Biomedical subjects

Yuji Nimura

Publications and source records attributed to Yuji Nimura.

At least 19 recordsLinked to original sources

PubMed2007

Prognostic value of tumor architecture, tumor-associated vascular characteristics, and expression of angiogenic molecules in pancreatic endocrine tumors.

PURPOSE: It is difficult to predict the biological behavior of pancreatic endocrine tumors (PETs). Our aim was to evaluate the prognostic significance of certain variables in PETs. EXPERIMENTAL DESIGN: The following variables were examined in 37 patients with PETs and then compared with other clinicopathologic characteristics: histologic tumor structure; microvessel density (MVD) measured by three different methods, including a unique method involving calculation of solid area MVD; endothelial proliferation; and the immunohistochemical expression of vascular endothelial growth factor-A and CXC chemokine CXCL-12. Intratumoral vascular structures were analyzed by double immunofluorescence using 30-microm-thick sections. RESULTS: The presence of focal and intensive solid growth of tumor cells (large solid nests; P = 0.003), low solid area MVD (P = 0.002), a high endothelial cell proliferation index (EPI; P = 0.005), and high expression of CXCL-12 in PET cells (P = 0.018) were significant unfavorable prognostic indicators. The predominant structure of the overall tumor histology and the expression of vascular endothelial growth factor-A did not separate aggressive PETs. In areas of focal solid growth, tumor-associated blood vessels had obviously low MVD and high EPI, and their structures were poorly formed with highly abnormal features, in comparison with other areas. High expression of CXCL-12 in tumor cells was significantly associated with variables representing tumor growth, hematogenous tumor spread, low MVD, high EPI, and the presence of large solid nests. CONCLUSIONS: This study has provided novel findings on the prognostic features of tumor architecture and tumor-associated angiogenesis in PETs. CXCL-12 is the first candidate molecule in association with neoangiogenesis in PETs.

Adolescent↗

PubMed2006

Is there any effect of renal failure on the hepatic regeneration capacity following partial hepatectomy in rats?

The effects of renal dysfunction on liver regeneration capacity have not been fully elucidated before, although many patients with renal failure are subjected to hepatectomy due to hepatobiliary diseases. In this study, we sought to determine the effects of renal dysfunction on the hepatic regeneration capacity using rat chronic renal failure model. After establishing chronic renal failure (CRF group) by semi-total renal resection, the rats were subjected to 70% partial hepatectomy (PHx). Rats without renal failure were used as control (Sham group). The hepatic regeneration rate, histology of the liver, clearance of indocyanine green into the bile, and the expression of hepatic regeneration-associated genes in the liver were evaluated. The hepatic regeneration rate was lower in CRF group as compared to Sham group on day 1 after PHx. Mitotic index evaluated by histologic examination on day 1 after PHx was also significantly lower in CRF group. However, no difference in these indices was observed on day 2 and 7 between Sham and CRF. Indocyanine green clearance rate was almost identical between Sham and CRF on day 7 following PHx. The baseline expressions of the hepatic regeneration-associated genes, such as IL-6, TNF-alpha, HGF, c-fos, and c-jun, in the liver of CRF were significantly lower than those of Sham. However, the rate of upregulation of these genes was not significantly different between Sham and CRF. These results clearly demonstrate that the renal dysfunction, although initially delays the onset, does not suppress the total hepatic regeneration capacity following partial hepatectomy. The function of the regenerated liver on day 7 after PHx also was not different. Our results provide a possibility that the hepatectomy can be indicated even for the patient with a chronic renal failure.

Animals↗

PubMed2006

Does estrogen contribute to the hepatic regeneration following portal branch ligation in rats?

The aim of this study was to determine whether estrogen plays any role in the hepatic regeneration of nonligated lobe following portal branch ligation (PBL). Male rats were subjected to PBL on the left and middle lobes. Two and 7 days after PBL, the rats were killed and blood and liver samples were analyzed. Sham animals underwent only laparotomy. The serum estradiol levels were significantly elevated on day 2 following PBL and returned to normal levels on day 7. The expression of estrogen receptors (ER) in the liver evaluated by Western blotting did not show any change in the nonligated lobe compared with shams. Immunohistochemical study for ER showed a predominant ER expression in the hepatocyte nucleus in periportal area (zone 1), although there was no apparent difference in the amount and expression pattern between sham and PBL. However, chronic inhibition of ER by an ER antagonist (ICI 182,780) showed a significantly lower regeneration rate of the nonligated lobe compared with vehicle treatment. Liver regeneration-associated genes also were less activated in the ICI group. Moreover, portal venous flow, determined by fluorescent microsphere injection, was significantly lower in the ICI group compared with vehicle group. These changes correlated with the attenuated expression of endothelial nitric oxide synthase mRNA in both superior mesenteric arteries and veins. In conclusion, these results indicate that the estrogen's contribution on hepatic regeneration following PBL is at least partly mediated through maintaining mesenteric blood flow by mesenteric endothelial nitric oxide synthase upregulation rather than directly activating liver regeneration in the liver.

Alanine Transaminase↗

PubMed2006

Disruption of phospholipase Cdelta4 gene modulates the liver regeneration in cooperation with nuclear protein kinase C.

Phospholipase Cdelta4 (PLC delta4) gene has been cloned from the cDNA library of regenerating rat liver. Using PLC delta4 gene-disrupted mice (PLC delta4(-/-)), we studied a role of PLC delta4 during liver regeneration after partial hepatectomy (PH). In PLC delta4(-/-), liver regeneration occurred in an apparently normal way. However, BrdU-indices indicated that PLC delta4 gene disruption delayed the onset of DNA synthesis by 2 h. Noticeably, the BrdU-indices in PLC delta4(+/+) remained rather constant throughout S phase, 25-35%, whereas in PLC delta4(-/-), it fluctuated drastically from 25% at 34 h to 65% at late S, 42 h after PH. This fact showed that PLC delta4 gene disruption caused a higher synchronization of cell proliferation. The mRNA for PLC delta4 in PLC delta4(+/+) appeared at late G1, and the expression continued throughout S phase. PLC activity increased transiently in chromatin at the late G1 and S phases in only PLC delta4(+/+), but not in PLC delta4(-/-). The specific increases in PLC activity well correlated with the transient increases of protein kinase C (PKC) alpha in chromatin of PLC delta4(+/+). PKC epsilon also increased transiently in chromatin from PLC delta4(+/+) at late S. It is concluded that PLC delta4 regulates the liver regeneration in cooperation with nuclear PKC alpha and epsilon.

Animals↗

PubMed2006

Urinary gamma-glutamyltransferase (GGT) as a potential marker of bone resorption.

We recently identified gamma-glutamyltransferase (GGT) as a novel bone-resorbing factor. The present study was undertaken to determine whether GGT is a marker of bone resorption in two genetic models of hyper- and hypo-function of osteoclasts, as well as in postmenopausal women with accelerated bone resorption, using type I collagen N-telopeptide (NTX) and deoxypyridinoline (DPD) as established biochemical markers. Urinary excretion of GGT, corrected for creatinine, was found to be increased in osteoprotegerin (OPG)-deficient osteoporotic mice as well as in patients with postmenopausal osteoporosis (67-83 years of age); in both cases the urinary level decreased after treatment of patients or mice with alendronate, a selective inhibitor of bone resorption, concomitantly with a reduction in DPD and NTX. Conversely, in osteopetrotic op/op mice, urinary GGT increased in parallel with DPD after induction of osteoclasts with M-CSF injection. Constant infusion of parathyroid hormone (PTH) also increased urinary GGT along with DPD. In a survey of 551 postmenopausal women (50-89 years of age) at their regular health checkup, urinary GGT excretion exhibited a high correlation with DPD (rho = 0.49, p < 0.0001). The calculated sensitivity and specificity for diagnosing elevated bone resorption, as determined by a DPD value higher than 7.6 nM/mM Cr, were 61% and 92%, respectively, when a cut-off value of 40 IU/g Cr was assigned for urinary GGT. Since GGT activity can be measured inexpensively in large numbers in a very short time, the measurement of urinary level may provide a convenient and useful method for mass screening to identify those with increased bone turnover and hence at increased risk for bone fracture.

Aged↗

PubMed2006

Biphasic activation of liver regeneration-associated signals in an early stage after portal vein branch ligation.

At an early stage in liver regeneration, a variety of factors including transcriptional factors, proinflammatory cytokines, and proto-oncogenes are activated or expressed. However, these responses are affected by surgical stress in the conventional portal vein branch ligation model (PVL). We sought to determine the net activation of early regeneration-associated signals after PVL using a newly developed non-surgical stress PVL model. Male Wistar rats were assigned into two groups, a stress-PVL (sPVL) model with laparotomy and portal vein branch ligation, and a non-stress-PVL (nsPVL) one subjected to portal vein branch ligation 1 week after laparotomy in which the effects of surgical stress were subsided. The activation of transcriptional factors and expression of immediate early genes were analyzed at an early time point (within 24 h) by Western blotting and RT-PCR, respectively. A monophasic upregulation of nuclear factor-kappaB (NF-kappaB) and phosphorylated-signal transducer and activator of transcription 3 (p-STAT3) peaked at 3h after sPVL was observed. In contrast, the expression pattern of these factors was biphasic (first peak at 0.5-1 h, second peak at 3-6 h) in nsPVL group. The expression pattern of immediate early genes showed a similar trend between sPVL and nsPVL. cDNA array analysis for the non-ligated lobe at 2 h after PVL revealed a much higher gene activation in sPVL than in nsPVL. These results indicate that previously observed activation pattern of regeneration-associated signals after PVL is significantly affected by the effect of laparotomy and our results using nsPVL model may more accurately represent liver regeneration-associated signal pattern.

Animals↗

PubMed2006

Evaluation of hepatic interleukin-6 secretion following portal vein ligation using a minimal surgical stress model.

BACKGROUND: Animal portal vein ligation (PVL) model requires laparotomy under general anesthesia, which induces systemic inflammatory response, and makes the analysis of early signals for hepatic regeneration difficult. We developed a nonstress PVL model, which performs the ligation after surgical stress is subsided, and evaluated the hepatic IL-6 production at early phase of PVL. MATERIALS AND METHODS: After laparotomy under general anesthesia, a monofilament suture was placed around the left portal vein and knotted, but not tied, and the two ends were delivered through each flank. Seven days after laparotomy, PVL was created by pulling the two ends of the ligature, tightening the ligature. RESULTS: Biochemical assays indicated that the surgical stress of laparotomy resolved on day 7. Rate of liver regeneration of the nonligated lobe in this model was similar to that in the conventional PVL model. The serum interleukin-6 concentration rose rapidly (within 3 h) after PVL and remained elevated until 6 h. RT-PCR demonstrated that transcripts of IL-6 gene significantly increased 3 h after ligation in the nonembolized lobes. Furthermore, in situ hybridization for IL-6 mRNA was stained at sinusoidal endothelial cells, especially periportal area. CONCLUSIONS: Our PVL model minimizing surgical stress was comparable to the stress of clinical portal vein embolization. Using this model, we found an increased expression of IL-6 mRNA in the sinusoidal endothelial cells predominantly at the periportal area.

Animals↗

PubMed2006

Establishment of perineural invasion models and analysis of gene expression revealed an invariant chain (CD74) as a possible molecule involved in perineural invasion in pancreatic cancer.

PURPOSE: Perineural invasion causes frequent local recurrence even after resection and a poor prognosis for pancreatic cancer. We established perineural invasion models and analyzed the molecular mechanism of perineural invasion in pancreatic cancer. EXPERIMENTAL DESIGN: Seven pancreatic cancer cell lines with or without human peripheral nerves were s.c. implanted in nonobese diabetes/severe combined immunodeficient mice. We compared expression profiles among high and low perineural invasion cell lines by using an oligonucleotide microarray. We examined up-regulation of the invariant chain (CD74) in high perineural invasion cell lines in mRNA and protein levels and surgical cases immunohistochemically. RESULTS: Four of seven pancreatic cancer cell lines (CaPan1, CaPan2, CFPAC, and MPanc96) showed perineural invasion to s.c. transplanted human peripheral nerves. Moreover, CaPan1 and CaPan2 (high perineural invasion group) also resulted in a high frequency of perineural invasion to mouse s.c. peripheral nerves, whereas three pancreatic cancer cell lines HPAFII, AsPC1, and Panc1 (low perineural invasion group) did not show perineural invasion to either human or mouse nerves. We identified 37 up-regulated genes and 12 down-regulated genes in the high perineural invasion group compared with the low perineural invasion group. Among them, CD74 was up-regulated in the high perineural invasion group in mRNA and protein levels. Furthermore, immunohistochemical expression of CD74 in clinical cases revealed its significant overexpression in pancreatic cancer with perineural invasion (P < 0.008). CONCLUSIONS: This is the first report of perineural invasion models using human pancreatic cancer cell lines. In combination with gene expression profiling, it was indicated that CD74 could be a candidate molecule involved in perineural invasion. These models provide new approaches for study of perineural invasion in pancreatic cancer.

Aged↗

PubMed2006

Solid-pseudopapillary neoplasms of the pancreas in men and women: do they differ?

Solid-pseudopapillary neoplasms (SPNs) of the pancreas are uncommon and occur preferentially in young women. The question whether the features of SPNs occurring in men differ from those in women has not yet been studied. For a better understanding of the clinicopathological features of SPNs of both sexes, we studied a series of 14 tumors surgically resected at a Japanese hospital within a period of 14 years. This series was composed of seven men and seven women. All these SPNs demonstrated nuclear and cytoplasmic accumulation of beta-catenin protein in immunohistochemistry and 86% of them had activating mutations of beta-catenin gene. No pancreatic neuroendocrine tumors showed such immunohistochemical findings and genetic alterations. In our series, most SPNs in women showed encapsulation by thick fibrous tissue and massive degenerative changes. Most SPNs in men exhibited solid components without prominent degenerative changes, even though they were of a similar size to those in women. These findings suggest that SPNs in men tend to be a solid mass with slower progression of degenerative changes during their growth compared to that in women. Nuclear accumulation of beta-catenin appears to be a useful marker of SPN, which allows male SPNs to be correctly diagnosed despite their less typical features.

Adult↗

PubMed2006

Bi-phasic activation of eNOS in response to uni-axial cyclic stretch is mediated by differential mechanisms in BAECs.

We investigated the signaling mechanism of stretch-induced NO (Nitric oxide) production in bovine arterial endothelial cells (BAECs). BAECs cultured on an elastic silicone chamber coated with fibronectin were subjected to uni-axial cyclic stretch (1 Hz, 20% in length) and the amount of produced NO was measured by a cGMP assay. NO production increased in a bi-phasic manner and peaked at 5 min and 20 min after stretch onset. Correspondingly, the activities of endothelial nitric oxide synthase (eNOS) and Akt/PKB (measured by phosphorylation at serine 1,177 and serine 473, respectively), showed two peaks over time. Application of Gd(3+), a potent SA channel blocker, and depletion of external Ca(2+) exclusively inhibited the first peaks of eNOS and Akt activity, but exerted little effect on the second peak. On the other hand, the PI3K inhibitors, Wortmannin, LY294002, almost completely inhibited the second peak but not the first. These results suggest that up-regulation of eNOS in response to cyclic stretch was mediated by two distinct pathways, [Ca(2+)](i) increases via the SA channel in an early phase (partially Akt/PKB), and PI3K-Akt/PKB pathways in a late phase.

Androstadienes↗

PubMed2006

An important role of Tyk2 in APC function of dendritic cells for priming CD8+ T cells producing IFN-gamma.

Tyrosine kinase 2 (Tyk2) contributes to the signals triggered by IL-12 for IFN-gamma production by NK cells and T cells. We found in this study that Tyk2-deficient (-/-) mice showed increased susceptibility at the early stage after an i.p. infection with Listeria monocytogenes, accompanied by impaired IFN-gamma production. The numbers of both MHC class Ib (H2-M3)- or MHC class Ia (Kb)-restricted CD8+ T cells producing IFN-gamma and exhibiting cytotoxicity were significantly decreased in Tyk2-/- mice after infection with L. monocytogenes. Using an adoptive transfer system of OT-I cells expressing OVA(257-264)/Kb-specific TCR into Tyk2-/- mice followed by challenge with recombinant L. monocytogenes expressing OVA, we found that the defective Tyk2 signaling in the host environment was at least partially responsible for the impaired CD8+ T cytotoxic-1 (Tc1) cell responses in Tyk2-/- mice following the infection. Adoptive transfer with MHC class Ib- or MHC class Ia-binding peptide-pulsed BM-derived DC from Tyk2-/- mice induced lower levels of the Ag-specific CD8+ Tc1 cells producing IFN-gamma. These results suggest that Tyk2 signaling is also important for DC function in the induction of MHC class Ia- and class Ib-restricted CD8+ Tc1 cells following L. monocytogenes infection.

Adoptive Transfer↗

PubMed2006

Clinicopathologic comparison of Siewert type II and III adenocarcinomas of the gastroesophageal junction.

BACKGROUND: Since Misumi et al. and Siewert proposed a new classification for carcinoma of the gastroesophageal junction (GEJ), few surgical studies using these criteria have been reported from Eastern countries. Siewert type II adenocarcinomas are managed using general rules for either gastric or esophageal cancer. We set out to determine whether type II adenocarcinoma is a distinct clinical entity requiring a more specific treatment plan. METHODS: Among 125 Japanese patients who underwent resection of adenocarcinoma of the GEJ (type I, 2; type II, 44; type III, 79), 101 who underwent R0 resections (type II, 40; type III, 61) were analyzed to evaluate surgical results and compare clinicopathologic factors. RESULTS: Barrett's epithelium was recognized in two patients with type II adenocarcinoma. Type II differed significantly from type III in higher prevalence of Borrmann macroscopic type 2, more frequent lymph node metastasis (58% vs. 34%), higher metastatic rate to lower mediastinal lymph nodes (13%), increased risk of hepatic recurrence, and lower 5-year survival after R0 resection (67.4% vs. 87.1%). CONCLUSIONS: Clinicopathologic differences were evident between type II and III adenocarcinomas. Siewert type II adenocarcinoma differs sufficiently to be considered a clinical entity distinct and independent from type III.

Adenocarcinoma↗

PubMed2006

A study of the subvesical bile duct (duct of Luschka) in resected liver specimens.

BACKGROUND: Injury to the duct of Luschka is associated with biliary fistula from the gallbladder bed after cholecystectomy. However, few studies have reported on the detailed anatomy. We elucidated the anatomy and frequency of the duct of Luschka METHODS: A total of 128 specimens from patients who underwent right hepatectomy or more extensive right-sided liver resection between February 1992 and December 2003 were examined. Specimens were fixed in formalin, and serial sections were prepared to trace the course of the bile ducts from the subsegmental branch level. RESULTS: The duct of Luschka was observed in 6 (4.6%) specimens. The sites of confluence were as follows: right anterior inferior dorsal branch (2 patients), right anterior branch (2 patients), right hepatic duct (1 patient), and common hepatic duct (1 patient). The upstream end was located in the liver parenchyma of the right anterior inferior dorsal subsegment (5b) and connective tissue of the gallbladder bed in 4 and 2 specimens, respectively. CONCLUSIONS: The duct of Luschka never crosses the segmental (5b) border. Therefore, its upstream region may not be injured by segmentectomy or more extensive liver resection. However, it is possible to injure the duct of Luschka at the common hepatic duct, even if right-sided hepatectomy is performed, as the sites of confluence included the common hepatic duct.

Adult↗

PubMed2006

Hepatectomy for colorectal liver metastases with macroscopic intrabiliary tumor growth.

OBJECTIVES: We set out to clarify the clinicopathologic characteristics of colorectal liver metastases with macroscopic intrabiliary tumor growth and to determine optimal surgical management. METHODS: Over 15 years, 6 of 103 patients undergoing hepatectomy for colorectal liver metastases had macroscopic intrabiliary tumor growth and were analyzed retrospectively. RESULTS: We performed 11 operations for the 6 patients, consisting of 10 hepatectomies (including 1 hepatopancreatoduodenectomy) and 1 pancreatoduodenectomy. Three patients survived more than 5 years: 1 died of pulmonary emphysema with no sign of recurrence 101 months after initial hepatectomy; the 2 others were alive with no sign of recurrence at 74 and 145 months after initial hepatectomy. Median survival time of all 6 patients was 87.5 months. Histologically, intrabiliary tumor growth had two components: intraluminal and intraepithelial extension. In the proximal direction, distance between these two components ranged from 4-10 mm. CONCLUSION: Aggressive surgical treatment can improve chances of long-term survival for patients with macroscopic intrabiliary growth of colorectal liver metastasis. Although nonanatomic limited resection is a common procedure for colorectal liver metastasis, anatomic hepatobiliary resection is recommended.

Adenocarcinoma↗

PubMed2006

Treatment of colorectal liver metastasis with biliary and portal vein tumor thrombi by hepatopancreatoduodenectomy.

We present a case of a large colorectal liver metastasis with portal vein and biliary tumor thrombi and duodenal and jejunal direct invasion that required hepatopancreatoduodenectomy. A 38-year-old woman presented to her local hospital with right back pain and jaundice. She had undergone transverse colectomy and limited liver resection for transverse colon cancer with a synchronous liver metastasis in September 1991, and low anterior resection for rectal carcinoma in January 1996. She was diagnosed as having colorectal liver metastasis and was referred to our hospital for possible surgery. Radiologic and endoscopic examinations revealed a large liver tumor occupying the right lobe, biliary dilation in the left lateral section, and a portal vein tumor thrombus. Invasion of the inferior vena cava and the right renal vein were also suspected. Intraoperative findings revealed a large liver tumor that occupied the right lobe and invaded the duodenum and jejunum. The tumor was resected successfully by right trisectionectomy, caudate lobectomy, pancreatoduodenectomy, partial resection of the jejunum, and combined portal vein resection and reconstruction. The inferior vena cava, right kidney, and renal vein could be detached from the tumor. The patient has enjoyed an active life without recurrence for 2 years since the operation.

Adult↗

PubMed2006

Computed tomographic demonstration of a fish bone in abdominal actinomycosis: report of a case.

A 53-year-old man who had the habit of consuming fish bones was referred to our clinic because of a suspected malignant abdominal wall tumor. Computed tomography (CT) showed a mass (10 x 5 cm) in continuity with the transverse abdominal muscle, containing a small calcification. A laparotomy was performed with a preoperative diagnosis of an inflammatory mass due to fish bone penetration from the sigmoid colon. A fish bone, measuring 2.3 cm in length, was detected within the tumor by specimen radiography. The pathological findings demonstrated actinomycotic colonies. We herein present the first case of a CT demonstration showing a fish bone in an abdominal mass which was pathologically confirmed to be actinomycosis. Evidence of the presence of a foreign body is valuable for diagnosing inflammatory nodules such as actinomycosis and differentiation from malignancies.

Abdominal Pain↗

PubMed2006

Hedgehog signal activation in gastric pit cell and in diffuse-type gastric cancer.

BACKGROUND & AIMS: Sonic hedgehog (SHH) and Indian hedgehog (IHH) have cell-specific actions in some organs. Only SHH has been shown to regulate parietal cell differentiation. This study examined whether SHH, 2 other ligands IHH and Desert hedgehog, and receptors or downstream targets are expressed in normal gastric epithelium or in intestinal and diffuse-type gastric cancers. The effects of a Hedgehog (Hh) inhibitor, cyclopamine, were assessed in primary gastric epithelium cultures and gastric cancer cell lines. METHODS: Reverse-transcription polymerase chain reaction and immunostaining compared expression and localization of Hh signaling molecules and phenotypic markers of pit, neck, and gland cells in situ and in cultured cells treated with cyclopamine. Bromodeoxyuridine staining assessed the effects of cyclopamine on proliferation. RESULTS: Hh signaling molecules were expressed differentially in pit, neck, and gland cells. IHH co-expressed with most downstream targets in the pit. IHH, SHH, Patched (PTCH), Smoothened (SMO), and downstream targets were expressed more frequently and highly in the diffuse as compared with intestinal type cancers. In diffuse cancers, IHH was expressed in cells with an epithelial phenotype and SHH in cells with a mesenchymal phenotype. Cyclopamine reduced the number of cells with a pit phenotype but not a gland phenotype in primary cultures. Cyclopamine had particularly potent effects of inhibiting the growth of cell lines that expressed high levels of SMO. CONCLUSIONS: Expression of IHH and downstream targets correlates with pit cells. IHH and SMO may be useful biomarkers of diffuse cancers that may show growth inhibition with Hh antagonists such as cyclopamine.

Animals↗

PubMed2006

"Anatomic" right hepatic trisectionectomy (extended right hepatectomy) with caudate lobectomy for hilar cholangiocarcinoma.

BACKGROUND: The techniques of right hepatic trisectionectomy are now standardized in patients with hepatocellular or metastatic carcinoma, but not in those with hilar cholangiocarcinoma. METHODS: Under preoperative diagnosis of hilar cholangiocarcinoma, 8 patients underwent "anatomic" right hepatic trisectionectomy with en bloc resection of the caudate lobe and the extrahepatic bile duct, in which the bile ducts of the left lateral section were divided at the left side of the umbilical fissure following complete dissection of the umbilical plate. RESULTS: Liver resection was successfully performed, and all patients were discharged from the hospital in good condition, giving a mortality of 0%. All patients were histologically diagnosed as having cholangiocarcinoma. The proximal resection margins were cancer-negative in 7 patients and cancer-positive in 1 patient. Four patients with multiple lymph node metastases died of cancer recurrence within 3 years after hepatectomy. One patient died of liver failure without recurrence 42 months after hepatectomy. The remaining 3 patients without lymph node metastasis are now alive after more than 5 years. CONCLUSIONS: Anatomic right hepatic trisectionectomy with caudate lobectomy can produce a longer proximal resection margin and can offer a better chance of long-term survival in some selected patients with advanced hilar cholangiocarcinoma.

Adult↗