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Biomedical subjects

Masao Omata

Publications and source records attributed to Masao Omata.

At least 19 recordsLinked to original sources
PubMed2007

Effect of rapamycin on hepatocyte function and proliferation induced by growth factors.

BACKGROUND: Rapamycin is a specific inhibitor of the mammalian target of rapamycin (mTOR). The effect of rapamycin on proliferation and cellular function was studied in hepatocytes stimulated by hepatocyte growth factor (HGF) or transforming growth factor-alpha (TGFalpha). METHODS AND RESULTS: When isolated rat hepatocytes were cultured at low density, the addition of HGF or TGFalpha increased DNA synthesis but did not affect albumin or fibrinogen concentrations in the medium. In contrast, in hepatocytes cultured at high density, the albumin and fibrinogen concentrations, but not DNA synthesis, were increased by HGF or TGFalpha. The HGF- or TGFalpha-induced increase in DNA synthesis and in albumin or fibrinogen concentrations was suppressed by the addition of rapamycin, as well as wortmannin, a phosphatidylinositol-3 kinase inhibitor. CONCLUSION: HGF and TGFalpha stimulate proliferation and function of hepatocytes depending upon the conditions, and rapamycin inhibited these stimulatory effects, possibly by inhibiting the mTOR-dependent signaling pathway.

Albumins↗
PubMed2006

A retrospective study of radiotherapy for spinal bone metastases from hepatocellular carcinoma (HCC).

OBJECTIVE: To evaluate the therapeutic effects of radiotherapy on spinal bone metastases from hepatocellular carcinoma (HCC). METHODS: A retrospective review was conducted on 24 ambulatory patients with spinal bone metastases from HCC treated by radiotherapy from 1995 to 2004. Ambulatory rate and local progression-free rate after radiotherapy were analyzed. Eight (33%) of 24 patients had radiographic spinal cord compression from the spinal bone metastases before the treatment. Two (8.3%) of the 24 patients had some spinal deficits before the treatment. Biological equivalent dose (BED) with alpha/beta ratios of 10 ranged from 39 to 50.7 Gy (median 44.8 Gy). RESULTS: The median observation period was 5.1 months ranging from 0.9 to 36.0 months. Among the 24 patients, five (21%) underwent salvage therapies, while of the remaining 19 patients four (21%) became nonambulatory by the last follow-up. The ambulatory rates at 3 months and 6 months were 85 and 63%, respectively. The local progression-free rates at 3 months and 6 months were 53 and 47%, respectively. CONCLUSIONS: Radiotherapy with a BED of 39-50.7 Gy (median 44.8 Gy) is not sufficiently effective for the patients with spinal bone metastases from HCC to prevent paralysis. Dose escalation with a highly precise radiation technique will need to be evaluated.

Aged↗
PubMed2006

Dysregulated expression of stem cell factor Bmi1 in precancerous lesions of the gastrointestinal tract.

PURPOSE: It is important to identify the definitive molecular switches involved in the malignant transformation of premalignant tissues. Cellular senescence is a specific characteristic of precancerous tissues, but not of cancers, which might reflect tumorigenesis-protecting mechanisms in premalignant lesions. Polycomb protein Bmi1, which is a potent negative regulator of the p16INK4 gene, suppresses senescence in primary cells and is overexpressed in various cancers. We hypothesized that Bmi1 expression would also be dysregulated in precancerous lesions in human digestive precancerous tissues. EXPERIMENTAL DESIGN: Bmi1 expression was investigated in cancerous and precancerous tissues of the digestive tract. The expression of p16, beta-catenin, and Gli1 and the in vivo methylation status of the p16 gene were also analyzed in serial sections of colonic precancerous lesions. RESULTS: Bmi1 was clearly overexpressed across a broad spectrum of gastrointestinal cancers, and the expression of Bmi1 increased in a manner that reflected the pathologic malignant features of precancerous colonic tissues (low-grade dysplasia, 12.9 +/- 2.0%; high-grade dysplasia, 82.9 +/- 1.6%; cancer, 87.5 +/- 2.4%). p16 was also strongly expressed in high-grade dysplasia, but not in cancers. p16 promoter methylation was detected only in some Bmi1-positive neoplastic cells. CONCLUSIONS: Bmi1 overexpression was correlated with the malignant grades of human digestive precancerous tissues, which suggests that advanced Bmi1 dysregulation might predict malignant progression. The abnormal Bmi1 expression might link to malignant transformation via the disturbance of orderly histone modification.

Cell Line, Tumor↗
PubMed2006

A randomized controlled trial evaluating the usefulness of a transparent hood attached to the tip of the colonoscope.

OBJECTIVES: Considering the increasing demand for colonoscopy, auxiliary devices that could facilitate the examination would be useful. A hood attached to the tip of the colonoscope has been reported to be helpful in detecting and removing colorectal polyps. However, its usefulness in aiding scope intubation has not been fully evaluated. METHODS: Patients for colonoscopy between July 2004 and May 2005 in Tokyo University Hospital were enrolled to this randomized controlled trial, and assigned to colonoscopy with a transparent hood, a short hood, or no hood. Colonoscopies were conducted by trainees without sedation. The evaluated outcomes were cecal intubation rate, trainee intubation rate (cecal intubation within 15 min), cecal intubation time, and polyp detection rate. RESULTS: Enrolled 684 patients were randomly assigned to transparent hood (N = 221), short hood (N = 228), and no hood (N = 235) groups. The overall cecal intubation rate was 95.3% (652/684) and did not differ among the groups. The overall trainee intubation rate was 55.1% (377/684) and significantly higher in the transparent hood group than in the no hood group for female patients (60.7%vs 37.4%, P = 0.003). Cecal intubation time was 11.5, 13.5, and 14.0 min in the transparent, short, and no hood groups, respectively, and significantly shorter in the transparent hood group than in the no hood group among overall (P = 0.008), female (P = 0.001), and old (P = 0.04) patients. Polyp detection rate was higher in the transparent hood group than in the no hood group (49.3%vs 39.1%, P = 0.04). CONCLUSIONS: The transparent hood was useful in shortening the cecal intubation time especially in difficult cases.

Clinical Competence↗
PubMed2006

Nucleotide change of codon 38 in the X gene of hepatitis B virus genotype C is associated with an increased risk of hepatocellular carcinoma.

BACKGROUND/AIMS: The hepatitis B virus (HBV) genotype C is associated with the development of hepatocellular carcinoma (HCC). In addition, the HBV X gene, which encodes the pleiotropic transactivator HBx, has also been associated with the development of HCC. In this study, we investigated whether nucleotide changes in the X gene of genotype C are associated with the development of HCC. METHODS/RESULTS: We sequenced the X gene in age- and sex-matched 39 HBV-infected patients with HCC and 36 HBV-infected patients without HCC. A novel nucleotide change that resulted in a proline to serine substitution at codon 38 in HBx (codon-38 change) was preferentially found in patients with HCC. Then, sera were collected from a new group of age- and sex-matched 52 patients with HCC and 51 patients without HCC. In this cohort also, the codon-38 change was associated with HCC. Multiple logistic regression analysis showed the prevalence of the codon-38 change was significantly associated with HCC in all patients (P=0.001, odds ratio: 4.89). CONCLUSION: The codon-38 change in genotype C is an independent risk factor for the development of HCC and may serve as a useful molecular marker for predicting the clinical outcomes in patients infected with HBV.

Biopsy↗
PubMed2006

Microbubble-induced increase in ablation of liver tumors by high-intensity focused ultrasound.

We studied the possibility of using high-intensity focused ultrasound (HIFU) together with a microbubble agent to treat hepatocellular carcinoma. Development of liver tumors in rats was induced by administration of Dimethylnitrosamin (100ppm). Rats with liver tumors were anesthetized, underwent laparotomy, and were given the microbubble agent Levovist or saline intravenously. After the injection, the liver was exposed to HIFU for 30s (2.18MHz, 600W/cm(2), 40mm in diameter). Immediately after HIFU exposure, ultrasound images of the HIFU area were evaluated. Then the liver was excised and the volume of coagulated tissue was measured. The mean volumes of hyperechoic areas after HIFU were as follows (mm(3), Levovist versus saline: 355.3+/-180.7 versus 47.4+/-35.6, P<0.001, n=13). The volumes of liver tissue coagulated by HIFU were as follows (mm(3), Levovist versus saline: 275.3+/-120.0 versus 60.1+/-23.6, P<0.001, n=13). On microscopic examination of areas exposed to HIFU, implosion cysts were seen, and many cancer cells were found to have been destroyed completely (loss of cell membranes or nuclei). In conclusion, the microbubble agent Levovist can increase the volume of tissue coagulated by HIFU.

Journal Article↗
PubMed2006

Pancreatic cancer in patients with pancreatic cystic lesions: a prospective study in 197 patients.

BACKGROUND & AIMS: K-ras mutation is frequently detected in pancreatic juice of patients with pancreatic small cystic lesions, as well as those with pancreatic cancer. Those cystic lesions are often found by chance with modern radiologic imaging modalities. In this study, we prospectively examined the prognosis of patients with pancreatic cystic lesions, focusing on pancreatic cancer development. METHODS: A total of 197 patients with pancreatic cystic lesions, 80 with intraductal papillary mucinous neoplasm (IPMN) and 117 with non-IPMN cysts, were followed up for 3.8 years on average. Blood tests and imaging diagnosis were performed twice a year. The observed incidence of pancreatic cancer was compared with the expected incidence calculated on the basis of age- and gender-matched mortality of pancreatic cancer in the general Japanese population. RESULTS: Pancreatic cancer developed in 7 patients during the observation period (0.95% per year), infiltrating ductal carcinoma in 5 and intraductal papillary mucinous carcinoma in 2. Three of the ductal cancer cases had pancreatic non-IPMN cyst as preexisting lesion. At least 2 of the carcinomas arose in regions remote from preexisting lesions. The observed incidence of pancreatic cancer was 22.5 times higher (95% confidence interval, 11.0-45.3) than expected mortality from this cancer among general population. CONCLUSIONS: Patients with pancreatic cystic lesions are at a considerably high risk for pancreatic cancer, with a standardized incidence rate of 22.5. Cancer might develop in regions remote from the preexisting cystic lesion, suggesting diffuse pathologic changes predisposing to malignant transformation in the entire pancreas harboring cystic lesions.

Adult↗
PubMed2006

Endoscopic management of biliary complications after adult living donor liver transplantation.

OBJECTIVES: Biliary complications are one of the important issues to be addressed after liver transplantation. Endoscopic management of biliary complications after deceased donor liver transplantation (DDLT) is widely accepted, but it remains to be established in patients after living donor liver transplantation (LDLT). Endoscopic management in LDLT patients is difficult mainly because of the complexity of duct-to-duct reconstruction. METHODS: A total of 174 adult LDLTs with duct-to-duct reconstruction were performed in our institution. Biliary complications developed in 53 patients (30%). Among these, 18 patients were referred for endoscopic management and were the subjects of the present study. Success rate, early morbidity, and outcome were evaluated in these 18 patients. RESULTS: The type of graft was the right liver in six, left liver in eight, and right lateral sector in four patients. Ten out of 18 patients had one biliary anastomosis and the remaining eight had multiple anastomoses. Six patients had a previous history of surgical or percutaneous intervention for biliary complications after LDLT. Seventeen patients had one or more biliary strictures. Biliary casts were found in nine patients, three of whom had concomitant bile leaks. Strictures were successfully treated with endoscopic balloon dilation in 12 (71%) of the 17 patients (nasobiliary catheter placement in eight and stent placement in four patients). Bile leak was successfully managed in two of three patients. Biliary casts were removed by endoscopic papillary balloon dilation in eight of nine patients. Five patients with failed endoscopic therapy were converted to percutaneous or surgical intervention. Endoscopic-procedure-related cholangitis developed in one patient. During follow-up with median periods of 10 months (range 2-20 months), four of nine patients without stent placement developed biliary strictures, and these were relieved by additional endoscopic management. CONCLUSIONS: Endoscopic approach has the potential to be a first-line therapy for the management of biliary complications after LDLT.

Adult↗
PubMed2006

MDM2 promoter SNP309 is associated with the risk of hepatocellular carcinoma in patients with chronic hepatitis C.

PURPOSE: A single nucleotide polymorphism (SNP) in the promoter region of MDM2 gene, SNP309, has recently been shown to be associated with accelerated tumor formation in both hereditary and sporadic cancers in humans. However, the association of SNP309 with hepatocellular carcinoma is unknown. We evaluated the association of SNP309 with the risk of hepatocellular carcinoma development among Japanese patients with chronic hepatitis C virus infection. EXPERIMENTAL DESIGN: We genotyped the SNP309 at the MDM2 promoter in 435 Japanese patients with chronic hepatitis C virus infection, including 187 patients with hepatocellular carcinoma and 48 healthy subjects, using a fluorogenic PCR. Presence of SNP was also confirmed by direct sequencing of the MDM2 promoter region. RESULTS: The proportion of G/G genotype of the SNP309 in patients with hepatocellular carcinoma (33%) was significantly higher than that in patients without hepatocellular carcinoma (23%), with an odds ratio (95% confidence interval) of 2.28 (1.30-3.98). A multivariate analysis revealed that MDM2 SNP309 (G/G versus T/T), age >60 years, male gender, presence of cirrhosis, serum alpha-fetoprotein >20 mug/L, and serum albumin <3.2 g/dL were independently associated with the hepatocellular carcinoma development at odds ratio of 2.27, 2.46, 3.08, 4.15, 4.87, and 6.33, respectively. CONCLUSIONS: The MDM2 promoter SNP309 is associated with the presence of hepatocellular carcinoma in Japanese patients with chronic hepatitis C.

Adult↗
PubMed2006

Cholecystitis after metallic stent placement in patients with malignant distal biliary obstruction.

BACKGROUND & AIMS: Cholecystitis after metallic stent (MS) placement is an issue requiring attention. From our experience, cholecystitis seemed to occur mainly in patients with tumor involvement to the cystic duct orifice. The aim of the present study was to identify risk factors for cholecystitis in patients treated with covered or uncovered MS. METHODS: We analyzed 246 patients who received MS placement (covered MS in 171 and uncovered in 75) between August 1997 and May 2005 for the treatment of unresectable distal malignant biliary obstruction. Causative diseases were as follows: pancreatic cancer in 162, papillary cancer in 10, bile duct cancer in 41, and metastatic nodes in 33 patients. Tumor involvement to orifice of the cystic duct (OCD) was diagnosed based on cholangiography and intraductal ultrasonography. RESULTS: Cholecystitis after MS placement was found in 13 patients (5.3%). There was no significant difference in the incidence of cholecystitis between covered (5.8%) and uncovered (4.0%) MS. By univariate analysis, tumor involvement of the OCD, MS placed above the papilla, and stricture located at midportion were associated significantly with cholecystitis. By multivariate analysis, only tumor involvement of the OCD was a risk factor, with an odds ratio of 47.206 (95% confidence interval, 5.84-381.60). CONCLUSIONS: Cholecystitis after MS placement is associated with tumor involvement to the orifice of the cystic duct, regardless of the type of stent.

Aged↗
PubMed2006

Endoscopic submucosal dissection of esophageal squamous cell neoplasms.

BACKGROUND & AIMS: Endoscopic submucosal dissection (ESD) has recently been developed for en bloc resection of stomach neoplasms, which results in high tumor eradication rates as well as a modality for the precise histologic assessment of the entire lesion. Application of the technique is desirable for esophageal squamous cell neoplasms (SCNs), but there have been no reports on the use of this procedure in the esophagus. METHODS: An ESD with methods similar to those used for resections of early gastric cancer was performed on 58 consecutive esophageal SCNs with preoperative diagnoses of intraepithelial neoplasm or intramucosal invasive carcinoma occurring in 43 enrolled patients. The therapeutic efficacy, complications, and follow-up results were assessed. RESULTS: The rate of en bloc resection was 100% (58/58), and en bloc resection with tumor-free lateral/basal margins (R0 resection) was 78% (45/58). There was no evidence of significant bleeding. Perforation occurred in 4 (6.9%) patients during the ESD, who were managed by conservative medical treatments after endoscopic closure of the perforation. Removal of 9 (16%) lesions resulted in esophageal stricture requiring balloon dilation after ESD. Of 40 lesions occurring in 31 patients fulfilling the criteria of node-negative tumors (mean follow-up, 17 months), 1 lesion resected by en bloc resection with nonevaluable tumor-free lateral margins (Rx [lateral] resection) recurred locally 6 months after ESD, which was treated successfully by a second ESD procedure. CONCLUSIONS: The ESD is applicable to the esophagus with promising results, but notification of risk is essential.

Coloring Agents↗
PubMed2006

Combination therapy of intraarterial 5-fluorouracil and systemic interferon-alpha for advanced hepatocellular carcinoma with portal venous invasion.

BACKGROUND: Hepatocellular carcinoma (HCC) with portal venous invasion (PVI) has a very poor prognosis, with a median survival of 3 months and virtually no survival at 1 year. The combination of intraarterial 5-fluorouracil (FU) and systemic interferon-alpha (IFNalpha) was recently reported to be effective against HCC with PVI, but these were small pilot studies. METHODS: One hundred and sixteen patients with HCC with PVI received IFNalpha (5,000,000 U intramuscularly on Days 1, 3, and 5 of each week of treatment) and 5-FU (500 mg into hepatic artery on Days 1-5 of the first and second week of each 4-week cycle). The therapy was either terminated at the end of the first cycle in cases with progressive disease, or continued for at least 3 cycles, when responses to treatment were evaluated by Eastern Cooperative Oncology Group criteria. The survival rate was compared with that of historical controls (n = 40). RESULTS: Nineteen (16%) patients showed complete response and another 42 (36%) showed partial response. Adverse events were limited to nausea and appetite loss. The survival rates at 12 and 24 months among overall patients were 34% and 18%, respectively, in contrast to 15% and 5% among the historical controls. Survival rates at 12 and 24 months were 81% and 59% among complete responders, respectively, and 43% and 18% among partial responders. CONCLUSION: The combination therapy with 5-FU and IFN was safe, and substantially improved the survival rate among the complete responders. These results provide a rationale for future randomized controlled trials.

Aged↗
PubMed2006

TRAIL-induced cell death cooperates with IFN-gamma activation in the graft-versus-tumor effect against colon tumors.

The graft-versus-tumor (GVT) effect that occurs following allogeneic bone marrow transplantation (BMT) and donor lymphocyte infusion (DLI) is currently being subjected to intensive investigation because of clinical evidence for GVT efficacy against leukemia. In this report, we investigate the efficacy and molecular mechanisms of GVT against solid tumors, using a modification of the mouse parent-to-F1 BMT model. Mouse Colon26 cells in which tumor necrosis factor related apoptosis-inducing ligand (TRAIL) receptor expression was stably knocked down were transplanted to investigate the role of the TRAIL-TRAIL receptor system in the GVT effect. In addition, Fas ligand-(FasL) deficient mice on a C57BL6 (B6) background were used as donors, to determine the significance of the Fas-FasL system for the antitumor effect. The group that received B6 DLI followed by preconditioning with 950 rad irradiation underwent tumor reduction associated with the induction of IFN-gamma, TRAIL and tumor-cell apoptosis. In vitro cultured Colon26 cells were resistant to TRAIL but susceptible to the combination of IFN-gamma and TRAIL in a TRAIL-dose-dependent manner. The infusion of lymphocytes from FasL-defective donors reduced the tumor progression, although efficacy was decreased in the TRAIL receptor knockdown tumors but not in wild-type ones, compared with infusion of B6-derived lymphocytes. The findings indicate that GVT activity against subcutaneous colon tumors is efficiently induced by preconditioning with irradiation and allogeneic DLI, and that TRAIL and IFN-gamma act cooperatively in the antitumor effect.

Animals↗
PubMed2006

MyD88 and TNF receptor-associated factor 6 are critical signal transducers in Helicobacter pylori-infected human epithelial cells.

Helicobacter pylori induces NF-kappaB activation, leading to mucosal inflammation via cag pathogenicity island. Although recent studies have implicated several candidate proteins of both H. pylori and host, the molecular mechanism by which H. pylori activates NF-kappaB remains unclear. The aim of this study was to analyze the mechanism of cag pathogenicity island-mediated NF-kappaB activation in epithelial cells. The responses of human cell lines and mouse embryonic fibroblasts to infection with wild-type H. pylori or cagE mutant were investigated. The effect of small interfering RNAs (siRNAs) for several NF-kappaB signaling intermediate molecules was evaluated in H. pylori-induced IkappaBalpha phosphorylation and IL-8 production. Protein interactions of exogenously expressed TNFR-associated factor 6 (TRAF6) and MyD88 or receptor-interacting protein 2 and nucleotide-binding oligomerization domain 1 or those of endogenous IkappaB kinase, TGF-beta-activated kinase 1 (TAK1), and TRAF6 were assessed by immunoprecipitation. Cag pathogenicity island-dependent NF-kappaB activation was observed in human cell lines, but not in mouse fibroblasts. In human epithelial cells, H. pylori-induced IkappaBalpha phosphorylation and IL-8 production were severely inhibited by siRNAs directed against TAK1, TRAF6, and MyD88. In contrast, siRNAs for TRAF2, IL-1R-associated kinases 1 and 4, and cell surface receptor proteins did not affect these responses. H. pylori infection greatly enhanced MyD88 and TRAF6 complex formation in a cag-dependent manner, but did not enhance Nod1 and receptor-interacting protein 2 complex formation. H. pylori also induced TAK1 and TRAF6 complexes. These results suggest that the cag pathogenicity island of H. pylori is a cell type-specific NF-kappaB activator. TAK1, TRAF6, and MyD88 are important signal transducers in H. pylori-infected human epithelial cells.

Adaptor Proteins, Signal Transducing↗
PubMed2006

Serum IgG4 concentrations in pancreatic and biliary diseases.

BACKGROUND: Recently, it has been reported that the serum concentration of IgG4, a minor component of IgG subclasses, is increased in autoimmune pancreatitis. However, data regarding IgG4 concentrations in other pancreatic or biliary diseases have been insufficient. METHODS: Serum IgG4 was measured in 116 patients with pancreatic or biliary diseases (35 autoimmune pancreatitis, 24 chronic pancreatitis except autoimmune pancreatitis, 11 primary sclerosing cholangitis, 23 pancreatic cancer, 3 islet cell tumor, 2 papilla cancer, 15 bile duct cancer, and 3 gallbladder cancer patients). The cut-off concentration of IgG4 was 135 mg/dl. RESULTS: Increased serum IgG4 was observed in 33 of 35 patients with autoimmune pancreatitis, 0 of 24 with chronic pancreatitis, 4 of 11 with primary sclerosing cholangitis, 0 of 23 with pancreatic cancer, 0 of 3 with islet cell tumor, 0 of 2 with duodenal papilla cancer, 0 of 15 with bile duct cancer and 0 of 3 with gallbladder cancer patients. CONCLUSIONS: Serum IgG4 was increased in autoimmune pancreatitis and was within normal limits for other pancreatic or biliary diseases except primary sclerosing cholangitis.

Adolescent↗
PubMed2006

Radiofrequency ablation for hepatocellular carcinoma in so-called high-risk locations.

We evaluated the efficacy and safety of radiofrequency (RF) ablation for hepatocellular carcinoma (HCC) in presumably high-risk locations. Between February 1999 and December 2001, we performed RF ablation on 1419 nodules in 636 consecutive HCC patients, of which 231 nodules in 207 patients were in high-risk locations, defined as less than 5 mm from a large vessel or an extrahepatic organ. Eighty-one patients had a nodule adjacent to a large vessel, 145 patients had a nodule adjacent to an extrahepatic organ, of whom 19 also had one adjacent to a large vessel. Early complications and local tumor progression were analyzed with regard to the location of each nodule. The mean nodule diameter and average number per patient were 27 mm and 2.3, respectively. Early complications, within 30 days after ablation, occurred in 12 of 207 patients (5.8%) with a nodule in a high-risk location and in 15 of 429 patients (3.5%) without (P = .1776). There was no significant difference in local tumor progression rate between nodules in high-risk locations (1 year: 2.1%, 2 years: 3.1%, 3 years: 3.1%) and those elsewhere (1 year: 0.6%, 2 years: 1.7%, 3 years: 2.5%) (P = .2745). In conclusion, HCC nodules adjacent to a large vessel or extrahepatic organ were treated with RF ablation without compromising the efficacy of the procedure. However, even though without significant difference, some complications occurred at risky locations and need to be carefully considered.

Aged↗
PubMed2006

Prediction of recurrence of hepatocellular carcinoma after curative ablation using three tumor markers.

Three tumor markers for hepatocellular carcinoma (HCC) are available in daily practice in Japan: alpha-fetoprotein (AFP), des-gamma-carboxy prothrombin (DCP), and lens culinaris agglutinin-reactive fraction of alpha-fetoprotein (AFP-L3). To elucidate the predictability of these tumor markers on HCC recurrence after curative ablation, we enrolled 416 consecutive patients with naïve HCC who had been treated by percutaneous ablation at our department from July 1997 to December 2002. Tumor marker levels were determined immediately before and 2 months after the treatment. Complete ablation was defined on CT findings as nonenhancement in the entire lesion with a safety margin. Tumor recurrence was also defined as newly developed lesions on CT that showed hyperattenuation in the arterial phase with washout in the late phase. We assessed the predictability of recurrence via tumor markers in multivariate analysis, using proportional hazard regression after adjusting for other significant factors in univariate analysis. Until the end of follow-up, tumor recurrence was identified in 277 patients. Univariate analysis revealed the following factors to be significant for recurrence: platelet count; size and number of tumors; AFP, AFP-L3, and DCP preablation; and AFP and AFP-L3 postablation. Multivariate analysis indicated that AFP >100 ng/mL and AFP-L3 >15%, both pre- and postablation, were significant predictors. The positivity of AFP and AFP-L3 preablation that turned negative postablation was not significant. In conclusion, tumor markers pre- and post-ablation were significant predictors for HCC recurrence and can complement imaging modalities in the evaluation of treatment efficacy.

Aged↗