Landscape and prognostic values of lymphocytes in patients with hepatocellular carcinoma undergoing transarterial embolization.

Transarterial embolization, the first-line treatment for hepatocellular carcinoma, does not always lead to promising outcomes in all patients. A better understanding of how the immune lymphocyte changes after transarterial embolization might be the key to improve the efficacy of transarterial embolization. However, there are few studies evaluating immune lymphocytes in transarterial embolization patients. Therefore, we aimed to evaluate the short- and long-term effects of transarterial embolization on lymphocyte subsets in patients with hepatocellular carcinoma to identify those that predict transarterial embolization prognosis. Peripheral blood samples were collected from 44 patients with hepatocellular carcinoma at the following time points: 1 d before the initial transarterial embolization, 3 d after the initial transarterial embolization, and 1 mo after the initial transarterial embolization and subjected to peripheral blood mononuclear cell isolation and flow cytometry. Dynamic changes in 75 lymphocyte subsets were recorded, and their absolute counts were calculated. Tumor assessments were made every 4 to 6 wk via computed tomography or magnetic resonance imaging. Our results revealed that almost all lymphocyte subsets fluctuated 3 d after transarterial embolization, but only Tfh and B cells decreased 1 mo after transarterial embolization. Univariate and multivariate Cox regression showed that high levels of Th2 and conventional killer Vδ2 cells were associated with longer progressive-free survival after transarterial embolization. Longer overall survival after transarterial embolization was associated with high levels of Th17 and viral infection-specific Vδ1 cells and low levels of immature natural killer cells. In conclusion, transarterial embolization has a dynamic influence on the status of lymphocytes. Accordingly, several lymphocyte subsets can be used as prognostic markers for transarterial embolization.

Targeting cyclin D1 as a therapeutic approach for papillary thyroid carcinoma.

Cyclin D1 functions as a mitogenic sensor that specifically binds to CDK4/6, thereby integrating external mitogenic inputs and cell cycle progression. Cyclin D1 interacts with transcription factors and regulates various important cellular processes, including differentiation, proliferation, apoptosis, and DNA repair. Therefore, its dysregulation contributes to carcinogenesis. Cyclin D1 is highly expressed in papillary thyroid carcinoma (PTC). However, the particular cellular mechanisms through which abnormal cyclin D1 expression causes PTC are poorly understood. Unveiling the regulatory mechanisms of cyclin D1 and its function in PTC may help determine clinically effective strategies, and open up better opportunities for further research, leading to the development of novel PTC regimens that are clinically effective. This review explores the mechanisms underlying cyclin D1 overexpression in PTC. Furthermore, we discuss the role of cyclin D1 in PTC tumorigenesis via its interactions with other regulatory elements. Finally, recent progress in the development of therapeutic options targeting cyclin D1 in PTC is examined and summarized.