Serologic and molecular biomarkers for recurrence of hepatocellular carcinoma after liver transplantation: A systematic review and meta-analysis

analysis revealed comparable survival rates between patients received ETV and those received LAM (4 weeks: RR = 1.03, 95%CI [0.89, 1.18], P = 0.73; 8 weeks: RR = 0.98, 95% CI [0.85, 1.14], P = 0.84; 12 weeks: RR = 0.98, 95% CI [0.90, 1.08], P = 0.70; 24 weeks: RR = 1.02, 95% CI [0.94, 1.10], P = 0.66). After 24 weeks of treatment, patients treated with ETV had a significantly lower TBIL levels (MD = -37.34, 95% CI [-63.57, -11.11], P = 0.005), higher PTA levels (MD = 11.10, 95% CI [2.47, 19.73], P = 0.01) and higher HBV DNA negative rates (RR = 2.76, 95% CI [1.69, 4.51], P < 0.0001) than those treated with LAM. In addition, no drug related adverse effects were observed in the two treatment groups. Conclusions: ETV and LAM treatments had similar effects to improve 24 weeks survival rate of patients with CHB-associated liver failure, but ETV was associated with greater clinical improvement. Both drugs were tolerated well during the treatment. It is suggested to perform further studies to verify the results.

Entecavir versus Lamivudine therapy for patients with chronic hepatitis B-associated liver failure: a meta-analysis.

The present study aimed to evaluate changes in the expression patterns at the gene and protein levels associated with drug resistance. The study group included 48 women who had a histopathologically confirmed diagnosis of stage I-IV ovarian cancer, they were divided into two subgroups (groups A and B). In group A, there were 36 patients in whom surgical treatment was supplemented with first-line chemotherapy according to current standards. Within this patient group, 5 had stage I (14%), 5 had stage II (14%), 25 had stage III (69%), and 1 had stage IV ovarian cancer (3%). Drug resistance was found after the third cycle of chemotherapy in 17 patients (71%) and after the sixth cycle in 7 patients (29%). Group B included 12 women with type I ovarian cancer, including 11 with stage I and 1 patient with stage IV ovarian cancer. The oncological treatment required only surgery. The control group (C) included 50 women in whom the uterus and adnexa were surgically removed for non-oncological reasons. Significantly higher levels of carcinoma antigen 125 CA-125 and human epididymis protein 4 HE4 were observed in group A and in menopausal women. Moreover, drug resistance was associated with significantly higher levels of CA-125 (p < 0.05). The genes UBA2, GLO1, STATH, and TUFT1 were differentiated in test samples from control samples. Moreover, drug resistance was associated with significantly higher expression of GLO1. The results of these assessments indicated the strong link between UBA2 and hsa-miR-133a-3p and hsa-miR-133b; GLO1 and hsa-miR-561-5p; STATH and hsa-miR-137-3p and hsa-miR-580-3p; and TUFT1 and hsa-miR-1233-3p and hsa-miR-2052. Correlation analysis showed a significant correlation between CA-125 and HE4 levels. Moreover, a significant correlation between TUFT1 mRNA and UBA2, GLO1, STATH (negative correlation), and TUFT1 in relation to CA-125 and HE4 (p < 0.05) was noted in all patients. In view of the lack of screening tests for ovarian cancer, the occurrence of the described correlation may be inscribed as an attempt to establish an assay that meets the criteria of a screening test and thus increase the early diagnosis of ovarian cancer.

/pdf/clinical-and-molecular-evaluation-of-patients-with-ovarian-15kedk7x.pdf

Clinical and molecular evaluation of patients with ovarian cancer in the context of drug resistance to chemotherapy

Methylenetetrahyfrofolate reductase (MTHFR) is the key enzyme for one carbon and folate metabolism. Previous studies have drawn different conclusions about the relationship between the mutation of MTHFR and hepatocellular carcinoma (HCC) occurrence. MTHFR polymorphisms' influence on liver transplantation for HCC recurrence has yet not been reported. Aim of this study was to clarify the impact of MTHFR polymorphism on hepatocarcinogenesis and the prognosis of liver transplant recipient with HCC. This study enrolled 244 HCC patients and 487 healthy individuals in Chinese Han population to analyze the influence of MTHFR polymorphism on HCC susceptibility first. Furthermore, this research choose another 100 donors’ and 104 recipients’ specimens to detect the association between polymorphism of MTHFR and post-transplant HCC recurrence. rs1801131 polymorphism A to C was associated with the occurrence of HCC in Chinese Han population (p < 0.05), especially in age exceeding 50 years (p < 0.01). No association was observed with rs1801133 polymorphism and HCC occurrence. The mean tumor-free survival for recipients with donor liver graft rs1801133 C to T variants was shorter than CC type (12.63 ± 3.84 vs 22.43 ± 4.74 months, p < 0.05). Multivariate analysis revealed that Donor rs1801133 and Hangzhou criteria were two independent prognostic factors for tumor-free survival (p < 0.05). Neither donor rs1801131 polymorphism nor recipients’ MTHFR polymorphisms was associated with HCC recurrence. This study demonstrated that MTHFR polymorphism was associated with HCC occurrence and post-transplant HCC recurrence. rs1801131 mutation A to C is a valuable molecular biomarker for predicting HCC occurrence in Chinese Han population. Donor MTHFR rs1801133 C to T polymorphism could present as a promising prognostic biomarkers for HCC recurrence in liver transplant recipients.

The MTHFR polymorphism affect the susceptibility of HCC and the prognosis of HCC liver transplantation

Immunity-related GTPase M (IRGM), an Interferon-inducible protein, functions as a pivotal immunoregulator in multiple autoimmune diseases and infection. However, the role of IRGM in hepatocellular carcinoma (HCC) development remains unveiled. Here, we found interferon-γ (IFN-γ) treatment in HCC drastically triggered the expression of IRGM, and the high level of IRGM indicated poor prognosis in HCC patients. Functionally, IRGM promoted the malignant progression of HCC. Single-cell sequencing revealed that IRGM inhibition promoted the infiltration of CD8+ cytotoxic T lymphocytes (CTLs) with significant downregulation of PD-L1 expression in HCC. Furthermore, Immunoprecipitation-Mass Spectrometry assay revealed that IRGM interacted with transcription factor YBX1, which facilitated PD-L1 transcription. Mechanistically, IRGM promoted the interaction of YBX1 and phosphokinase S6K1, increasing phosphorylation and nuclear localization of YBX1, transcription of PD-L1. Additionally, the combination of IRGM inhibition with α-PD1 demonstrated a stronger anti-tumor effect compared to the single application of α-PD1. In summary, IRGM is a novel regulator of PD-L1, which suppresses CD8+ CTLs infiltration and function in HCC, resulting in cancer progression. This study may raise a novel therapeutic strategy combined with immune checkpoint inhibitors (ICIs) against HCC. 

IRGM is a novel regulator of PD-L1 via promoting S6K1-mediated phosphorylation of YBX1 in hepatocellular carcinoma.

Lack of association between genetic polymorphisms in cytokine genes and tumor recurrence in patients with hepatocellular carcinoma undergoing transplantation.

High nuclear ABCG1 expression is a poor predictor for hepatocellular carcinoma patient survival.

Immune checkpoint blockades have been widely used to treat various malignancies. Programmed cell death protein 1 (PD-1) inhibitor-induced alopecia areata, one of the immune-related adverse events, is rarely reported. We present a case of alopecia universalis during the treatment of Sintilimab, a monoclonal anti-PD-1 antibody, in a patient with hepatocellular carcinoma. A 65-year-old male was diagnosed with hepatocellular carcinoma in liver segment VI (S6) and chose to receive Sintilimab due to predicted insufficient residual liver volume for hepatectomy. He presented extensive hair loss in all the parts of the body 4 weeks after Sintilimab treatment. And without using any dermatologic drug, the alopecia areata gradually developed to be alopecia universalis after Sintilimab continuous treatment for 21 months. The pathological examination of skin revealed remarkable increased lymphocytes infiltration around the hair follicles, which contained predominantly CD8 positive T cells in the dermis. During single immunotherapy, the tumor marker of serum alpha-fetoprotein level soon decreased from 512.1 mg/L to a normal level within 3 months, accompanied with a remarkable tumor regression in liver S6 by magnetic resonance imaging scans. The patient received hepatectomy and pathological examination demonstrated the nodule was full of extensive necrosis. By combining immunotherapy and hepatectomy, the patient finally achieved a remarkable anti-tumor effect of complete remission. Immune checkpoint blockades-induced alopecia areata is a rare immune-related adverse event and accompanied with a good anti-tumor efficacy in our case. Regardless of alopecia treatment, PD-1 inhibitor treatment is recommended to be continued, especially when the immunotherapy is effective.

Sintilimab-induced Alopecia Universalis in a Patient With the Anti-tumor Effect of Complete Remission After Hepatectomy

OBJECTIVE
This study aims to investigate how miR-561-5p regulated the expression of RAC1 and whether its effects on RAC1 was associated with the proliferation, migration, invasion, and apoptosis in pancreatic ductal adenocarcinoma (PDAC) cells.


MATERIALS AND METHODS
RT-qPCR was performed to assess miR-561-5p expression in human PDAC tissues. A series of in vitro experiments including cell counting Kit-8, colony formation, cell migration and invasion, and apoptosis assays were used to assess the PDAC cell biological behaviors. TargetScan v7.2 was used to identify the miR-561-5p target genes, dual-luciferase reporter assay was performed to confirm the targeted relationship between miR-561-5p and Rac family small GTPase 1 (RAC1). Also, RAC1 was upregulated in miR561-5p overexpressed PDAC cells to evaluate the functional involvement of RAC1 in miR-561-5p mediated PDAC cell proliferation and invasion.


RESULTS
The results demonstrated that miR-561-5p expression was lower in PDAC tissues compared with in normal tissues. Overexpression of miR-561-5p inhibited PDAC cell proliferation, migration, and invasion, and promoted apoptosis in vitro, while miR-561-5p-knockdown had the opposite effects in the PDAC cell line BxPC3. Using bioinformatics analysis and dual-luciferase reporter assays, the present study revealed that RAC1 was a direct target of miR-561-5p and that RAC1 overexpression could partly rescue the suppressive effects of miR-561-5p mimics on PDAC cells.


CONCLUSION
The overexpression of miR-561-5p may suppress carcinogenesis in PDAC cells by targeting RAC1 and inhibit PDAC cell proliferation and invasion.

MicroRNA-561-5p Inhibits Cell Proliferation and Invasion by Targeting RAC1 in Pancreatic Ductal Adenocarcinoma.

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Papers

Lack of association between genetic polymorphisms in cytokine genes and tumor recurrence in patients with hepatocellular carcinoma undergoing transplantation.

High nuclear ABCG1 expression is a poor predictor for hepatocellular carcinoma patient survival.

Sintilimab-induced Alopecia Universalis in a Patient With the Anti-tumor Effect of Complete Remission After Hepatectomy

MicroRNA-561-5p Inhibits Cell Proliferation and Invasion by Targeting RAC1 in Pancreatic Ductal Adenocarcinoma.