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Global Translational Medicine                                         Cirrhosis and hepatocellular carcinoma




            Table 5. Occurrence of vascular invasion in patients with different tumor size
            First cohort                                    Tumor size                                  P‑value
                                   ≤2cm           >2 and≤5cm        >5 and≤10cm         >10 cm
                                  (n=34)           (n=153)            (n=106)           (n=41)
            Vascular invasion                                                                           <0.001
             Yes                   1 (2.9)          4 (2.6)           6 (5.7)           8 (19.5)
             No                   33 (97.1)        149 (97.4)        100 (94.3)         33 (80.5)
            Second cohort                                   Tumor size                                  P‑value
                                   ≤2cm           >2 and≤5cm        >5 and≤10cm         >10 cm
                                  (n=128)          (n=346)            (n=339)           (n=274)
            Vascular invasion                                                                           <0.001
             Yes                   8 (6.2)         35 (10.1)         131 (38.6)        176 (64.2)
             No                  120 (93.8)        311 (89.9)        208 (61.4)         98 (35.8)


            fibrosis may play a protective role [15-17] . Further, a recent   in these patients may also lead to a higher probability of
            study showed that the value of liver stiffness measurement   vascular invasion and extrahepatic metastases.
            inside the tumor and in the peri-tumoral tissue was   The present study also showed that globulin is a
            negatively correlated  with serum alpha-fetoprotein   risk factor for HCC tumor growth, while albumin is a
            (P < 0.05) , which to some extent supports the above   protective factor. This result is justifiable since the albumin
                    [18]
            idea  that cirrhosis is  an important factor  which  is   levels reflect the nutrition status of patients, and numerous
            negatively associated with the tumor size, since the value   studies have shown that malnourished patients with HCC
            of liver stiffness measurement would reflect the severity   with low serum albumin levels have poor overall survival
            of cirrhosis and the alpha-fetoprotein level is strongly   and high recurrence rate . In contrast, high levels of
                                                                                    [26]
            correlated with the tumor size . Besides, the importance   globulin  indicate  a  systematic  inflammatory  response,
                                    [19]
            of fibrosis as an activator of the immune system against   which plays an important role in proliferation, progression,
            cancer has been previously shown in pancreatic     development, and metastasis of tumor cells [26-28] .
            cancers [20,21] , where fibrosis development and cirrhosis-
            induced inflammation might prime the immune system   The current study is restrained by several limitations.
            and ensure a better response against malignant cells   Although we had excluded the patients having anti-HBV
            present in the liver . However, it should be emphasized   treatment within 6 months before prior to HCC diagnosis,
                           [9]
            that this process is harmful in the long term, as indicated   to reduce the potential influence of different screening
            by our results that patients with decompensated cirrhosis   frequency between patients with and without cirrhosis,
            had larger tumor size (a higher proportion of patients   some bias may still exist because of the retrospective and
            had tumor >5  cm) and a significantly higher rate of   cross-sectional nature of this study. In addition, the disease
            vascular invasion and extrahepatic metastasis than   background of both cohorts was not exactly the same;
            those with compensated cirrhosis and non-cirrhosis.   therefore, similar results observed from the two cohorts
            When cirrhosis progresses to decompensated cirrhosis,   might verify its reliability only to some extent but could not
            immune dysfunction in HCC patients with severely   be compared directly with each other. Further, only HBV-
            decompensated cirrhosis would result in significant   infected patients were investigated in this study; therefore,
            tumor growth and metastasis . Decreased efficiency of   future studies including patients with other etiological
                                    [13]
            cell durotaxis and increased level of stiffness from soft   factors of HCC are warranted.
            matrix to rigid matrix has been reported previously ,
                                                        [22]
            which may explain the limitation on HCC tumor margins   5. Conclusion
            as seen in the patients with cirrhosis. However, many   In summary, this retrospective multicenter study
            studies have shown that tumor cells would spread better   demonstrated that HCC patients with compensated
            and migrate faster in the rigid matrix than in the soft   cirrhosis tend to harbor smaller tumor but severe cirrhosis
            matrix [23-25] . These studies may also explain why vascular   favors tumor vascular invasion and metastasis, which
            invasion occurred more frequently in HCC patients with   affect tumor recurrence and survival of the patients.
            cirrhosis, especially in patients with decompensated   This  further  reminds  us that for  patients  with  cirrhosis,
            cirrhosis. In addition, changes of vascular permeability   especially those with decompensated cirrhosis, risk of


            Volume 1 Issue 2 (2022)                         7                       https://doi.org/10.36922/gtm.v1i2.94
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