metabolism in different cancers, providing insights into metabolic targeting strategies.