[Hepatic resection using glissonean pedicle transection].

K Takasaki

Home/Archive/PubMed

PubMed · 9642694

[Hepatic resection using glissonean pedicle transection].

K Takasaki

View original source ↗Export metadata ↓

Abstract

The basics of hepatic resection using the glissonean pedicle transection method are presented. The portal triad continues from the hepatoduodenal ligament to the intrahepatic portion in the from of the glissonean pedicle, i.e., the artery, portal vein, and bile duct are Combined with connective tissue and sheathed by the peritoneum in the form of a fibroid bundle. The full length of the primary branches and the origin of secondary branches are located extrahepatically, and the trunk of the secondary and more peripheral branches have an intrahepatic course. The ramification pattern of the tertiary branches of each secondary branch varies by individual. The liver is nourished by the 3 secondary branches of the glissonean pedicle. Each secondary branch supplies one segment, and therefore the liver can be divided into 3 segments and the additional caudate area. The area supplied by each of the tertiary branches is cone shaped ("cone unit"). Each segment is composed of from 6 to 8 cone units. The standard method for hepatic resection is the segmental resection method, in which one secondary branch is transected. In cases of limited resection, the number of cone units to be resected is adjusted, and the tertiary branches which supply them must also be transected selectively through the hilar or parenchymal approach. The author has performed hepatic resection using the glissonean pedicle transection method in 834 consecutive patients with hepatocellular carcinoma with no trouble.

Explore related subjects

Carcinoma, Hepatocellular Hepatectomy Humans Liver Liver Neoplasms Portal Vein Vascular Surgical Procedures English Abstract Journal Article Review

Keep this discovery

Explore connections, maps & timelines

BibTeX RIS

K Takasaki. 1998. [Hepatic resection using glissonean pedicle transection].. https://pubmed.ncbi.nlm.nih.gov/9642694/

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

PubMed2026

Pan-cancer analysis identifies KANSL2 as a cell-cycle-associated regulator of tumor progression and immunity in liver hepatocellular carcinoma.

KANSL2, a core component of the NSL histone acetyltransferase complex, has been implicated in tumorigenesis. However, its pan-cancer relevance and functional role in liver hepatocellular carcinoma (LIHC) remain unclear. Multi-omics data from TCGA, GEO, and HPA were integrated to systematically evaluate KANSL2 expression, clinical significance, genomic alterations, and immune associations across cancers. Functional enrichment, immune infiltration analyses, and single-cell transcriptomics were performed. In vitro assays were conducted to validate the biological effects of KANSL2 in LIHC cells. KANSL2 is broadly upregulated across cancers and exhibits strong diagnostic performance. Elevated KANSL2 expression correlates with unfavorable prognosis, particularly in LIHC. Mechanistically, KANSL2 and its co-expressed genes are enriched in cell-cycle progression. KANSL2 expression is also closely associated with immune infiltration and immunoregulatory signaling within the tumor microenvironment, with single-cell data indicating preferential expression in proliferative T-cell subsets. Functional experiments demonstrate that KANSL2 silencing suppresses proliferation, migration, and invasion, and induces G2/M phase arrest in LIHC cells. Notably, its effects on apoptosis are limited, suggesting that KANSL2 primarily drives tumor progression through cell-cycle-dependent mechanisms. This study identifies KANSL2 as a key regulator of tumor progression and immune remodeling in LIHC. By promoting malignancy predominantly via cell-cycle control, KANSL2 represents a promising biomarker for diagnosis and prognosis, and a potential therapeutic target.

Carcinoma, Hepatocellular↗

PubMed2026

LARS promotes hepatocellular carcinoma progression via the PI3K/AKT/mTOR pathway and interaction with RPS5, and serves as a prognostic biomarker.

BACKGROUND: Hepatocellular carcinoma (HCC) caused many cancer deaths around the world. Its progression involves complex mechanisms, creating an urgent need to identify new therapeutic targets. Leucine-tRNA synthetase (LARS) is a key enzyme for protein synthesis, but its specific role and mechanism in HCC are not well understood. PURPOSE: This research aims to investigate the biological function, molecular mechanism, and clinical relevance of the LARS gene in HCC progression, to assess its potential as a treatment target. METHODS: LARS expression was assessed in HCC cell lines (PLC-PRF-5, HCC-LM3) and in mouse subcutaneous tumor models using siRNA and adeno-associated virus (AAV). Techniques including Cell Counting Kit-8(CCK-8), colony formation, EdU, Transwell, wound healing, and flow cytometry were used to measure cell proliferation, migration, invasion, and apoptosis. RNA-seq, proteomics (TMT), western blot, co-immunoprecipitation (Co-IP) with mass spectrometry, molecular docking, and molecular dynamics simulation were employed to study the affected signaling pathway (PI3K/AKT/mTOR) and interacting protein (RPS5). The TCGA (The Cancer Genome Atlas) database and UALCAN platform were used to analyze links between LARS expression and clinicopathological features or prognosis in HCC patients. RESULTS: Reducing LARS expression significantly inhibited the proliferation, colony formation, migration, and invasion of HCC cells, while promoting apoptosis. In mice, LARS knockdown markedly slowed tumor growth. Mechanistic studies showed that reducing LARS expression levels affected the PI3K/AKT/mTOR signaling pathway and led to decreased levels of the key interacting protein RPS5. Overexpressing RPS5 partly reversed the proliferation inhibition caused by LARS depletion. Molecular docking and dynamics simulations suggested that the environmental contaminant triphenyl phosphate (TPP) might bind to the LARS protein. Clinical data analysis revealed that LARS expression is higher in HCC tissues. High LARS expression was significantly associated with shorter overall survival (OS) in patients and correlated positively with various clinical features like tumor stage, grade, and TP53 mutation status. CONCLUSION: LARS helped HCC become worse by affecting the PI3K/AKT/mTOR pathway and working with RPS5. High LARS meant a worse outcome for patients. This suggested LARS could be used to predict disease or as a treatment target in HCC.

Carcinoma, Hepatocellular↗

PubMed2026

Integrative Multi-Omics Mendelian Randomization Analysis Identifies NIT2 as a Potential Metabolic Risk Gene in Hepatocellular Carcinoma.

BACKGROUND: Metabolic pathways are crucial in hepatocellular carcinoma (HCC) pathogenesis, but causal metabolic genes remain unclear. This study used Summary data-based Mendelian Randomization (SMR) and colocalization to identify metabolism-related genetic loci influencing HCC risk. METHODS: Differentially expressed genes in hepatic malignancy phenotype versus normal tissues from TCGA and GTEx were analyzed. Metabolism-related candidates were examined via SMR and colocalization using multi-omics data: methylation (mQTL), expression (eQTL), and protein (pQTL) quantitative trait loci. RESULTS: Multi-omics integration identified NIT2 as a key metabolic regulator for HCC. The cg13016775 locus of NIT2 was associated with elevated HCC risk at gene (OR = 1.618, 95% CI: 1.199-2.182) and protein (OR = 4.432, 95% CI: 1.783-11.018) levels. Colocalization supported a shared causal variant (PPH4 > 0.6), linking NIT2 to hepatocarcinogenesis via metabolic regulation. CONCLUSIONS: This study provides multi-omics evidence for NIT2 as a potential causal gene in HCC, enhancing understanding of metabolic contributions to HCC pathogenesis and highlighting integrative genomics for uncovering causal relationships.

Carcinoma, Hepatocellular↗