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    Factors Relating to Tumor Size and Survival in Patients with Hepatocellular Carcinoma: Significance of Platelet-Lymphocyte Ratio, Portal Vein Thrombosis, and Albumin
    (Karger, 2026) Donghia, Rossella; Carr, Brian Irving; Yilmaz, Sezai
    Introduction: Maximum tumor diameter (MTD) is one of the key aggressiveness features of hepatocellular carcinoma (HCC). However, the clinical associations and causes of large size HCC are not well understood. The aim was to compare small and large MTD (<=/>6 cm) HCCs with respect to clinical associations. Methods: MTD <=/> 6 cm HCCs were compared by clinical characteristics and analyzed through logistical regression models, as well as Cox proportional hazard models for death, on clinical parameters. Results: Patients with larger HCCs had more portal vein thrombosis (PVT) and tumor multifocality, higher AST, ALKP and GGT levels and lower albumin levels. A logistic regression model of MTD (<=/>6 cm) showed the highest risk for PVT and platelet-lymphocyte ratio (PLR) >150, while albumin and female gender were protective. The combination of male gender, PLR >150, plus PVT had an odds ratio of 12.124. In Cox proportional hazard models, the highest hazard ratio for death was for PVT, and only albumin was significantly protective. PVT plus low albumin had a hazard ratio of 4.254. Conclusion: PVT, albumin, PLR, and gender were significant for <=/>6 cm MTD. PVT and albumin were significant for survival.
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    HBV viral load and tumor and non-tumor factors in patients with HBV-associated HCC
    (Kare Publ, 2024) Ataman, Engin; Harputluoglu, Murat; Carr, Brian Irving; Gozukara, Harika; Ince, Volkan; Yilmaz, Sezai
    Background and Aim: Several tumor and non-tumor factors affect the prognosis of hepatocellular carcinoma (HCC) patients. This study aimed to investigate the effects of hepatitis B virus (HBV) viral load on tumor and non-tumor factors in patients with HBV-associated HCC. Materials and Methods: Patients with hepatitis B and HCC who presented Transplantation Institute, were included in our study. Patients were divided into two groups according to the presence or absence of HBV-DNA, and it was determined whether there were differences between these two groups with respect to tumor and non-tumor parameters. Results: Comparison of serum alanine aminotransferase (ALT), gamma-glutamyl transferase (GGT), hepatitis B surface antigen (HBsAg), and C-reactive protein (CRP) levels between HBV-DNA negative and positive patients showed significant differences (respectively p<0.01, p<0.01, p<0.05, and p<0.05). A major finding was a very significant difference between the two patient groups in terms of portal vein invasion (PVI) and venous invasion (p<0.001 and p<0.01, respectively). However, there was no significant difference in metastasis or lymph node involvement between HBV-DNA negative and positive patients. Conclusion: Our findings suggest that HBV viral load plays an important role in PVI in HCC patients, and there is a significant relationship between HBV viral load and inflammation.
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    Inflammatory Mechanisms of HCC Development
    (Mdpi, 2020) Refolo, Maria Grazia; Messa, Caterina; Guerra, Vito; Carr, Brian Irving; D'Alessandro, Rosalba
    HCC (hepatocellular carcinoma) is the second leading cause of cancer deaths worldwide, with several etiologic causes, mostly inflammation-associated. Different inflammatory responses in the liver can be triggered by different etiological agents. The inflammatory process can be resolved or be persistent, depending on the etiology and multiple other factors. Chronic inflammation, tissue remodeling, genetic alterations, and modifications in cellular signaling are considered to be key processes promoting immunosuppression. The progressive immunosuppression leads to the inactivation of anti-tumor immunity involved in HCC carcinogenesis and progression. Tumor cellular processes including DNA damage, necrosis, and ER (endoplasmic reticulum) stress can affect both immune-surveillance and cancer-promoting inflammation, supporting a mutual interdependence. Here, we review the current understanding of how chronic liver injury and inflammation is triggered and sustained, and how inflammation is linked to HCC. The identification of many hepatic microenvironmental inflammatory processes and their effector molecules, has resulted in extensive translational work and promising clinical trials of new immunomodulatory agents.