Reappraisal of the Mawangdui Han Tomb Cadaver Thirty Years After Its Unearthing.

The Mawangdui tomb No.1 cadaver, a female corpse from the Western Han Dynasty, was unearthed in 1972. Forensic examination at the time of discovery indicated fairly remarkable presence of bodily constituents at the anatomical, histological, and molecular levels. The cadaver was preserved in a formalin-based fixative afterward, and maintained in the Hunan Museum. To better protect this rare human corpse, a reappraisal of the status of preservation was carried out using noninvasive approaches, including X-ray radiography, gross anatomical examination, and histological, microbiological, and molecular analyses of sampled tissues. The cadaver remained essentially intact from a gross anatomical perspective, with radiography of the skeletal system and arterial contrast filling appeared comparable with the original documentation. The light microscopic features of the skin, cartilage, and skeletal muscle remained detectable, as were the stratified ultrastructure of the collagen and muscle fibers. The levels of nitrogen and amino acidic elements appeared elevated in the cadaver and liver preservation fixatives, with a higher calcium and phosphate concentration in the former. These findings suggest that there existed a certain degree of macromolecule degradation and bone decalcification in the cadaver, likely irrelevant to biological decomposition. The reappraisal also led to the implementation of stronger scientific measures to better protect the cadaver through a renovated Museum-University coadministrative management agreement.

MicroRNA-34a inhibits metastasis in liver cancer cells.

MicroRNAs (miRNA/miRs) have the ability to target specific mRNAs, resulting in degradation of mRNA or inhibition of translation. Notably, miR-34a is able to regulate cell cycle and tumorigenicity. The level of miR-34a expression is usually low in tumors, and previous studies have indicated miR-34a to be an important tumor suppressor. In order to elucidate the association between miR-34a and metastasis, stable cell lines were established and transfected with miR-34a. Cell invasion assay was subsequently performed. The present study demonstrated that cell invasion was inhibited in cells that were transfected with miR-34a compared with the control group (P<0.05). Therefore, miR-34a was able to inhibit metastasis in liver cancer cells.

Inhibiting the proliferation and metastasis of hilar cholangiocarcinoma cells by blocking the expression of vascular endothelial growth factor with small interfering RNA.

The aim of the present study was to investigate whether the proliferation and metastasis of hilar cholangiocarcinoma cells can be suppressed and whether apoptosis can be induced by small interfering RNA (siRNA) repression of vascular endothelial growth factor (VEGF). siRNA sequences targeting the VEGF gene were designed and the human hilar cholangiocarcinoma QBC939, HCCC-9810 and RBE cell lines were transfected with VEGF-siRNA plasmids for 48 h. Reverse transcription-quantitative polymerase chain reaction and western blotting measured the levels of VEGF-A, VEGF-C and matrix metalloproteinase 2 (MMP2) mRNA expression and protein content. The cell invasion potential was evaluated using the Transwell invasion and migration assay and the MTT assay was employed to detect the proliferation of hilar cholangiocarcinoma cells. Flow cytometry was used to quantify cell apoptosis and necrosis. Following the transfection of VEGF-siRNA, a significant reduction of mRNA and protein levels of VEGF-A, VEGF-C and MMP2 was observed in the hilar cholangiocarcinoma cells. The invasion, migration and proliferation of tumor cells were also notably decreased. The rate of tumor cell apoptosis was increased in the VEGF-siRNA group (15.42%) compared with the non-siRNA control (2.22%) and the negative control (2.71%) groups. It was concluded that blocking the expression of VEGF via VEGF-siRNA effectively inhibited the invasion, migration and proliferation, and induced apoptosis in hilar cholangiocarcinoma cells. These observations suggested that targeting VEGF with RNAi may be an effective therapeutic strategy for treating hilar cholangiocarcinoma.

Aberrant Expression of MicroRNA-15a and MicroRNA-16 Synergistically Associates with Tumor Progression and Prognosis in Patients with Colorectal Cancer.

The aim of this study was to reveal the associations of microRNA miR-15a and miR-16 dysregulation with clinicopathological characteristics and prognosis in patients with colorectal cancer. As a result, we found that miR-15a and miR-16 expression, detected by quantitative real time-PCR, were both significantly downregulated in colorectal cancer tissues compared with adjacent colorectal mucosa (both P < 0.001). Particularly, the expression levels of miR-15a in colorectal cancer tissues were positively correlated with those of miR-16 significantly (Spearman correlation coefficient r = 0.652, P < 0.001). In addition, miR-15a and/or miR-16 downregulation were all significantly associated with advanced TNM stage (all P < 0.05), poorly histological grade (all P < 0.05), and positive lymph node metastasis (all P < 0.05). Moreover, the survival analysis identified miR-15a expression, miR-16 expression, and miR-15a/miR-16 combination as independent predictors of both unfavorable overall survival and disease-free survival. Interestingly, the prognostic value of miR-15a/miR-16 combination was more significant than miR-15a or miR-16 expression alone. Collectively, the aberrant expression of miR-15a and miR-16 could be used to stratify patients with aggressive tumor progression of colorectal cancer. The combined pattern of miR-15a and miR-16 downregulation has a significant value for distinguishing patients with a worse prognosis of colorectal cancer after surgery.

Silencing of CXCR4 inhibits tumor cell proliferation and neural invasion in human hilar cholangiocarcinoma.

BACKGROUND/AIMS: To evaluate the expression of CXC motif chemokine receptor 4 (CXCR4) in the tissues of patients with hilar cholangiocarcinoma (hilar-CCA) and to investigate the cell proliferation and frequency of neural invasion (NI) influenced by RNAi-mediated CXCR4 silencing. METHODS: An immunohistochemical technique was used to detect the expression of CXCR4 in 41 clinical tissues, including hilar-CCA, cholangitis, and normal bile duct tissues. The effects of small interference RNA (siRNA)-mediated CXCR4 silencing were detected in the hilar-CCA cell line QBC939. Cell proliferation was determined by MTT. Expression of CXCR4 was monitored by quantitative real time polymerase chain reaction and Western blot analysis. The NI ability of hilar-CCA cells was evaluated using a perineural cell and hilar-CCA cell coculture migration assay. RESULTS: The expression of CXCR4 was significantly induced in clinical hilar-CCA tissue. There was a positive correlation between the expression of CXCR4 and lymph node metastasis/NI in hilar-CCA patients (p<0.05). Silencing of CXCR4 in tumor cell lines by siRNA led to significantly decreased NI (p<0.05) and slightly decreased cell proliferation. CONCLUSIONS: CXCR4 is likely correlated with clinical recurrence of hilar-CCA. CXCR4 is involved in the invasion and proliferation of human hilar-CCA cell line QBC939, indicating that CXCR4 could be a promising therapeutic target for hilar-CCA.

In vitro neuraotropic growth of cholangiocarcinoma: an experimental study.

OBJECTIVE: Perineural invasion of cholangiocarcinoma happens in the early stage of the disease but is often not recognized until its later stages. Research about the behaviour and mechanism of perineural invasion by cholangiocarcinoma is urgently needed for a useful new model. The aim of this work is to establish a novel model to address the problem. DESIGN: Neural cells and cholangiocarcinoma cells were co-cultured to mimic the neurotropic invasion of cholangiocarcinoma. SETTING: Human embryonic stem cells were induced to form neural cells by glial cell-derived neurotropic factor and retinoic acid; neural cells and cholangiocarcinoma cells were co-cultured in Transwell chamber. PARTICIPANTS: Human embryonic stem cells and cholangiocarcinoma cells were applied. MAIN OUTCOME MEASURES: Paired t-test was used to compare the counts of penetrating cholangiocarcinoma cells in co-culture and control group. RESULTS: Formation of neurospheres and neural-like cells were observed following induction at 24 and 48 h, respectively; synapses were viewed to protrude from neural-like cell bodies after incubation for 96 h. Forty-eight hours after incubation, immunocytochemical staining of the cells showed that synaptophysin and glial fibrillary acidic protein were expressed in the neuron-like cells and gliocytes-like cells, respectively. The cholangiocarcinoma cells that had penetrated through the Matrigel/polyethylene terephthalate membrane from the upper chamber to the lower chamber of the Transwell in the co-culture group were significantly more numerous than those in the control group (68 ± 8.3/field versus 46 ± 5.7/field, P < 0.05). CONCLUSION: The novel model is a valuable tool to study the perineural invasion of cholangiocarcinoma.

A Disintegrin and Metalloprotease with Thrombospondin Motif 2 May Contribute to Cirrhosis in Humans through the Transforming Growth Factor-ß/SMAD Pathway.

BACKGROUND/AIMS: We aimed to investigate the correlation between a disintegrin and metalloprotease with thrombospondin motif 2 (ADAMTS-2) and transforming growth factor-ß1 (TGF-ß1) in clinical human cirrhotic tissues. METHODS: The liver tissues of 24 patients (16 cases with cirrhotic portal hypertension as the cirrhosis group and eight cases with healthy livers as the normal group) were collected. Immunohistochemistry and Western blots were performed to evaluate the protein expression levels of ADAMTS-2 and TGF-ß1. Western blots for other key mediators of cirrhotic progression, including SMAD2, SMAD3, TGF-ß receptor II (TGFßRII), matrix metalloproteinases 2 (MMP2), and tissue inhibitor of matrix metalloproteinases 2 (TIMP2), were also performed. RESULTS: Cirrhotic tissues showed higher percentages of collagen. The protein expression levels of ADAMTS-2 and TGF-ß1 were significantly higher in the cirrhotic group as compared to the matched normal group (p<0.05), and there was a positive correlation between these two proteins (r=0.862, p<0.01). The protein expressions of MMP2, TIMP2, and TGFßRII, as well as the phosphorylated forms of SMAD2 and SMAD3, were significant higher in the cirrhotic group (p<0.01 or p<0.05). CONCLUSIONS: These findings suggested that ADAMTS-2 and TGF-ß1 may play important roles in the pathogenesis of human cirrhosis; specifically, TGF-ß1 may induce the expression of ADAMTS-2 through the TGFß/SMAD pathway.

Downregulation of microRNA-138 enhances the proliferation, migration and invasion of cholangiocarcinoma cells through the upregulation of RhoC/p-ERK/MMP-2/MMP-9.

microRNAs (miRs) play an important role in tumor initiation and progression in many types of cancer, including cholangiocarcinoma (CC). miR-138 dysregulation is frequently observed in a variety of tumors. In the present study, miR-138 was found to be downregulated in CC tissues by quantitative real-time RT-PCR. Furthermore, its potential target molecule, Ras homolog gene family, member C (RhoC) protein, was found to be highly expressed in CC tissues examined by western blot analysis. Luciferase reporter assay further demonstrated that miR-138 directly targeted RhoC. We found that the introduction of miR-138 mimics to RBE and QBC939 CC cells could reduced RhoC mRNA and protein expression, and suppressed the proliferation, G1/S transition, migration and invasion of CC cells. However, transfection with a miR-138 inhibitor induced an inverse effect in CC cells. The expression of phosphorylated extracellular signal-regulated kinase (p-ERK), matrix metalloproteinase (MMP)-2 and MMP-9 decreased following transfection with miR-138, and increased following transfection with miR-138 inhibitor in CC cells. In conclusion, RhoC upregulation induced by miR-138 downregulation promotes the malignant progression of CC cells and the underlying mechanisms of this effect involve the increase in the expression of p-ERK/MMP-2/MMP-9. Consequently, miR-138/RhoC is a potential target for the clinical diagnosis and treatment of CC.

Prognostic factors of distal cholangiocarcinoma after curative surgery: a series of 84 cases.

BACKGROUND/AIMS: The aim of this study was to identify useful prognostic factors for patients with distal cholangiocarcinoma. METHODOLOGY: The records of 84 patients with distal cholangiocarcinoma undergoing pancreatoduodenectomy were retrospectively reviewed. Potential clinicopathological prognostic factors that may affect survival were examined by univariate and multivariate analyses. RESULTS: There were two patients died within 30 days of surgery. Overall survival rates were 69.51%, 42.68%, and 36.59% for 1, 3 and 5 years, respectively (median survival time, 32.74 months). Univariate analysis found that alanine aminotransferase/aspartate aminotransferase (AST/ALT) ratio less than and equal to 2, serum bilirubin less than and equal to 171 micromol/L, CA19-9 level less than 150 U/L, tumor size less than 2 cm, absent neural invasion, and absent lymph node involvement were associated with higher survival rate (p < 0.05). Furthermore, multivariate analysis found that AST/ALT ratio more than 2, present lymph node involvement and present neural invasion were the independent risk factors of poor survival (p < 0.01). CONCLUSIONS: These results suggest that not only the well-known lymph node involvement, but also neural invasion and AST/ALT ratio more than 2 might be useful prognostic factors for long-term survival in distal cholangiocarcinoma.

The regulatory roles of miRNA and methylation on oncogene and tumor suppressor gene expression in pancreatic cancer cells.

Carcinogenesis is driven by an accumulation of mutations and genetic lesions, which leads to activation of oncogenes and inactivation of tumor suppressor genes. However, the molecular mechanisms by which the expression of these genes was regulated in pancreatic cancer remains unclear. In this study, we investigated the regulatory effects of microRNA and methylation on the expression of k-ras, TP53 and PTEN genes in pancreatic cancer cells. The protein and miRNA levels were measured by Western blotting and Northern blotting, respectively. Xenograft pancreatic tumor models were established by inoculating BxPC-1, Capan-2, and Panc-1 tumor cells into athymic nu/nu mice. A disparate level of KRAS, p53, PTEN, Dnmts, and Dicer 1 proteins as well as let-7i, miR-22, miR-143, and miR-29b miRNA was observed in BxPC-1, Capan-2, and Panc-1 cells. Knockdown of Dicer 1 expression in BxPC-3 and Panc-1 cells resulted in significant increases in KRAS, p53, PTEN, and Dnmts protein levels and significant decreases in miR-22, miR-143, let-7i, and miR-29b expression. Knockdown of Dicer 1 expression in Capan-2 cells significantly increased p53 and PTEN expression, while significantly decreased miR-22 and miR-143 expression, but had no effects on PTEN, Dnmts, let-7i, and miR-29b expression. Knockdown of Dicer 1 expression significantly inhibited xenograft BxPC-3 tumor growth, but promoted xenograft Panc-1 tumor growth. In contrast, knockdown of Dicer 1 expression had no effect on xenograft Capan-2 tumor growth. Our study suggested that different pancreatic cancer cell lines exhibited obvious discrepancies in gene expression profiles, implying that different molecular mechanisms are involved in the carcinogenesis of pancreatic cancer subclasses. Our study highlighted the importance of personalized therapy.

Prognostic value of miR-93 overexpression in resectable gastric adenocarcinomas.

BACKGROUND AND STUDY AIMS: MicroRNAs (miRNAs) have been shown to be aberrantly expressed in many human carcinomas. Emerging evidence indicates that miR-93 plays important oncogenic roles in human carcinogenesis and is often up-regulated. However, its relationship with the clinicopathological features and prognosis of human gastric cancer (GC) has yet to be addressed. In this study, we investigate the expression and clinical significance of miR-93 in human gastric cancer. PATIENTS AND METHODS: 158 patients with gastric adenocarcinoma who had undergone gastrectomy were enrolled. Specimens including the tumor and non-neoplastic were detected for the expression of miR-93 by Real-Time reverse transcription-polymerase chain reaction (RT-PCR). Furthermore, the correlation of miR-93 levels with clinicopathologic variables and prognosis was analyzed. RESULTS: miR-93 was significantly up-regulated in 128 cases (81%) of the 158 gastric cancer (P < 0.05). Furthermore, the elevated expression of miR-93 was significantly associated with advanced disease stage (P < 0.001), deep invasion level (P < 0.001) and the presence of nodal metastases (P < 0.001). Moreover, gastric cancer patients with high miR-93 expression levels had shorter overall survival (P = 0.001) and disease-free survival (P = 0.006) than that with low miR-93 expression levels. CONCLUSIONS: miR-93 is highly elevated in gastric cancer, especially in advanced and metastasized gastric cancer, suggesting miR-93 may play critical roles in carcinogenesis of gastric cancer. Overexpression of miR-93 can serve as a novel prognostic marker for gastric cancer.

miR-17-5p as a novel prognostic marker for hepatocellular carcinoma.

OBJECTIVES: miRNAs are frequently deregulated in cancer and have shown promise as tissue-based markers for cancer classification and prognostication. Emerging evidence indicates that miR-17-5p plays an important role in carcinogenesis. However, the expression of miR-17-5p in HCC tissues and its clinical relevance has not been systematically studied yet, and whether miR-17-5p expression has influence on prognosis of HCC is still unknown. In this study, we investigate the expression and clinical significance of miR-17-5p in human HCC. METHODS: The expression levels of miR-17-5p were measured in 120 paired hepatocellular carcinoma (HCC) and paracarcinomatous liver tissues (PCLTs) derived from patients who underwent hepatic resection by qRT-PCR. Furthermore, the correlation of miR-17-5p levels with clinicopathologic variables and prognosis was analyzed. RESULTS: miR-17-5p was significantly upregulated in HCCs (p < .001). Furthermore, HCC with metastasis had higher miR-17-5p levels than that without metastasis (p < .001). Importantly, the elevated expression of miR-17-5p correlated with multiple tumor nodules (p = .046), worse Edmondson-Steiner grade (p = .024), vein invasion (p = .001), shortened overall survival (p = .012), and disease-free survival (p = .011) of HCC. Multivariable Cox regression analysis revealed that miR-17-5p was an independent risk factor for overall survival and disease-free survival (p = .002 and p = .042, respectively). CONCLUSION: miR-17-5p is highly elevated in HCC, especially in HCC with metastasis. miR-17-5p can serve as a novel prognostic marker for HCC.

A standard approach to expose the recurrent laryngeal nerve during endoscopic thyroidectomy.

PURPOSE: Exposing the recurrent laryngeal nerve (RLN) during all types of thyroid surgery is essential to protect this nerve. Endoscopic thyroidectomy (ET) has gained acceptance from both patients and physicians, in part due to the cosmetic benefits. Therefore, the avoidance of intraoperative RLN impairment during ET is of critical significance. We have developed a standard approach to expose the RLN during ET that prevents RNL impairment. PATIENTS AND METHODS: ET was performed in 120 consecutive patients with thyroid disease. In order to develop a standard procedure that protects the RLN, several steps that differed from the traditional open procedure were introduced. First, the thyroid gland was freed from the isthmus instead of the superior pole. Then, the inferior pole of the thyroid gland was meticulously freed, and the lateral side of the thyroid gland was freed followed by the superior pole. At this point, the RLN was easily visualized in the tracheoesophageal groove. The thyroidectomy was then performed simultaneously with exposure of the RLN from the inferior to superior aspects. All RLNs were exposed when hemithyroidectomies, subtotal thyroidectomies, or total thyroidectomies were performed. The operative time and parathyroid hormone (PTH) and calcium levels were recorded prospectively and analyzed. RESULTS: Using this method, all RLNs were easily exposed within 15 minutes. Only one case of transient RLN palsy occurred due to accidental contact of the harmonic scalpel to the nerve. Postoperative hypocalcemia occurred in 23 cases (19.2%), and the PTH level decreased significantly in 33 cases (27.5%). The PTH levels returned to normal within 3 months. CONCLUSION: Use of the described approach to expose and protect the RLN when performing ET is safe and feasible.

[The effect of sevoflurane inhalation anesthesia only and propofol total intravenous anesthesia on perioperative cytokine balance in lung cancer patients].

AIM: To investigate the effects of sevoflurane inhalation anesthesia only and propofol total intravenous anesthesia on perioperative cytokine balance in lung cancer patients. METHODS: ASA I or II patients undergoing lobectomy for lung cancer were randomly divided into two groups with 45 cases each. In group A, patients received g sevoflurane inhalation anesthesia only and patients in group B received propofol total intravenous anesthesia. The cervical venous blood samples were obtained at the following time points: before induetion of anesthesia(T0), before the start of one-lung ventilation(T1), before the end of one-lung ventilation(T2), after closed chest surgery(T3), after 24 h (T4) . The serum concentrations of IL-6, IL-8 and IL-10 were measured by ELISA. RESULTS: (1) In both groups the concentration of IL-6 increased at T1 and kept raising to a high level at T4 which showed significant differences with that of pre-operation(P < 0.05).Compared between the groups, the concentration of IL-6 at T1 and T2 in group B was lower than that of group A(P < 0.05). (2) In both groups the concentration of IL-8 kept at T1 and T3 which were significant with that of pre-operation(P < 0.01). The concentration of IL-8 decreased apparantly at T4 in both groups, it was significant with that of pre-operation though(P < 0.01).Compared between the groups, the concentration of IL-8 at T1, T2 and T3 in group B were all lower than that of group A (P < 0.05). (3) In both groups the concentration of IL-10 increased at T1 which was significant with that of pre-operation(P < 0.05)and kept at T2 and T3. It dropped somehow at T4 but still maintained at a high level.Compared between the groups, the concentration of IL-10 in group B at T1, T2, T3 and T4 was singicantly higher than that of group A(P < 0.05). CONCLUSION: Propofol causes less inflammatory mediator release and can also modulate the balance of cytokines. It is a better anesthetic for lung cancer than sevoflurane.

Fibro-C-Index: comprehensive, morphology-based quantification of liver fibrosis using second harmonic generation and two-photon microscopy.

We develop a standardized, fully automated, quantification system for liver fibrosis assessment using second harmonic generation microscopy and a morphology-based quantification algorithm. Liver fibrosis is associated with an abnormal increase in collagen as a result of chronic liver diseases. Histopathological scoring is the most commonly used method for liver fibrosis assessment, where a liver biopsy is stained and scored by experienced pathologists. Due to the intrinsic limited sensitivity and operator-dependent variations, there exist high inter- and intraobserver discrepancies. We validate our quantification system, Fibro-C-Index, with a comprehensive animal study and demonstrate its potential application in clinical diagnosis to reduce inter- and intraobserver discrepancies.

[Clinical trial on pancreatic duct stones caused by chronic pancreatitis].

OBJECTIVE: To determine the possible mechanism for chronic pancreatitis causing pancreatic duct stones. METHODS: A total of 172 patients with chronic pancreatitis (n=67), pancreatic duct stones (n=62), and pancreatic injury (n=43), admitted to from August 2000 to October 2008, preoperatively diagnosed by endoscopic retrograde cholangiopancreatograpby(ERCP) or computed tomography(CT), and intraoperatively confirmed by exploration and biopsy, were divided into 3 groups. Pancreatic fluid was drawn to test the concentrations of pancreatic stone protein (PSP), lactoferrin (LF) and Ca2+. RESULTS: The chronic pancreatitis (the CP group) presented hard consistency, shrinkage and nodular fibrosis of the pancreas; besides the above symptoms, the pancreatic duct stones (the PS group) presented dilatation of the pancreatic ductal system with various stones; pancreatic injury (the PI group) presented broken pancreas of different grades with fluid or blood. Compared with that of the PI group, PSP concentration of both the PS group and the CP group was elevated (P<0.05), and was more apparent in the CP group. Concentrations of LF and Ca2+ were also elevated (P<0.05), which were more obvious in the PS group. CONCLUSION: Decreased concentrations of PSP and increased concentrations of LF and Ca2+ may play very important roles in chronic pancreatitis causing pancreatic duct stones.

Tumor-enhancing activity of Basigin expression in gallbladder carcinoma and its prognostic role.

Basigin (EMMPRIN/CD147) is a multifunctional membrane glycoprotein that is overexpressed in many solid tumors and is involved in tumor invasion and angiogenesis. The main purpose of this study was to investigate the tumor-enhancing activity of Basigin in a gallbladder carcinoma (GC) cell line and in primary GC tissues. A system that blocks Basigin in the human primary GC cell line GBC-SD was developed using RNA interference. GBC-SD cells were transfected with the small interfering RNA that target Basigin, then the proliferative, invasive and migration activities of the cells were assayed in vitro. Additionally, tissue samples from 98 patients with GC and 26 patients with chronic cholecystitis were stained with anti-Basigin antibody for immunohistochemical analysis. Furthermore, the association of Basigin expression with the clinicopathological characteristics and prognosis of the patients was analyzed. siRNA-treated GBC-SD cells exhibited significantly decreased growth ability, invasion and migration capacities compared to control cells in vitro. Moreover, clinicopathological analysis demonstrated that the intensity of Basigin staining in cancerous tissue was significantly associated with the histological type (p=0.02), distant metastasis (p<0.01) and Nevin stage (p<0.01) of GC. A proportional hazards model revealed the survival rate of patients with stronger Basigin expression to be the lowest (p<0.01). These results suggest that Basigin is a prognostic marker and potential therapeutic target for patients with GC.

[Expression and clinical significance of highly expressed protein in cancer (Hec 1) in human primary gallbladder carcinoma].

AIM: To investigate the relationship between the expression of highly expressed protein in cancer (Hec 1) and infiltration, metastasis and prognosis of human primary gallbladder carcinoma (PGC). METHODS: The expression of Hec 1 in was detected 108 patients with PGC by SABC immunohistochemistry with 15 cases of chronic cholecystitis as control. Then, a 5 year follow-up was carnedout in 96 out of 108 patients to analyze the correlation between Hec 1 and prognosis of the patients. RESULTS: The clinical pathological characteristics of PGC and clinical outcome of the patients were associated with the expression of Hec 1. Hec 1 was highhy expressed in cancer tissues with lymph node metastasis and poor differentiation. Especially, a statistical correlation was found with more advanced Nevin stages of PGC (P < 0.05). Moreover, the 5-year survival rate of the patients with PGC whose expression of Hec 1 was positive was significantly lower than that of the patients without Hec 1 expression (P < 0.01). CONCLUSION: Hec 1 may be associated with the development, infiltration and metastasis of PGC. The combination of Hec 1 expression in cancer tissues with clinical staging may faliliate the auurate predication of patients' prognosis.

CD147 expression as a significant prognostic factor in differentiated thyroid carcinoma.

CD147 is 1 of the molecules involved in regulating the expression of matrix metalloproteinases (MMPs). The goal of this study was to analyze the expression of CD147 in differentiated thyroid carcinoma (DTC) tissues as well as its association with the clinicopathologic features of DTC patients and its prognostic significance. During our research, CD147 expression in 156 patients who underwent operation for DTC [100 with papillary thyroid carcinoma (PTC) and 56 with follicular thyroid carcinoma (FTC)] were examined by immunostaining on paraffin-embedded tumor specimens. Then, the association of CD147 expression with clinicopathologic characteristics and patients' prognosis was analyzed. As a result, CD147 was expressed in cancerous lesions but not in normal tissues. Overall, 55 of 156 (35.26%) cases showed low CD147-positive expression, 52 of 156 (33.33%) showed intermediate CD147-positive expression, and 49 of 156 (31.41%) showed high CD147-positive expression. Positive CD147 staining was associated significantly with various clinicopathologic features, such as extrathyroidal invasion (P = 0.02), lymph node metastasis (P = 0.01), and depth of tumor invasion (P < 0.01). Patients with low CD147 expression showed better survival rates than those with intermediate and high expression (90.91% for low expression, 82.69% for intermediate expression, and 65.31% in high expression, respectively; P < 0.05 for analyses). Using Cox regression analysis of the 156 patients, high expression of CD147, extrathyroidal invasion, lymph node metastasis, and the pathologic grading of tumor invasion seemed to be independent prognostic indicators (P < 0.01, P = 0.02, P < 0.01, and P < 0.01, respectively). Therefore, we conclude that the expression of CD147 may be useful to predict the prognosis of DTC patients.