A Comparative Study of Laparoscopic and Open Approaches for Right Hemihepatectomy in Hepatocellular Carcinoma Patients: Safety and Short-Term Outcomes.

BACKGROUND Hepatocellular carcinoma (HCC) is a leading cause of cancer deaths worldwide, with China reporting over half of global cases. While traditional open liver resection is effective, it often results in large incisions and significant complications. Laparoscopic hepatectomy, particularly for right hemi-hepatectomy, features smaller incisions and quicker recovery, but its widespread adoption is hindered by its procedural complexity and a steep learning curve. This study compares the safety and efficacy of laparoscopic versus open right hemi-hepatectomy with an anterior approach in 57 patients with HCC. MATERIAL AND METHODS The data of patients with HCC who underwent treatment at our center from January 2016 to December 2020 were retrospectively analyzed. RESULTS We included a total of 57 patients with histopathologically-confirmed HCC - 23 in the laparoscopic group and 34 in the open group. Operation time was significantly shorter in the open group than in the laparoscopic group (234.5±66.9 vs 297.0±74.9, P=0.002). Intraoperative bleeding was significantly less in the laparoscopic group (P=0.042). There were no statistically significant differences in postoperative complications between the 2 groups. Postoperative hospital stay was significantly shorter in the laparoscopic group (12 days vs 15 days, P=0.044). There was no significant difference in postoperative overall survival (OS) and disease-free survival (DFS) between the 2 groups (P>0.05). CONCLUSIONS In patients with hepatocellular carcinoma, the laparoscopic right hemi-hepatectomy with the anterior approach technique has the same safety and comparable short-term outcomes as open surgery.

Megamitochondria plasticity: Function transition from adaption to disease.

As the cell's energy factory and metabolic hub, mitochondria are critical for ATP synthesis to maintain cellular function. Mitochondria are highly dynamic organelles that continuously undergo fusion and fission to alter their size, shape, and position, with mitochondrial fusion and fission being interdependent to maintain the balance of mitochondrial morphological changes. However, in response to metabolic and functional damage, mitochondria can grow in size, resulting in a form of abnormal mitochondrial morphology known as megamitochondria. Megamitochondria are characterized by their considerably larger size, pale matrix, and marginal cristae structure and have been observed in various human diseases. In energy-intensive cells like hepatocytes or cardiomyocytes, the pathological process can lead to the growth of megamitochondria, which can further cause metabolic disorders, cell damage and aggravates the progression of the disease. Nonetheless, megamitochondria can also form in response to short-term environmental stimulation as a compensatory mechanism to support cell survival. However, extended stimulation can reverse the benefits of megamitochondria leading to adverse effects. In this review, we will focus on the findings of the different roles of megamitochondria, and their link to disease development to identify promising clinical therapeutic targets.

Bile is a reliable and valuable source to study cfDNA in biliary tract cancers.

Objective: The aim of this study is to determine the clinical efficacy of bile-derived liquid biopsy compared with plasma and tumor tissue biopsy in patients with biliary tract carcinoma (BTC). Methods: A total of 13 patients with BTC were enrolled in this cohort. Tumor tissue, bile, and plasma samples were obtained and analyzed using next-generation sequencing for genomic profiling. Results: Bile and plasma samples were collected from all 13 patients, and 11 patients also had matched tumor tissues available. The cell-free DNA (cfDNA) concentration was significantly higher in the bile supernatant than in plasma (median: 1918 vs. 63.1 ng/ml, p = 0.0017). The bile supernatant and pellet had a significantly higher mean mutation allele frequency (MF) than plasma (median: 3.84% vs. 4.22% vs. 0.16%; p < 0.001). Genomic alterations were predominantly missense. Both bile supernatant and pellet had significantly more genomic alterations than plasma (average: 9.3 vs. 7.2 vs. 2.3 alterations per sample; p < 0.01). Among the top 10 most frequent genomic alterations, the consistency between bile supernatant and tumor tissue was 90.00% (18/20), that between bile pellet and tumor tissue was 85.00% (17/20), and that between the plasma and tissue was only 35.00% (7/20). MAF of both bile supernatant and pellet was positively correlated with that in tissue samples (ρ < 0.0001, spearman r = 0.777, and ρ < 0.0001, spearman r = 0.787, respectively), but no significant correlation with tissue was found in the plasma (ρ = 0.966, spearman r = 0.008). Furthermore, additional genomic alterations could be detected in bile supernatant and pellet than in tissue. Potential targets for targeted therapy were identified in bile supernatant and pellet. Regarding copy number variation (CNV) and chromosomal instability (CIN) detection, four additional CNVs from two patients were detected in the bile supernatant that was not detected in tissues (i.e., amplification of TERC, IL7R, RICTOR, and TERT). CIN was significantly higher in tumor tissue than in plasma. The CIN of the bile was also significantly higher than that of plasma. There was no significant difference in CIN between the tissue and the bile supernatant. Conclusion: The consistency of all genomic alterations and tumor tissue-determined genomic alteration in the bile supernatant/pellet was significantly higher than in plasma. Bile supernatants/pellets are better for genetic sequencing and may also have potential clinical value to guide targeted therapy and evaluate prognosis. Bile cfDNA may be a feasible substitute for tumor tissue in the genetic testing of patients with BTC.

PCAT6 May Be a Whistler and Checkpoint Target for Precision Therapy in Human Cancers.

LncRNAs are involved in the occurrence and progressions of multiple cancers. Emerging evidence has shown that PCAT6, a newly discovered carcinogenic lncRNA, is abnormally elevated in various human malignant tumors. Until now, PCAT6 has been found to sponge various miRNAs to activate the signaling pathways, which further affects tumor cell proliferation, migration, invasion, cycle, apoptosis, radioresistance, and chemoresistance. Moreover, PCAT6 has been shown to exert biological functions beyond ceRNAs. In this review, we summarize the biological characteristics of PCAT6 in a variety of human malignancies and describe the biological mechanisms by which PCAT6 can facilitate tumor progression. Finally, we discuss its diagnostic and prognostic values and clinical applications in various human malignancies.