包裹肿瘤簇的血管（VETC）代表了肝细胞癌（HCC）的不良预后形态学特征，这与免疫抑制性肿瘤免疫微环境（TIM）有关。然而，具有 VETC 模式的 HCC（VETC 阳性 HCC）中肿瘤细胞和 TIM 特征的潜在因素仍不确定。制瘤素 M (OSM) 是白细胞介素 6 家族的一种多效细胞因子，调节多种生物过程，包括肿瘤细胞的炎症、增殖和侵袭。我们的目的是检验 OSM 与 VETC 阳性 HCC 的免疫抑制 TIM 相关的假设。总共纳入了 397 例连续接受根治性肝切除术的 HCC 患者。对 OSM 阳性细胞和炎症细胞（包括 CD4、CD8、CD163、FOXP3 阳性细胞）进行免疫组织化学评估。我们根据细胞数量比较了 VETC 阳性和 VETC 阴性 HCC。我们在 62 名患者 (15.6%) 中发现了 VETC 模式。我们的分析显示，在 VETC 阳性 HCC 中，精氨酸酶 1（一种与成熟肝细胞分化相关的标志物）的表达显着下降（P = 0.046）。 VETC 阳性 HCC 中肿瘤浸润 OSM 阳性细胞的数量显着较低 (P = 0.0057)。值得注意的是，在 VETC 阳性 HCC 中，OSM 阳性细胞数量与血管侵犯无关，而在 VETC 阴性 HCC 中，OSM 阳性细胞数量增加与血管侵犯相关（P = 0.042）。我们揭示了 VETC 阳性 HCC 的独特病理特征，例如肝细胞分化低、OSM 阳性细胞减少和 OSM 独立的血管侵袭。这些发现强调了 VETC 阳性 HCC 细胞与其 TIM 之间通过减少 OSM 表达细胞的潜在相互作用。本文受版权保护。保留所有权利。本文受版权保护。版权所有。

Vessels encapsulating tumor clusters (VETC) represents an adverse prognostic morphological feature of hepatocellular carcinoma (HCC), which is associated with an immunosuppressive tumor-immune microenvironment (TIM). However, the underlying factors characterizing the tumor cells and TIM in HCC with a VETC pattern (VETC-positive HCC) remain uncertain. Oncostatin M (OSM), a pleiotropic cytokine of the interleukin-6 family, regulates various biological processes, including inflammation, proliferation, and invasiveness of tumor cells. We aimed to test a hypothesis that OSM is associated with the immunosuppressive TIM of VETC-positive HCC.A total of 397 consecutive HCC patients with curative-intent hepatectomy were included. OSM-positive cells and inflammatory cells including CD4-, CD8-, CD163-, FOXP3-positive cells were immunohistochemically evaluated. We compared VETC-positive and VETC-negative HCCs in terms of the number of these cells.We found the VETC pattern in 62 patients (15.6%). Our analysis revealed a significant decrease in the expression of arginase-1, a marker associated with mature hepatocyte differentiation, in VETC-positive HCC (P = 0.046). The number of tumor-infiltrating OSM-positive cells was significantly low in VETC-positive HCC (P = 0.0057). Notably, in VETC-positive HCC, the number of OSM-positive cells was not associated with vascular invasion, whereas in VETC-negative HCC, an increase in the number of OSM-positive cells was associated with vascular invasion (P = 0.042).We revealed the unique pathological features of VETC-positive HCC, such as low hepatocyte differentiation, decreased OSM-positive cells, and OSM-independent vascular invasion. These findings highlight the potential interaction between VETC-positive HCC cells and their TIM through the reduction of OSM-expressing cells. This article is protected by copyright. All rights reserved.This article is protected by copyright. All rights reserved.