The values of contrast-enhanced computed tomogramphy and ultrasound in radiofrequency ablation for liver cancer / 肿瘤

Objective: To investigate the values of CECT (contrast-enhanced computed tomogramphy) and CEUS (contrast-enhanced ultrasonography) in the diagnosis of cancerous lesions in the liver before and after RFA (radiofrequency ablation) for liver cancer. Methods: The clinical records of 90 patients with liver cancer (65 primary liver cancer and 25 metastatic liver cancer) undergoing RFA between May 2008 and September 2010 were retrospectively analyzed. A total of 104 cancerous lesions in the liver were treated with CT- or ultrasound-guided RFA. Each patient underwent CEUS and CECT one week before RFA and one month after RFA. The diagnostic abilities of CEUS and CECT before RFA and the values of CEUS and CECT in the evaluation of therapeutic effect of RFA were assessed. Results: Before RFA, 93 and 96 cancerous lesions in the liver were detected by CECT and CEUS, respectively. However, CECT combined with CEUS found 104 lesions. One month after RFA, 90 lesions showed no enhancement on CECT, and 91 lesions showed no enhancement on CEUS. CECT combined with CEUS found that 86 lesions showed no enhancement. CECT, CEUS and the CECT combined with CEUS found 5, 8 and 11 recurrent lesions in the liver, respectively. Conclusion: CECT combined with CEUS can increase the detection rates of cancerous lesions in the liver before RFA and the residual lesions and recurrent lesions after RFA. © 2012 by Tumor.

Prognosis after hepatectomy for primary liver cancer of segment 7 or 8 / 中华外科杂志

<p><b>OBJECTIVE</b>To investigate the results of surgical treatment for primary liver cancer of segment VII or VIII.</p><p><b>METHODS</b>The clinical data of 149 patients with primary liver cancer who underwent hepatectomy between January 2005 and December 2010 was retrospectively analyzed. There were 120 male and 29 female patients, aging from 19 to 75 years with a mean of 53.1 years. Among 149 patients, tumors were located at segment VII, VIII or several segments containing VII or VIII (VII/VIII group) in 53 patients, located at other segments (non-VII/VIII group) in 96 patients. The results of surgical treatment for VII/VIII group and non-VII/VIII group were compared by using t test, χ(2) test, Kaplan-Meier survival analysis and Cox proportion hazard regression analysis.</p><p><b>RESULTS</b>Right liver lobe was turned over completely in VII/VIII group, hepatic lobe which tumor was located at was not or partly turned over in non-VII/VIII group. Compared with non-VII/VIII group, VII/VIII group had longer operative time ((215 ± 68) min vs. (123 ± 36) min, t = 2.860, P = 0.01). No significant difference was found for tumor size, tumor number, tumor encapsulation, microvascular invasion, Edmondson grade, pTNM stage, intraoperative blood loss, blood transfusion rate, R0 resection rate and postoperative complication rate between two groups. The cumulative 1-, 3-, and 5-year overall survival rates were 74.6%, 42.3%, 15.4% respectively, in VII/VIII group, and 89.3%, 63.0%, 40.4% respectively, in non-VII/VIII group (χ(2) = 13.501, P = 0.000). Univariate and multivariate analysis of prognostic factors indicated that tumor location (tumor was located at segment VII or VIII) had unfavorable prognostic influence on overall survival (χ(2) = 10.329, P = 0.001; HR = 1.693, 95%CI: 1.232 - 2.694, P = 0.013).</p><p><b>CONCLUSION</b>The results of surgical treatment for primary liver cancer located at segment VII or VIII are worse than that located at other segments.</p>

Effects of celecoxib combined with fluvastatin on tumor growth and cell apoptosis in a xenograft model of hepatocellular carcinoma / 中华肝脏病杂志

<p><b>OBJECTIVE</b>To evaluate effects of celecoxib (a selective cox-2 inhibitor)combined with fluvastatin (a HMG-CoA reductase inhibitor) on tumor growth and cell apoptosis in hepatocellular carcinoma xenograft in nude mice.</p><p><b>METHODS</b>Hepatocellular carcinoma BEL-7402 cells were inoculated subcutaneously into the left armpit of nude mice, the mice (n = 32) were then randomly divided into 4 groups: the control group, the celecoxib group,the fluvastatin group and the combination group. At the end of the study, Tumor Tissues were collected for analysis. Cell apoptosis was determined by flow cytometry analysis and TUNEL assay. Akt, p-Akt and survivin protein levels were measured by Western blot. Statistical comparisons were made using factorial analysis of variance (ANOVA) and multiple comparisons between each two groups were calculated using SNK-q test.</p><p><b>RESULTS</b>The combination of Celecoxib and fluvastatin resulted in a greater inhibition of tumor growth than either agent alone, the tumor inhibitory rate was 34.0% in the Celecoxib group, 25.0% in the fluvastatin group and 72.2% in the combination group. The percentages of TUNEL--positive cancer cells in the celecoxib and fluvastatin alone treatment groups were 8.5%+/-1.4% and 9.4%+/-1.7% respectively as compared to the control group which was 3.5%+/-0.8%. Combination therapy showed a significantly greater increase in tumor cell apoptosis in comparison with the control and single-therapy groups (apoptotic index: 19.4%+/-3.0%; P value is less than 0.01 versus celecoxib or fluvastatin groups). The results of flow cytometry analysis also showed the same tendency. a small number of apoptotic cells were detected in the control tumours (4.1%+/-1.6%), whereas a large number of apoptotic cells were detected in tumours treated with celecoxib (9.1%+/-2.1%) or fluvastatin (10.1%+/-2.3%) alone; and the combination therapy resulted in even more apoptotic cells (23.6%+/-5.8%; P value is less than 0.01 versus celecoxib or fluvastatin groups). Western blot analysis demonstrated that the combination of celecoxib and fluvastatin significantly down-regulated p-Akt (0.23+/-0.08 versus 1.12+/-0.07 and surviving (0.50+/-0.07 versus 1.47+/-0.19) in BEL-7402 tumours compared with the control (P value is less than 0.01 for all).</p><p><b>CONCLUSION</b>The present study provided evidence that treatment with celecoxib in combination with fluvastatin resulted in the inhibition of HCC tumour growth in an in vivo mouse model.</p>

Expression of estrogen receptor α in hepatitis B-related hepatocellular carcinoma and its clinical significance / 中华外科杂志

<p><b>OBJECTIVE</b>To investigate the expression and its clinical significance of estrogen receptor (ERα) and phosphorylated estrogen receptor (p-ERα) in patients with hepatocellular carcinoma. The associations between ERα, p-ERα and IL-6 were also analyzed.</p><p><b>METHODS</b>Immunohistochemistry was used to detect the expression of ERα, p-ERα and IL-6 in tumor tissues from 77 cases with hepatocellular carcinoma. The relations between ERα and the clinical pathological parameters and prognosis were also analyzed.</p><p><b>RESULTS</b>The positive rates of ERα, p-ERα and IL-6 in hepatocellular carcinoma were 39.0% (30/77), 45.4% (35/77) and 72.7% (56/77), respectively. The expression of ERα and p-ERα were negatively correlated with the expression of IL-6 (r=-0.468, P<0.01; r=-0.370, P<0.01, respectively). The positive rate of ERα in patients with tumor size≤5 cm, serum level of alpha-fetoprotein<400 µg/L, with complete encapsulation and non-microvascular invasion was significantly higher than those with tumor size>5 cm, serum level of alpha-fetoprotein≥400 µg/L, non-complete encapsulation and with microvascular invasion (all P<0.05). The overall survival rates of ERα-positive and ERα-negative patients were 66.7% and 23.4% (P<0.05). And the disease-free survival rates of ERα-positive and ERα-negative patients were 83.3% and 57.4% (P<0.05).</p><p><b>CONCLUSIONS</b>The tumor biological features of ERα-positive patients are better than that of ERα-negative patients. The role of ERα in hepatocellular carcinoma may be related to IL-6 level.</p>

Prevention of hepatic tumor growth and metastasis in rats with rapamycin / 中华肝脏病杂志

<p><b>OBJECTIVES</b>To test the effect of rapamycin (RAPA) on hepatic tumor growth and metastasis in Sprague-Dawley (SD) rat model and explore the possible mechanism.</p><p><b>METHODS</b>SD rat hepatocellular carcinoma (HCC) model with metastatic potential was induced by diethylnitrosamine (DEN) and N-nitrosomorpholine (NMOR). 120 SD rats were randomized into four groups 16 weeks after DEN and NMOR treatment, and received 4-week intraperitoneal injection of RAPA (1.5 or 4.5 mg x kg(-1) x d(-1)), CsA (25 mg x kg(-1) x d(-1)) or equal volume of 0.9% saline, respectively. Tumor growth and metastasis were checked after the 4-week treatment. Serum vascular endothelial growth factor (VEGF) was determined by enzyme-linked immunosorbent assay (ELISA). Antiangiogenetic effects were assessed by CD34 immunostaining. The levels of hypoxia-inducible factor 1 alpha (HIF-1 alpha) and VEGF proteins and mRNAs were detected by immunohistochemistry, western blot and reverse transcriptase-polymerase chain reaction (RT-PCR).</p><p><b>RESULTS</b>The mean liver weight (5.58% +/- 0.42% and 5.69% +/- 0.74%), the metastatic liver nodules (5.12 +/- 0.68 and 5.67 +/-1.12), the metastasis lung nodules (0.43 +/- 0.11 and 0.45 +/- 0.83), and the lung metastasis rate (17.2% and 14.8%) were lower in rats treated with RAPA 1.5 mg x kg(-1) x d(-1) or 4.5 mg x kg(-1) x d(-1) than those in rats treated with saline, which were 10.42% +/- 1.86%, 12.36 +/- 3.45, 1.81 +/- 0.3 and 50.0% respectively (P < 0.01 or P < 0.05). The intratumoral microvessel density (MVD), serum VEGF, and the levels of HIF-1 alpha and VEGF were lower in RAPA-treated rats than those in control rats. However, CsA-treated rats showed an opposite trend compared with the RAPA-treated rats.</p><p><b>CONCLUSION</b>RAPA can repress the expression of angiogenesis-promoting factors HIF-1 alpha and VEGF, and significantly inhibits the growth and metastasis of HCC.</p>

Study the value of screening hereditary nonpolyposis colorectal cancer kindreds by detecting the expression of hMLH1/hMSH2 with tissue microarray / 中华胃肠外科杂志

<p><b>OBJECTIVE</b>To study the value of screening hereditary nonpolyposis colorectal cancer (HNPCC) kindreds by detecting the expressions of hMLH1/hMSH2 with tissue microarray.</p><p><b>METHODS</b>A tissue microarray with 22 colorectal cancers from HNPCC families and 15 sporadic colorectal cancers was established, and the expressions of hMLH1/hMSH2 were detected by immunohistochemistry (IHC).</p><p><b>RESULTS</b>The expressions of hMLH1 or hMSH2 were negative in 15 of 22 HNPCC and 1 of 15 sporadic colorectal cancers in routine IHC. The expressions of hMLH1 or hMSH2 were negative in 17 of 22 HNPCC and 2 of 15 sporadic colorectal cancers in tissue microarray. The examination of hMSH2 expression yielded same results between routine IHC and tissue microarray. There were no difference on the hMLH1 expressions between routine IHC and tissue microarray.</p><p><b>CONCLUSION</b>Tissue microarray is a high-throughput way to detect the expressions of hMLH1/hMSH2 and is applicable to screen HNPCC kindreds.</p>

Detection of microsatellite instability in colorectal cancer by fluorescence multiplex polymerase chain reaction and its clinical value / 中华胃肠外科杂志

<p><b>OBJECTIVE</b>To detect microsatellite instability(MSI) in colorectal cancer by fluorescence multiplex polymerase chain reaction(FM-PCR) and explore its clinical value.</p><p><b>METHODS</b>MSI of 110 colorectal cancer patients undergone surgical resection in our department from 2004 to 2005 were examined by FM-PCR, and the pathological characteristics were compared between MSI and microsatellite stable (MSS) colorectal cancer patients.</p><p><b>RESULTS</b>Among 110 cases, the male were 66 and the female were 44. Mean age was 60.8 (26-94) yrs. All 5 microsatellite markers were amplified. Out of them, 10 cases (8.1%) were MSI-H, 13 cases (11.8%) were MSI-L and 87 cases (79.1%) were MSS. Instability of BAT-26 was found in 9 cases (8.2%), BAT-25 was in 11 cases (10.0%), D2S123 was in 11 cases (10.0%), D5S346 was in 6 cases (8.2%) and D17S250 was in 8 cases (7.3%). Age between MSI and MSS colorectal cancer patients was significant and other pathological characteristics were not significant.</p><p><b>CONCLUSIONS</b>FM-PCR is a clinically stable method for MSI detection in colorectal cancer patients. There are no significant differences between MSI and MSS pathological characteristics of colorectal cancer patients.</p>