West China Medical Center of Sichuan University

The traditional Tumor-Node-Metastasis (TNM) staging system for solid tumors relies on anatomical assessment but possesses inherent limitations in capturing systemic micrometastases and molecular-level disease burden. Recently, the Tumor-Node-Metastasis-Blood (TNMB) staging system has garnered significant attention. It aims to provide a systematic synthesis of the origin of the TNMB staging system, its current applications in tumors, and its future prospects, while evaluating its potential value in enhancing early diagnosis, prognostic assessment, and the precision of therapeutic decision-making. A systematic literature search was conducted in PubMed and Web of Science databases from 2018 to 2026 using keywords related to neoplasms and TNMB staging system. Articles were screened for inclusion, and 21 studies focusing on cutaneous T-cell lymphoma and lung cancer were included for analysis. The TNMB staging system enhances risk stratification and prognostic accuracy in both cutaneous T-cell lymphoma and non-small cell lung cancer. In cutaneous lymphoma, TNMB staging system correlates with disease progression, treatment response, and molecular biomarkers. In lung cancer, integrating circulating tumor DNA (ctDNA) into TNMB staging system improves recurrence prediction and guides adjuvant therapy decisions, outperforming traditional TNM staging in prognostic discrimination. Beyond CTCL and non-small cell lung cancer (NSCLC), the utility of key biomarkers such as ctDNA for refining staging precision suggests a broader potential for the TNMB framework, even in cancers where its formal application is still forthcoming. The TNMB staging system represents a transformative approach in oncology by incorporating blood-based molecular data into traditional anatomical staging. It enables earlier detection of micrometastases, improves risk stratification, and supports personalized treatment strategies. Despite challenges in standardization and clinical integration, TNMB staging system holds significant promise for advancing precision oncology across multiple cancer types.

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Cellular and molecular heterogeneity in the liver has been increasingly recognized to drive liver fibrosis progression, but the particular events that occur initially in response to liver injury and trigger the immune cell recruitment remain unclear. Here, we identify epigenetically aberrant liver sinusoidal endothelial cells (LSECs) as key players in this process. Mechanistically, the epigenetic readers like bromodomain-containing protein 4 (BRD4)-dependent super-enhancers (SEs) activate proinflammatory genes, including promyelocytic leukemia (PML). PML in turn binds BRD4 and amplifies proinflammatory angiocrine signaling through phase separation-dependent SE-activation via PML/BRD4 condensate formation. In mouse models, LSEC-specific depletion of the PML/BRD4 complex mitigates liver inflammation and fibrosis. Single-cell RNA-sequencing reveals that epigenetically aberrant LSECs exhibit a reprogrammed proinflammatory angiocrine landscape in mouse fibrotic livers. TIMP1+ LSECs promote the recruitment of CD63+ monocyte-derived macrophages (MoMFs) during liver fibrosis progression. Thereby, PML/BRD4 in LSECs governs inflammatory immune cell recruitment in liver fibrosis. Pharmacological BRD4 inhibition or epigenetic PML-SE repression alleviates liver inflammation and fibrosis. In conclusion, PML/BRD4-mediated SE activation via phase separation drives proinflammatory angiocrine signaling in LSECs, initiating the inflammatory cascade and subsequent immune cell recruitment during liver fibrosis.

Hematologic malignancies are frequently complicated by malnutrition, a condition that remains underrecognized yet strongly associated with impaired treatment tolerance, immune recovery, and survival. Unlike solid tumors, hematologic malignancies are characterized by diffuse marrow and immune system involvement, rendering host metabolism highly vulnerable to tumor-driven inflammation and therapy-induced immune stress. Accumulating evidence indicates that nutritional deterioration in hematologic malignancies reflects a state of integrated immunometabolic vulnerability—driven by hyperinflammation, anabolic resistance, gastrointestinal injury, and psychosocial stress—rather than inadequate caloric intake alone. This review synthesizes current evidence on the biological basis, clinical assessment, and management of malnutrition in hematologic malignancies, with particular emphasis on hematopoietic stem cell transplantation and cellular therapies. We propose that nutritional care in hematologic malignancies should evolve from supportive supplementation toward mechanism-informed, precision nutritional strategies aimed at modulating host metabolism and immune function to improve clinical outcomes.

A study indicates that elevated aldosterone levels increase the risk of hypertension by 16%. This retrospective cohort study examines the relationship between blood pressure and renin-aldosterone levels in patients with essential hypertension (EH), aiming to elucidate the clinical features and risk factors of inappropriate hyperaldosteronism in Chinese individuals with essential hypertension. Clinical data of 309 EH patients were analyzed. The participants were divided into three groups with a high (H)/medium (M)/low (L) blood pressure level: Group H (BP≥160 / (or) 100 mmHg, n=151), Group M (BP 140-160/90-100 mmHg, n=101), Group L (BP < 140/90 mmHg, n=57). Since the data were all non-normal distributions, they were represented by the median and extreme values, and the Wilcoxon rank sum test was used. Categorical data were analyzed using the χ2 test. In the one-factor variance analysis, those with P<0.05 were included in the multivariate analysis, and the multiple linear regression analysis method was used for the multivariate analysis. The study assessed the relationship between the plasma renin activity (PRA), plasma aldosterone concentration (PAC), and the aldosterone/renin activity ratio (ARR) in patients with EH and their blood pressure levels. Among the 309 EH patients, 65 cases (21.04%) had elevated aldosterone levels, and 94 cases (30.42%) had increased renin activity. The diastolic blood pressure of patients with elevated aldosterone levels was higher than that of patients with normal or decreased aldosterone levels (100 vs. 95, 87, p<0.05), while there was no significant difference in systolic blood pressure between patients with elevated aldosterone levels and those with normal or decreased aldosterone levels (152 vs. 151.5, 142, p>0.05). The proportion of patients with heightened aldosterone levels was greater in Group H compared to the others (23.8% vs. 20.8% and 14.0%, p<0.05). Multiple linear stepwise regression indicated that higher aldosterone levels correlated with increased diastolic blood pressure. PAC increased by 3.66 ng/dL for every 10 mmHg of DBP. The increase in aldosterone levels is relatively common among EH patients in China. The increase in aldosterone levels is correlated with the elevation of diastolic blood pressure. The elevated aldosterone levels are an independent risk factor for the increase in diastolic blood pressure in EH patients.