Hepatocellular Cancer

NRM model demonstrated favorable performance in predicting early recurrence in NRM-HCC patients. This novel model will be helpful to guide postoperative follow-up and adjuvant therapy.

Treatment options of drugs targeting ferroptosis are further concluded. Determining different triggers of ferroptosis can clarify the mechanism of ferroptosis occurs at both physiological and pathological levels.

Radiomics has potential to link TME immune phenotypes with HCC prognosis. CD2 is a key biomarker connecting NK cells with radiomic features, offering a new classification of HCC into radiogenomic subtypes. This approach supports the use of radiogenomics in personalized HCC treatment.

Overall, farrerol suppresss HCC by inhibiting migration, invasiveness, the EMT, and angiogenesis, implying that farrerol could be a promising antimetastasis agent for HCC.

Docking studies revealed interactions between the derivatives and the signaling proteins AKT (PDB ID: 6HHF) and BRAF (PDB ID: 8C7Y) with binding affinities ranging from -7.10 to -9.91, highlighting their pivotal role in targeting key players in hepatocellular carcinoma progression. The findings of this study underscore the therapeutic potential of these derivatives against HepG2 cells and offer valuable insights for further experimental validation of their efficacy as inhibitors targeting AKT or BRAF signaling pathways.

The normal function of liver and dendritic cells was also associated with a good prognosis in HCC. This study analyzed the interaction of the immune microenvironment with HCC prognosis, identifying ZNF296 as a promising diagnostic and therapeutic target for HCC.

Our study establishes the prognostic significance of TIGIT and NKG2A expression in predicting OS and RFS following radical liver resection for HCC patients. The developed prognostic models incorporating TIGIT and NKG2A expression hold promise for improving risk stratification and clinical management of HCC patients.

Studies have not specifically examined the impact of PNPLA3 in lean individuals.

This seven-gene-based model showed stable outcomes in predicting HCC prognosis as well as responses to immunotherapy.

The results of the present study suggested that druggable gene alterations may provide useful information not only in proposing alternative treatment after standard of care but also in selecting second-line targeted treatments after immunotherapy for patients with advanced HCC.

These findings emphasize the need for comprehensive pediatric surgical guidelines for HCC. We recommend LT over LR in pediatric cases. Extrahepatic disease post-neoadjuvant chemotherapy remains the only absolute contraindication.

Nlrp6 overexpression inhibits lipid synthesis in HCC cells by regulating the AMPK-Srebp1c axis, which might be a key pathway for suppressing HCC cell proliferation.

Finally, GPN1 upregulation was confirmed to promote the migration of HCC cells. This study provides a comprehensive overview of GPN1 in human cancer and demonstrates that GPN1 contributes to the migration of HCC cells, potentially serving as a prognostic and immunotherapy biomarker.

Hepatic TYMP expression level may serve as a promising imaging biomarker for differential diagnosis of SS and MASH. SPECT imaging using [123I]IIMU potentially provides a novel noninvasive diagnostic method to differentiate MASH and SS.

This investigation shows that during the process of AG ameliorating BDL-induced liver fibrosis, bile acid derivatives such as CDCA, TCDCA, 3-DHC, UCA, DCA, among others, play significant roles. In this study, we identified that several non-bile acid metabolites, such as Deltarasin, Thr-Ile-Arg, etc., are entailed in the process of AG improving liver fibrosis.

Therefore, the Notch1/Hes1/PTEN pathway may act upstream of SPINK13 to downregulate the PI3K/Akt signaling pathway. Our study helps elucidate the underlying mechanism of SPINK13 in anti-hepatocellular carcinoma and lays a theoretical foundation for the development of novel therapeutic serine protease inhibitors.

Our study revealed that the expression of miR-192-2, a crucial tumor suppressor gene, was suppressed by the presence of HBV.

The results from differential analysis using three R packages are robust, revealing genes closely linked to immune cell infiltration in the tumor microenvironment. Additionally, a validated prognostic model for liver cancer was established based on key genes.

On days 0, 7, and 14, the percentages of CD4+ T cells, CD8+ T cells, and NK cells in the spleen of group C were significantly increased compared with groups A and B. Additionally, the Th1/Th2 ratio was significantly increased in group C. Serum TGF-β1 expression was elevated after cryoablation, but KCl solution reduced the high TGF-β1 expression after cryoablation and decreased the invasiveness of cancer cells. Finally, the proliferative activity of untreated tumor tissue was significantly reduced in group C compared to groups A and B. In summary, Cryoablation triggered a systemic immune response in tumor-bearing mice, which was further boosted by combining cryoablation with a KCl solution.

Conversely, fluorescein did not attenuate the phosphorylation of JNK. These results strongly suggest that Gβγ subunits act as positive regulators in TGF-α-induced migration of HCC cells via the JNK signalling pathway.

In this pilot study, we observed the association of MT levels in healthy probands and malignant liver tumor patients. Many previous studies show that MT concentrations are increasing as the illness progresses. We assume that this increase is connected to the high metabolic activity of cancer cells. This study will continue with collecting a larger number of samples.

Additionally, HURP partially overlaps with the microtubule-binding site of the Kif18A motor domain, indicating that excess HURP inhibits Kif18A motility by steric exclusion. We also observe that HURP and Kif18A function together to suppress dynamics of the microtubule plus-end, providing a mechanistic basis for how they collectively serve in microtubule length control.

CKD-581 prohibits LIHC progression via inhibiting the cell cycle signaling pathway. CKD-581 holds promise as a therapeutic agent for the clinical management of LIHC.

Our findings suggest that the mutual validation of big data analysis and functional experiments may facilitate the precise identification and definition of biomarkers, and our m6A risk models may have the potential to guide personalized chemotherapy, targeted treatment, and immunotherapy decisions in HCC.

Our study indicates that the miRAGe panel has low rate of both missed diagnosis and misdiagnosis rates, potentially serving as a useful diagnostic tool for HBV-related HCC in early stage, which may subsequently contribute to improve the prognosis.

Mechanistically, MANF enhanced the HSF1-HSP70-1 interaction, restricted HSF1 in the cytoplasm of macrophages, and decreased both mRNA and protein levels of HSP70-1, which in turn led to reprogramming TAMs, and suppressing neovascularization of HCC. Our study contributes to the exploration the mechanism of TAMs reprogramming, which may provide insights for future therapeutic exploitation of HCC neovascularization.

Furthermore, as in bladder urothelial carcinoma (BLCA), breast invasive carcinoma (BRCA), and kidney renal papillary cell carcinoma (KIRP), HDAC1 expression was found to be correlated with inflammatory cell infiltration. The levels of HDAC1 are expected to adapt to clinical adjuvant targeted therapy in most types of solid cancer.

Molecular docking and dynamic studies confirmed strong binding affinity and stability of Baicalein, Chrysin, Quercetin, and Myricetin with receptor targets within simulation time. This study provides insight into the mechanism of action of EKP on HCC and identifies AKR1C3 and MAPK1 as candidate target treatments for future drug development.

Finally, immunohistochemical (IHC) analysis not only validates our findings but also reiterates the novelty of the identified genes. Overall, elucidating the role of these novel genes and regulatory elements could pave the way for an earlier and more accurate diagnosis of liver diseases.

Comparison between low ( n = 464 patients) and high ( n = 302 patients) galectin-3 levels showed that mean serum galectin-3 levels were significantly higher in patients with HCC who had hepatitis C virus (HCV) infection ( p = 0.0001), higher Child-Pugh score (CPS) ( p = 0.0009), and higher Cancer of the Liver Italian Program (CLIP) score ( p = 0.0015). Our study shows that serum galectin-3 level is a valid prognostic biomarker candidate.

Similarly, in mouse models, PMEPA1 overexpression promotes HCC development, which demonstrates its oncogenic role. The identification of PMEPA1 as oncogenic driver in HCC and its role in immune exhaustion and poor clinical outcomes enhances our understanding of HCC pathogenesis and opens new avenues for targeted therapeutic interventions.

The combined use of GSTA1 and CTNNB1 inhibitors demonstrated synergistic anti-tumour effects through the induction of ferroptosis both in vitro and in vivo. Our findings reveal a novel regulatory role of the GSTA1/CTNNB1 axis in ferroptosis, suggesting that targeting GSTA1 and CTNNB1 could be a promising strategy to circumvent sorafenib resistance in HCC.

Gla regulates the expression levels of DUSP5, ZFP36, KLF10, NR4A1, and RMI2 to against HCC, providing valuable insights for the application of Gla in HCC treatment.

In addition, the high expression of model gene produced drug resistance to trametinib, selumetinib and RDEA119 (refametinib). The prognostic risk model based on six prognostic related DEGs is an independent prognostic factor of HCC, which can effectively predict the survival and prognosis of HCC patients.

Overall, the recent studies presented at the ASCO meeting highlight progress in HCC treatment, underscoring the importance of continued innovation. Future research should focus on overcoming resistance mechanisms, optimizing combination therapies, and integrating biomarker-driven approaches to improve patient outcomes and enhance personalized treatment strategies.

This article examines the role of the Nrf2/HO-1 signaling pathway in MASLD and highlights natural compounds that protect against MASLD by targeting Nrf2/HO-1 activation. The findings indicate that the Nrf2/HO-1 signaling pathway holds great promise as a therapeutic target for MASLD.

Our results confirmed that the CHI3L1 could serve as an independent predictor for OS in HCC patients after hepatectomy. The nomogram showed a good performance in prognosis prediction of HCC.

Additionally, HBV gene expression was shown to activate the PI3K/AKT pathway by modulating Foxp4 mRNA stability in HCC cells. This study provides valuable insights into the underlying mechanisms of HBV infection and its potential implications for cancer development.

The hRipk3-KI and hMlkl-KI mice showed significantly more and larger tumor nodules. Our study provides the first direct evidence that inflammation induced by necroptosis arising from hepatocytes can lead to the progression of hepatic steatosis to fibrosis in obese mice that eventually results in an increased incidence in hepatocellular adenomas.

The effectiveness of anti-CXCR4/PD1 therapy was compromised entirely in Batf3-KO mice deficient in cDC1s. Thus, combined CXCR4/PD1 blockade can reprogram intra-tumoral cDC1s and holds the potential to potentiate antitumor immune response against HCC.

Masitinib counteracted PGK1 upregulation by CSTF2 and suppressed the growth of HCC xenograft and patient-derived organoid models. In conclusion, this study revealed a function of CSTF2 in supporting HCC survival under hypoxia conditions through m6A modification evasion and metabolic reprogramming, indicating inhibiting CSTF2 may overcome hypoxia tolerance in HCC.

This study identified trans-kingdom microbial signatures associated with ICI in multi-cancer and specific cancer types. Trans-kingdom microbial biomarkers are potential predictors of ICI response in patients with cancer.