Exosomes, which are extracellular vesicles with a diameter ranging from 40 to 160 nm, are abundantly present in various body fluids. Exosomal microRNA (ex-miR), due to its exceptional sensitivity and specificity, has garnered significant attention. Notably, ex-miR is consistently detected in almost all bodily fluids, highlighting its potential as a reliable biomarker. This attribute of ex-miR has piqued considerable interest in its application as a diagnostic tool for the early detection, continuous monitoring, and prognosis evaluation of cancer. Given the critical role of exosomes and their cargo in cancer biology, this review explores the intricate processes of exosome biogenesis and uptake, their multifaceted roles in cancer development and progression, and the potential of ex-miRs as biomarkers for tumor diagnosis and prognosis.

This study aims to systematically review the molecular and cellular mechanisms by which the interleukin 17 (IL-17)/T helper cells (Th17) signalling axis contributes to Graves' disease (GD) and Hashimoto's thyroiditis (HT), with particular focus on IL-17/Th17/T regulatory cells (Treg) balance, and to summarize the development of IL-17-targeted therapies for autoimmune thyroid disease (AITD). A comprehensive literature review (up to 2025) was conducted, encompassing human studies, animal models, and pre-clinical investigations related to IL-17/Th17 biology in AITD. IL-17 levels are elevated in both untreated and intractable GD. IL-17/IL-17RA signalling enhances the expression of IL-6, chemokine CXC ligand 10, and intercellular cell adhesion molecule-1, thereby amplifying thyroid inflammation. The IL-23/IL-17 axis and Th17/Treg imbalance are strongly associated with thyroid-associated ophthalmopathy. Serum and tissue IL-17 concentrations correlate positively with TPOAb or TgAb titres and early fibrosis, while Th17 predominance precedes Th1-mediated tissue destruction. Excessive iodine intake further drives naïve Tregs toward Th17 differentiation. Shared TGF-β signalling drives the reciprocal development of Th17 and Treg cells, with retinoid-related orphan receptor gamma t and Forkhead box protein P3 acting as molecular switches. Disruption of this balance contributes to the progression of AITD. Several pre-clinical agents (JiaYanKangTai, Yanghe decoction, LY294002) have been found to ameliorate experimental autoimmune thyroiditis by inhibiting IL-17 signalling or restoring Th17/Treg equilibrium; however, clinical translation remains limited. IL-23/IL-17 axis and Th17/Treg imbalance are critical checkpoints in the AITD pathogenesis. IL-17 represents a promising, yet still experimental immunotherapeutic target, warranting rigorous clinical investigation.

In recent years, indocyanine green (ICG) fluorescence has been widely used as a new tracer in sentinel lymph node biopsy (SLNB) for breast cancer. This self-controlled study identified the benefits in SLNB between methylene blue (MB) tracer alone and MB combined with ICG fluorescence imaging (MB + ICG) dual tracing modality in patients with breast cancer. One hundred seventy-nine SLNB with MB + ICG dual tracing in 178 cN0 breast cancer patients were enrolled, and their clinical data were analyzed. The results showed that the identification rate (IR) of sentinel lymph nodes (SLNs) by MB staining alone was 92% (165/179), the mean number of detected SLNs was 2.1 ± 1.2, the rate of ≥3 SLNs was 33% (55/165), and the number of positive (metastatic) lymph nodes was 40. The IR of SLN by MB + ICG dual tracing imaging was 93.9% (168/179), the mean number of detected SLNs was 3.8 ± 1.8, the rate of ≥3 SLNs was 70.8% (119/168), and the number of positive lymph nodes was 40. Compared to MB staining alone, because of the addition of ICG fluorescence imaging, SLN status changed from N0 to N1 or the number of positive SLNs increased in 9 patients, and there was an alteration of axillary management from SLNB to axillary lymph node dissection in 4 patients. Although MB + ICG dual tracing did not significantly improve the IR of SLNs, it increased the average number of SLNs, rate of ≥3 SLNs, number of positive SLNs. This may reduce the false negative rate of SLNB and lead to an alteration in axillary management.

Background: Ductal carcinoma in situ with microinvasion (DCIS-MI) is a special type of breast cancer. It is an invasive lesion less than 1.0 mm in size related to simple ductal carcinoma in situ (DCIS). Lymph node metastasis (LNM) in DCIS-MI often indicates a poor prognosis. Therefore, the management of lymph nodes plays a vital role in the treatment strategy of DCIS-MI. Since DCIS-MI is often diagnosed by postoperative paraffin section and immunohistochemical detection, to obtain the best clinical benefits for such patients, we aim to establish and verify a nomogram to predict the possibility of lymph node metastasis in DCIS-MI patients and help preoperative or intraoperative clinical decision-making. Methods: A retrospective analysis of patients with DCIS-MI in the Surveillance, Epidemiology, and End Results (SEER) database from 2010 to 2019 was performed. The study cohort was randomly divided into a training cohort and a validation cohort at a ratio of 7:3. The risk factors were determined by univariate and multivariate logistic regression analyses in the training cohort, and a nomogram was constructed. The receiver operating characteristic (ROC) curve, calibration curve, and decision curve analysis (DCA) were used to evaluate the nomogram in the training set and validation set. An independent data cohort was obtained from the Shanghai Jiao Tong University Breast Cancer Database (SJTU-BCDB) for external validation. Results: This study included 3951 female patients from SEER with DCIS-MI, including 244 patients with regional lymph node metastasis, accounting for 6.18% of the total. An independent test set of 323 patients from SJTU-BCDB was used for external validation. According to the multifactorial logistic regression analysis results, age at diagnosis, ethnicity, grade, and surgical modality were included in the prediction model. The areas under the ROC curves (AUCs) were 0.739 (95% CI: 0.702~0.775), 0.732 (95% CI: 0.675~0.788), and 0.707 (95%CI: 0.607–0.807) in the training, validation and external test groups, suggesting that the column line graphs had excellent differentiation. The calibration curves slope was close to 1, and the model’s predicted values were in good agreement with the actual values. The DCA curves showed good clinical utility. Conclusion: In this study, we constructed accurate and practical columnar maps with some clinical benefit to predict the likelihood of lymph node metastasis in patients with postoperatively diagnosed DCIS-MI and provide a reference value for specifying treatment strategies.

Thyroid dysfunction is associated with the risk of cardiovascular disease; however, whether plasma thyroid-stimulating hormone (TSH) levels in subjects with euthyroidism affect the risk of cardiovascular disease remains unclear. This study aimed to investigate the causal association between plasma TSH levels and cardiovascular diseases, particularly ischemic heart disease and heart failure (HF). Summary statistics from the Integrative Epidemiology Unit Open genome-wide association studies Project and FinnGen consortium were used to investigate the causal relationship between plasma TSH levels and the risk of cardiovascular diseases. Two-sample Mendelian randomization analysis using inverse-variance weighting as the primary method was performed. The MR Pleiotropy RESidual Sum and Outlier and leave-one-out methods were used to ensure the robustness of our findings. Genetically determined plasma TSH levels were associated with major coronary heart disease events (OR 1.0557, 95% CI 1.0141–1.0991), all-cause HF (OR 0.9587, 95% CI 0.9231–0.9956), and HF + non-ischemic cardiomyopathy (OR 0.9318, 95% CI 0.8786–0.9882). After the Bonferroni correction, the causation described above disappeared. In the secondary analysis, genetically determined higher TSH levels were associated with a higher risk for unstable angina pectoris (OR 1.0913, 95% CI 1.0350–1.1507), but were associated with a lower risk for HF + overweight (OR 0.9265, 95% CI 0.8821–0.9731). These results were further validated using sensitivity analysis. Our findings show that increased plasma TSH levels in patients with euthyroidism may increase the risk of unstable angina pectoris but reduce the risk of HF in overweight patients. This evidence indicates that plasma TSH levels may need to be carefully controlled in specific patients.

SGO2 maintains the binding of sisters chromatids by protecting the adhesive complex at the centromere, thus ensuring the correct separation of chromosomes during mitosis and meiosis. And this study explored its role in breast cancer (BC) progression. SGO2 expression in breast cancer was analyzed utilizing data from TCGA, GTEX, and HPA databases. Our study leveraged clinical data to predict outcomes. Subsequently, we conducted a GSEA enrichment analysis, dove into co-expression profiling, explored immune cell infiltration patterns, examined drug sensitivity, and analyzed single-cell data. To delve deeper, we validated the functional role of SGO2 through in vitro cellular experiments. Survival analysis demonstrated a notable correlation between heightened SGO2 expression and unfavorable cancer survival rates. Gene set enrichment analysis (GSEA) highlighted the participation of SGO2 in DNA replication. Immunoinfiltration analysis indicated a connection between SGO2 and several immune cell types, with single-cell analysis verifying SGO2 expression across diverse cell populations. SGO2 may serve as a valuable prognostic biomarker and a potential therapeutic target in breast cancer.