Histopathological nature of myofascial trigger points at different stages of recovery from injury in a rat model.

OBJECTIVE: To investigate the histopathological nature of myofascial trigger points (MTrPs) or spots (MTrSs) at different stages of recovery from injury in a rat model. METHODS: Forty Sprague-Dawley rats were randomly divided into two groups: a control group (CG) and experimental group (EG). The CG was further randomly subdivided into CG1 and CG2 subgroups. The CG2 was used for palpating the taut band and CG1 as a blank. EG was subdivided into three groups according to recovery times: 4 weeks (4W), 8 weeks (8W) and 12 weeks (12W); these groups consisted of eight rats each. All CG rats received no intervention, whereas the intervention in EG rats was by a blunt strike to the vastus medialis and eccentric exercise for 8 weeks. The taut bands with spontaneous electrical activity were then detected in the muscle to guide a muscle biopsy. The histopathological findings were investigated under optical and electron microscopes in all groups. RESULTS: Under optical microscopy, the differently augmented sizes of round fibres (contracture knots) with deep staining in the transverse section and fusiform shapes in a longitudinal view were clearly seen in CG2 and EGs with a large diameter; the number of contracture knots was significantly more in EGs than in CGs. Under an electron microscope, the mitochondria in EGs significantly decreased with abnormal structures. The sarcomeres were significantly shortened in the 8W and 12W EGs. CONCLUSION: An injury can cause activation of MTrSs in a muscle and an activated level of MTrPs depending on the number of contracture knots in muscle with impaired energy production.

P300/CBP-associated factor (PCAF) inhibits the growth of hepatocellular carcinoma by promoting cell autophagy.

Aberrant autophagic processes have been found to have fundamental roles in the pathogenesis of different kinds of tumors, including hepatocellular carcinoma (HCC). P300/CBP-associated factor (PCAF), a histone acetyltransferase (HAT), performs its function by acetylating both histone and non-histone proteins. Our previous studies showed that PCAF was downregulated in HCC tissues and its high expression was significantly associated with patient survival after surgery, serving as a prognostic marker. In this study we found that overexpression of PCAF induced autophagy of HCC cells and its knockdown depressed autophagy. As type II programmed cell death, autophagy induced by PCAF-elicited cell death in HCC cells. In vivo experiments confirmed that PCAF-induced autophagy inhibited tumor growth. Subsequent in vitro experiments showed that PCAF promoted autophagy by inhibiting Akt/mTOR signaling pathway. Our findings show that PCAF is a novel modulator of autophagy in HCC, and can serve as an attractive therapeutic strategy of HCC treatment.

Systematic review and meta-analysis of prophylactic abdominal drainage after pancreatic resection.

AIM: To investigate whether prophylactic abdominal drainage is necessary after pancreatic resection. METHODS: PubMed, Web of Science, and the Cochrane Library were systematically searched to obtain relevant articles published before January 2014. Publications were retrieved if they met the selection criteria. The outcomes of interest included: mortality, morbidity, postoperative pancreatic fistula (POPF), clinically relevant pancreatic fistula (CR-PF), abdominal abscess, reoperation rate, the rate of interventional radiology drainage, and the length of hospital stay. Subgroup analyses were also performed for pancreaticoduodenectomy (PD) and for distal pancreatectomy. Begg's funnel plot and the Egger regression test were employed to assess potential publication bias. RESULTS: Nine eligible studies involving a total of 2794 patients were identified and included in this meta-analysis. Of the included patients, 1373 received prophylactic abdominal drainage. A fixed-effects model meta-analysis showed that placement of prophylactic drainage did not have beneficial effects on clinical outcomes, including morbidity, POPF, CR-PF, reoperation, interventional radiology drainage, and length of hospital stay (Ps > 0.05). In addition, prophylactic drainage did not significantly increase the risk of abdominal abscess. Overall analysis showed that omitting prophylactic abdominal drainage resulted in higher mortality after pancreatectomy (OR = 1.56; 95%CI: 0.93-2.92). Subgroup analysis of PD showed similar results to those in the overall analysis. Elimination of prophylactic abdominal drainage after PD led to a significant increase in mortality (OR = 2.39; 95%CI: 1.22-4.69; P = 0.01). CONCLUSION: Prophylactic abdominal drainage after pancreatic resection is still necessary, though more evidence from randomized controlled trials assessing prophylactic drainage after PD and distal pancreatectomy are needed.

Does Braun enteroenterostomy reduce delayed gastric emptying after pancreaticoduodenectomy?

Whether an additional Braun enteroenterostomy is necessary in reducing delayed gastric emptying (DGE) after pancreaticoduodenectomy (PD) has not yet been well investigated. Herein, in this retrospective study, 395 consecutive cases of patients undergoing classic PD from 2009 to 2013 were reviewed. Patients with and without Braun enteroenterostomy were compared in preoperative baseline characteristics, surgical procedure, postoperative diagnosis, and morbidity including DGE. The DGE was defined and classified by the International Study Group of Pancreatic Surgery recommendation. The incidence of DGE was similar in patients with or without Braun enteroenterostomy following PD (37/347, 10.7% vs 8/48, 16.7%, P = 0.220). The patients in the 2 groups were not different in patient characteristics, lesions, surgical procedure, or postoperative complications, although patients without Braun enteroenterostomy more frequently presented postoperative vomiting than those with Braun enteroenterostomy (33.3% vs 15.3%, P = 0.002). Bile leakage, pancreatic fistula, and intraperitoneal abscess were risk factors for postoperative DGE (all P < 0.05). Prokinetic agents and acupuncture were effective in symptom relief of DGE in 24 out of 45 patients and 12 out of 14 patients, respectively.The additional Braun enteroenterostomy following classic PD was not associated with a decreased rate of DGE. Postoperative abdominal complications were strongly correlated with the onset of DGE. Prokinetic agents and acupuncture could be utilized in some patients with DGE.

Concomitant Precise Hemihepatectomy to Improve the Efficacy of Surgical Treatment for Hilar Cholangiocarcinoma: Analysis of 38 Cases.

UNLABELLED: Background/Aims: Hilar cholangiocarcinoma (HC) is associated with low rates of resectability and curability, high morbidity and mortality, and poor long-term survival. Radical tumor resection with negative surgical margins provides the only chance of cure and long-term survival. The present study was to investigate the efficacy of concomitant precise hemihepatectomy for HC. METHODOLOGY: The clinical data of 38 patients who underwent surgery for HC with concomitant precise hemihepatectomy at our center from January 2009 to October 2012 were analyzed retrospectively. Survival curves were generated using the Kaplan-Meier method. Univariate and multivariate analysis were performed using the Cox proportional hazards model. RESULTS: R0 resection was performed in 32 patients (84.2%), R1 resection in 4 (10.5%), and R2 resection in 2 (5.3%). Two patients died during the perioperative period (mortality rate 5.3%). The most common postoperative complications were bile leakage (28.9%, 11/38) and hepatic dysfunction (21.1%, 8/38). The overall 1-, 2-, and 3-year survival rates were 65.8%, 36.8%, and 21.1%, respectively. The median survival time was 22.0 months. There were significant differences in survival between R0 and R1/R2 resection (χ2 = 4.516, P < 0.05) and between N0 and N1/N2 disease (χ2 = 10.397, P < 0.05). Univariate and multivariate analysis identified a positive surgical margin, lymph node metastasis and hepatic artery resection as prognostic indicators. CONCLUSIONS: Concomitant precise hemihepatectomy significantly improves the efficacy of radical surgical resection for HC. Precise liver resection, preservation of the hepatic artery, and selective preoperative biliary drainage are important to minimize postoperative morbidity and mortality.

[Expression of Fbxw7 and its correlation with cell proliferation in human hepatocellular carcinoma].

AIM: To observe the expression of Fbxw7 and explore its correlation with cell proliferation of hepatocellular carcinoma (HCC). METHODS: The expression of Fbxw7 in paired tumor and tumor-adjacent normal tissues from 40 patients with HCC were assessed using RT-PCR and immunohistochemistry. The expression level of Fbxw7 mRNA in normal liver cell line (LO2) and HCC cell lines (Hep3B and SMMC-7721) were detected by real-time RT-PCR. Colony formation assay and tumor xenograft assay were performed in different cell lines with different Fbxw7 expression respectively to investigate the ability of cell proliferation in vitro and in vivo. RESULTS: The expression of Fbxw7 at both mRNA and protein levels in HCC tissues were significantly down-regulated compared to tumor-adjacent normal tissues (P<0.05). Down-regulation of Fbxw7 was found apparently associated with high Edmonson-Steiner classification and advanced TNM stage (P<0.05). The expression of Fbxw7 mRNA in LO2 was significantly higher than that in Hep3B or SMMC-7721 (P<0.05). Cell lines with less Fbxw7 expression had not only more colonies in colony formation assay (P<0.05), but also bigger xenografts in vitro (P<0.05). CONCLUSION: The low expression of Fbxw7 correlates with the poor clinicopathological characteristics and cell proliferation of HCC.

[Downregulation of HSP70 gene expression and apoptosis in human hepatocellular carcinoma SMMC-7721 cells induced by nimesulide in vitro].

AIM: To investigate the effect of nimesulide on cell apoptosis and possible mechanism in human hepatocellular carcinoma SMMC-7721 cells. METHODS: SMMC-7721 cells were treated with nimesulide at different concentrations. Cell viability was assessed by MTT assay. Cell apoptosis rate was determined with flow cytometry. The cleavage activity of PARP and caspase-9 and the expression of HSP70 were evaluated using RT-PCR and Western blotting. The influence of HSP70 on cell apoptosis was observed using RNA interference silencing HSP70 expression. RESULTS: Nimesulide significantly inhibited cell growth in SMMC-7721 cells in a time- and concentration-dependent manner, and induced cell apoptosis in a concentration-dependent manner. Moreover, nimesulide promoted the cleavage of caspase-9 and PARP and inhibited the mRNA and protein expression of HSP70. Through the specific inhibition on HSP70 gene with siRNA, cell apoptosis increased, and the apoptosis was enhanced by the cleavage activity of caspase-9 and PARP. CONCLUSION: Nimesulide could inhibit cell growth and induce apoptosis in human hepatocellular carcinoma SMMC-7721 cells via the downregulation of HSP70.

[Gli1 expression and its relationship with the expression of Shh, Vimentin and E-cadherin in human hepatocellular carcinoma].

AIM: To investigate the expression and clinical features of glima-associated oncogene 1(Gli1) and its correlation with the expression of sonic hedgehog(Shh), one of the ligands of hedgehog (Hh) signaling, and two epithelial-mesenchymal transition (EMT) markers, Vimentin and E-cadherin in human hepatocellular carcinoma(HCC). METHODS: Paired HCC and normal tumor-adjacent tissues were collected from 63 HCC patients. Gli1 expression at both the protein and mRNA level were examined by immunohistochemistry and RT-PCR. The protein expression of Shh, Vimentin and E-cadherin were evaluated by immunohistochemistry to identify correlations with Gli1. RESULTS: The protein and mRNA expression of Gli1 were significantly up-regulated in the HCC tumor tissues compared to the normal tumor-adjacent tissues. Gli1 protein expression in HCC was closely correlated with intrahepatic metastases (x(2);=6.205, P<0.05), portal vein invasion (x(2);=4.014, P<0.05), high Edmonson-Steiner classification (x(2);=19.668, P<0.05) and advanced TNM stage (x(2);=7.091, P<0.05). Gli1 protein expression was positively correlated with Shh (r=0.574, P<0.05) and Vimentin(r=0.467, P<0.05), and negatively correlated with E-cadherin (r=-0.439, P<0.05). CONCLUSION: Gli1 is up-regulated in HCC tissues and closely correlated with clinicopathological characteristics, the increased expression of Gli1 in HCC tissues may be attributed to Shh, and Gli1 may play an important role in HCC progression and metastasis by inducing EMT.

[UbcH10 expression in hepatocellular carcinoma and its clinicopathological significance].

OBJECTIVE: To investigate UbcH10 expression in hepatocellular carcinoma and explore its clinicopathological implications. METHODS: We detected UbcH10 mRNA expression using RT-PCR in normal liver cell line, cancer cell lines, surgically removed hepatocellular carcinoma tissue and corresponding adjacent non-tumor tissue and evaluated the clinicopathological significance of UbcH10. Immunohistochemistry was performed to investigate UbcH10 protein expression in hepatocellular carcinoma tissue, the adjacent tissue, and normal liver tissue specimens. RESULTS: Normal liver cell line L02 showed significantly lower UbcH10 mRNA expression levels than the cancer cell lines BEL-7402, Hep3B, HepG2 and SMMC-7721 (P<0.05). UbcH10 mRNA expression was also was significantly higher in hepatocellular carcinoma tissues than in the corresponding non-tumor tissues (P<0.05). Clinicopathological evaluation suggested that UbcH10 expression was associated with tumor invasion of the portal vein, tumor size, TNM staging, and tumor differentiation (P<0.05). Immunohistochemistry identified stronger UbcH10 expression in hepatocellular carcinoma tissues than in the adjacent tissues and normal liver tissues (68.6%, 28.6%, and 26.7%, respectively). CONCLUSION: UbcH10 is over-expressed in hepatocellular carcinoma and may serve as a novel biomarker as well as a therapeutic target of hepatocellular carcinoma.

The role of miR-26 in tumors and normal tissues (Review).

miR-26, a functional miRNA, has received much attention from researchers in recent years. miRNAs may play crucial roles in numerous biological processes such as cell proliferation, apoptosis, tumorigenesis at different stages of non-tumor diseases, growth and development of normal tissues, and other biological processes. The expression of miR-26 has been found to be specific to different biological processes. Furthermore, its expression is frequently abnormal in tumors, indicating that miR-26 may play significant roles in tumor formation. Various reports exist regarding miR-26 involvement in non-tumor diseases, as well as the process of growth and development of normal tissues. In this review, we report findings of recent studies on the expression of miR-26 in different types of diseases and the process of growth and development and its predicted target genes in different tissue types. In conclusion, it is useful for researchers to understand the role of miR-26 in different biological processes.

Expression and clinical significance of p53, JunB and KAI1/CD82 in human hepatocellular carcinoma.

BACKGROUND: The mechanism of regulation of KAI1, a specific tumor metastasis suppression gene, is controversial. A recent study showed that the synergism of wild-type p53 and JunB has the function of regulating the expression of KAI1, a metastasis inhibiting factor in prostate cancer cells. The wild-type p53 gene is an activator of apoptosis and is closely related to malignant tumor cell multiplication. JunB, a member of the fos/jun family, is a key component of activator protein transcription factor and a major target element in the transmission pathway of mitosis. This study aimed to evaluate the relationship between the expression of KAI1 and p53 combined with JunB in tumor tissues and clinical outcomes in hepatocellular carcinoma (HCC) patients. METHODS: Quantitative real-time RT-PCR, Western blotting techniques and immunohistochemistry were used to evaluate the expression of KAI1 mRNA, KAI1/CD82, p53 and JunB in HCC patients, and the relationship between their expression and the clinicopathological prognostic parameters was analyzed. RESULTS: In cancer tissues, the values for positive expression of KAI1 mRNA, KAI1/CD82, p53 and JunB were 31.25%, 26.25%, 48.75%, and 20.00%, respectively, while in adjacent non-tumor tissues, they were 100%, 94.74%, 2.63%, and 76.32%, respectively. There was no correlation between the expression levels of p53 or JunB and KAI1 mRNA or KAI1/CD82. However, there were significant correlations between the expression levels of p53 combined with JunB and not only KAI1 mRNA but also KAI1/CD82 proteins. CONCLUSIONS: When p53 dysfunction and low expression of JunB are simultaneous, they may play an important role in down-regulating the expression of KAI1 by synergism in HCC. But further studies in vivo and in vitro are needed to verify these results.

Experimental study of specific immunotherapy induced by H22 autologous tumor as whole tumor cell vaccine.

This study explores the novel H22 whole-cell vaccine of active specific immunotherapy in the treatment of hepatocellular carcinoma. H22 hepatoma tumor vaccine modified by human interleukin-2 (hIL-2) and mouse granulocyte-monocyte colony-stimulating factor (mGM-CSF) fusion gene was prepared to study its specific anti-tumor immunity. Mice were inoculated by these vaccines. Then tumor cells were injected into mouse models. The (51)Cr release assay was used to examine the cytotoxicities of the splenocytes to H22 hepatoma cells in immunized mice, tumor-bearing mice and control mice. The blood was needed to test the level of IL-10 and interferon (IFN)-gamma in serum. Survival time of mice was calculated. Specific cytotoxicity rate of splenocytes from the immunized mice to H22 cancer cell was 38%, significantly higher than 13.6% in the tumor-bearing group, 7.5% in the control group, and 9.1% in S180 cells (p<0.05). Serum IFN-gamma in the immunized group was significantly increased compared with other groups (p<0.01), and serum IL-10 in the immunized group was significantly decreased compared with other groups (p<0.01). The survival time of the transgenic vaccinated group was significantly longer.

Relation among p130Cas, E-cadherin and beta-catenin expression, clinicopathologic significance and prognosis in human hepatocellular carcinoma.

BACKGROUND: p130Cas (p130Crk-associated substance) is a junction protein that is important to the adhesion between cytoskeleton and extracellular matrix. Also, the adhesion molecules E-cadherin and beta-catenin play important roles in the invasiveness of carcinoma. This study was undertaken to investigate the effects of p130Cas, E-cadherin and beta-catenin on the invasion, metastasis and prognosis of hepatocellular carcinoma (HCC). METHODS: Immunohistochemistry was used to evaluate the expression of p130Cas, E-cadherin, and beta-catenin in 40 patients with HCC. All patients were followed up postoperatively, and the relationship between expression and clinicopathological prognostic parameters was analyzed. RESULTS: The positive expression rates of p130Cas and E-cadherin in HCC tissue (n=40) were 62.50% and 55.00%, but in normal liver tissue 10%, and 100%, respectively (P<0.05). The abnormal expression rate of beta-catenin in HCC tissue was 70%, while in normal liver tissue it was 13.33% (P<0.05). The positive rate of p130Cas was correlated with lymph node invasion, pathological stage, TNM stage, and a worse prognosis, but not with gender, age, HBV infection, hepatic cirrhosis, alpha-fetoprotein (AFP) level before operation, and tumor diameter. Similarly, the expression of E-cadherin and beta-catenin was correlated with lymph node invasion, pathological stage, TNM stage, and worse prognosis, but not with gender, age, HBV infection, hepatic cirrhosis, AFP level before operation, and tumor size. Correlations were found between p130Cas and abnormal E-cadherin/beta-catenin expression (P<0.001 and <0.05, respectively). CONCLUSIONS: In HCC, there is a negative correlation between the positive expression of p130Cas and the normal expression of the adhesion molecules E-cadherin/beta-catenin, and p130Cas plays important roles in the invasion, metastasis and prognosis of HCC. p130Cas may be involved in alterating the structure and function of E-cadherin/beta-catenin, by regulating tyrosine phosphorylation via the p130Cas-Src signal pathway.

[Application of a tumor cell vaccine transfected with GM-CSF/IL-2 fusion gene for specific immunotherapy of hepatocellular carcinoma].

OBJECTIVE: To prepare a transgenic tumor cell vaccine transfected the fusion gene of murine granulocyte-monocyte colony stimulating factor (mGM-CSF) and human interleukin-2 (hIL-2) using H22 cells, and explore its specific antitumor immunity against hepatocellular carcinoma. METHODS: The eukaryotic vector expressing the fusion gene mGM-CSF/hIL-2 was transfected into H22 cells followed by radiation exposure to construct the tumor cell vaccine, which was used to immunize Balb/c mice by subcutaneous inoculation. The mice inoculated subcutaneously with H22 cells, cells transfected with the empty vector pcDNA(+), or with PBS served as the controls. A week later, H22 cells were injected peritoneally into Balb/c mice for establishing the tumor-bearing model, and their serum levels of interleukin-10 (IL-10) and interferon-gamma (IFN-gamma) were detected using enzyme-linked immunosorbent assay (ELISA) with the survival of the mice recorded. The spleen cells were obtained from the mice immunized with the tumor cell vaccine, the tumor-bearing mice and the normal control mice to assess their cytotoxicity against the parental H22 cells in vitro using (51)C(r)-release assay. RESULTS: The transgenic H22 cell vaccine transfected with mGM-CSF/hIL-2 fusion gene was successfully constructed. The killing rate of H22 cells by the spleen cells from the mice immunized with the transgenic cell vaccine was significantly higher than those by the spleen cells from the tumor-bearing mice or normal control mice (38.3% vs 13.6% and 7.5%, P<0.05). Serum IFN-gamma in the tumor-bearing mice immunized with the transgenic cell vaccine was significantly higher, and serum IL-10 significantly lower than those of the control groups (P<0.01). The survival time of the tumor-bearing mice injected with the transgenic cell vaccine was also significantly prolonged. CONCLUSION: Syngeneic tumor cell vaccine genetically modified by mGM-CSF/hIL-2 fusion gene transfection can elicit specific cellular immune response and enhance the host antitumor immune response to extend the survival time of tumor-bearing mice.

[Application of fusion gene mGM-CSF/hIL-2 to specific immunotherapy induced by hepatic tumor cell vaccine].

BACKGROUND & OBJECTIVE: Surgical resection is the main treatment for primary liver cancer, but there is no ideal treatment for postoperative recurrence and metastasis. Recently, due to the development of immunology, immunotherapy is regarded as a promising treatment for hepatoma. This study was to prepare H22 hepatoma tumor vaccine modified by the fusion gene of mouse granulocyte-monocyte colony stimulating factor (mGM-CSF) and human interleukin-2 (hIL-2), and explore its specific antitumor immunity. METHODS: Eukaryotic vector expressing fusion gene mGM-CSF/hIL-2 was transfected into H22 cells to establish tumor vaccine (H22/GM-CSF/IL-2) and inoculate mice; pcDNA3.1 was also transfected into H22 cells as empty control (H22/neo). Tumor-bearing mouse models were established. The cytotoxicities of the splenocytes from the mice in H22/GM-CSF/IL-2, H22/neo, and blank control groups were examined by 51Cr release assay. The serum levels of interleukin-10 (IL-10), interferon-gamma (IFN-gamma) were detected by ELISA. The survival of mice was observed. RESULTS: H22 cell vaccine modified by mGM-CSF/hIL-2 was successfully established. The killing rate of H22 cells by splenocytes was significantly higher in H22/GM-CSF/IL-2 group than in H22/neo and blank control groups (38.3% vs. 13.6% and 7.5%, P<0.05). The serum level of IFN-gamma was significantly higher and the serum level of IL-2 was significantly lower in H22/GM-CSF/IL-2 group than in H22/neo group [(12.83+/-0.75) pg/mL vs. (7.83+/-0.65) pg/mL, P<0.01; (4.58+/-0.34) pg/ml vs. (8.15+/-0.28) pg/mL, P<0.01]. The survival time of mice was significantly longer in H22/GM-CSF/IL-2 group than in H22/neo and blank control groups [(40+/-6) days vs. (30+/-3) days and (19+/-4) days, P<0.01]. CONCLUSION: Transfecting fusion gene mGM-CSF/hIL-2 into the novel autologous tumor vaccine H22 can elicit specific cellular immune response and improve the host's antitumor immune response, and prolong the survival of tumor-bearing mice.

[Expression of heparanase and nuclear factor kappa B in pancreatic adenocarcinoma].

OBJECTIVE: To detect the expressions of heparanase and nuclear factor kappa B p65 (NF-kappaB p65) in pancreatic adenocarcinomas and analyze their relation to patients' prognosis and the regulatory mechanism of NF-kappaB on heparanase expression. METHODS: Heparanase and NF-kappaB p65 proteins in the tumor and adjacent tissues were detected by immunohistochemistry in 48 patients with pancreatic adenocarcinoma and analyzed for their clinicopathological significance. RESULTS: Heparanase and NF-kappaB p65 proteins were found in 30 (62.5%) and 22 (45.9%) tumor specimens, respectively, a rate significantly higher than that in the adjacent tissues. High heparanase expression was closely related to advanced TNM stage (P=0.031), lymph node metastasis (P=0.003) and decreased 3-year postoperative survival (20.0% vs 0%, P=0.001). NF-kappaB p65 expression was associated with lymph node metastasis (P=0.017) and distant metastasis (P=0.031), but had a higher positive rate in heparanase-positive cases than in heparanase-negative cases (P=0.018). Multivariate analysis showed that neither heparanase nor NF-kappaB p65 was the independent prognostic factors. CONCLUSION: Heparanase is overexpressed in pancreatic adenocarcinomas in association with decreased postoperative survival. NF-kappaB may up-regulate heparanase expression and promote heparanase-dependent tumor invasion and metastasis.

[Clinical analysis of 9 cases of solid-cystic pseudopapillary tumor of the pancreas with literature review].

BACKGROUND & OBJECTIVE: Solid-cystic pseudopapillary tumor of the pancreas (SCPT) is a rare type of pancreatic tumor with low grade of malignancy. Its diagnosis and treatment remain controversial. This study was to discuss the diagnosis criteria and treatment strategy of SCPT. METHODS: Clinical data, including general history, medical history, treatment history and treatment outcome, of 9 SCPT patients, treated in the Department of Hepatobiliary Surgery of the First Affiliated Hospital of Xi'an Jiaotong University from Jan. 1997 to Feb. 2005, were analyzed retrospectively, and the related literature was reviewed to summarize the clinical characteristics, diagnosis, and treatment of SCPT. RESULTS: Among the 9 patients, 7 (77.8%) were women under 44 years old. The laboratory tests of liver function, serum amylase, and CEA, CA199 were normal. The accurate diagnosis rate of ultrasound was 22.2%, while that of CT was 77.8%. Most patients received local resection of the tumor. All patients were followed-up till Oct. 2005 and no metastasis was detected. CONCLUSIONS: SCPT is a rare disease with good prognosis. It occurs mainly in young women. In spite of unspecific laboratory tests, CT and fine needle aspiration method are useful to diagnose the disease. Based on literatures, operation could achieve satisfactory efficacy for SCPT patients.

Targeting radioimmunotherapy of hepatocellular carcinoma with iodine (131I) metuximab injection: clinical phase I/II trials.

PURPOSE: HAb18G/CD147 is a hepatocellular carcinoma (HCC)-associated antigen. We developed iodine (131I) metuximab injection (Licartin), a novel 131I-labeled HAb18G/CD147-specific monoclonal antibody Fab'2 fragment, and evaluated its safety, pharmacokinetics, and clinical efficacy on HCC in Phase I/II trials. METHODS AND MATERIALS: In a Phase I trial, 28 patients were randomly assigned to receive the injection in 9.25-, 18.5-, 27.75-, or 37-MBq/kg doses by hepatic artery infusion. In a multicenter Phase II trial, 106 patients received the injection (27.75 MBq/kg) on Day 1 of a 28-day cycle. Response rate and survival rate were the endpoints. RESULTS: No life-threatening toxic effects were found. The safe dosage was 27.75 MBq/kg. The blood clearance fitted a biphasic model, and its half-life was 90.56-63.93 h. In the Phase II trial, the injection was found to be targeted and concentrated to tumor tissues. Of the 73 patients completing two cycles, 6 (8.22%) had a partial response, 14 (19.18%) minor response, and 43 (58.90%) stable disease. The 21-month survival rate was 44.54%. The survival rate of progression-free patients was significantly higher than that of patients with progressive disease after either one or two cycles (p < 0.0001 or p = 0.0019). CONCLUSION: Iodine (131I) metuximab injection is safe and active for HCC patients.