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Sclerosing angiomatoid nodular transformation (SANT) is a rare benign splenic vascular lesion. Since it was first defined in 2004, a total of 132 cases of SANT have been reported in ~50 studies in the English literature. However, it remains difficult to form a definitive pre-operative differential diagnosis of SANT compared with other splenic tumors or malignant lesions. The present study reports a pathologically proven case of SANT in a 29-year-old man who initially presented with left upper quadrant and back discomfort. The study also provides a review of the current knowledge on the condition, including the clinical profile, imaging features, cytological features, differential diagnosis and treatment of SANT. The most important distinguishing features of SANT are its typical vascular character and lack of other features that are typical of a granuloma. A splenectomy is required and the diagnosis is based on pathological analysis.

The aim of this study was to construct a lentiviral vector of CXCR4-siRNA (Lenti-CXCR4-siRNA) and investigate whether the vector can inhibit the growth, migration, invasion and hepatic metastasis of colorectal cancer (CRC). RT-PCR and western blotting were employed to identify the ideal RNA interference sequence. Lenti-CXCR4-siRNA was constructed and transfected into the SW480 cell line. We used RT-PCR and western blotting to measure the expression of CXCR4 RNA and protein, respectively; the MTS assay to assess the proliferation of SW480 cells; transwell chambers to estimate the inhibitory effect on migration and invasion; and the Balb/c nude mouse model of CRC to examine the inhibition of hepatic metastasis. The relative expression of the CXCR4 gene and protein was 5.4 and 18.95%, respectively, in the siCXCR4 group. The genes in the expression plasmid pLenti-CXCR4-siRNA were in the correct order. In the SW480, nonsense control (NC) and the Lenti-CXCR4-siRNA groups CXCR4 RNA levels were, respectively, 0.54±0.06, 1.00±0.03 and 0.11±0.04 (P=0.0001); CXCR4 protein levels were 0.60±0.03, 0.72±0.03 and 0.18±0.02 (P=0.0001); the OD value was 1.38±0.04 (P=0.0050), 1.28±0.05 (P=0.0256) and 0.92±0.06; SW480 cell number in migration test was 32±6.85, 32.63±1.69 and 0.75±0.71 (P=0.0000); SW480 cell number in the invasion test was 29.13±10.3, 30.38±6.09 and 0.63±0.74 (P=0.0000); hepatic metastasis number was 7.10±3.98 (P=0.034), 7.50±4.09 (P=0.019) and (3.50±2.51); hepatic metastasis mean weight (in g) was 2.25±2.51 (P=0.000), 2.11±2.38 (P=0.000) and 1.45±2.07. Lenti-CXCR4-siRNA constructs were correctly constructed and effectively inhibit the expression of CXCR4 RNA and protein, reducing the proliferation, migration, invasion capacity of SW480 cells and hepatic metastasis of CRC.

To investigate whether Endostar can inhibit the angiogenesis and growth of gastrointestinal stromal tumor (GIST) xenografts in nude mice and the feasibility of antiangiogenesis as a treatment modality for GIST. Twenty Balb/c-nu/nu mice burdened with GIST were randomly divided into two groups. Endostar (2 mg/kg) was injected around the tumor once per day for 10 days in the experimental group and with normal saline (NS) (0.1 ml) in the control group. The tumor bulk was measured every 5 days until 5 days after the end of the injections. The inhibition tumor rate (ITR) was calculated. Tumor bulk, microvascular density (MVD), rate of bcl-2-positive expression, and AI were assessed in the two groups. Tumor volumes were compared before and after treatment in the experimental group. The difference in tumor bulk between the two groups was not statistically significant before treatment (P = 0.628), but at the end of test, the difference was significant (P

To investigate a novel therapeutic regiment for gastrointestinal stromal tumor (GIST) based on c-kit RNA interference (RNAi) under the mediation of AdMax adenovirus.c-kit shRNA, whose lateral sides were decorated with restriction endonuclease sequences, was designed. The joining of c-kit shRNA and PDC316-EGFP-U6 was catalyzed by T4 DNA ligase to construct PDC316-EGFP-U6-C-KIT. Homologous recombination of AdEGFP-U6-C-KIT was performed with AdMax system. Heterotopic transplantation of GIST in nude mice was established. AdEGFP-U6-C-KIT was intratumorally injected in experimental group while blank admax adenovirus AdEGFP-U6 in control group. The volume, inhibition ratio of tumor and CD117 expression of graft tumor were compared between test and control groups.The length of c-kit shRNA was around 50 bp in agarose electrophoresis. Gene sequencing revealed the designed c-kit RNAi sequence in PDC316-EGFP-U6-C-KIT. After transfection with AdEGFP-U6-C-KIT, 293 cells presented green fluorescence. The physical and infective titer of AdEGFP-U6-C-KIT was 5 × 10(11)vp/ml and 5.67 × 10(7) pfu/ml respectively. At the end of test, the mean volume of graft tumor was significantly smaller in test group than in control group [(75 ± 23) vs (989 ± 31) mm(3), P = 0.000]. The inhibition ratio of tumor was 59.6% in test group. Two cases (20%) in test group and 10 (100%) in control group had a positive expression of CD117 (P = 0.001).c-kit RNAi mediated by Admax vector system can inhibit effectively the expression of c-kit gene and the growth of GIST in nude mice.

To explore the clinical characteristics and the prognostic factors of patients with colorectal cancer.The data of 2042 cases of colorectal cancer, pathologically confirmed at our hospital from January 1995 to December 2007, were summarized and analyzed.The median age of all cases with colorectal cancer was 59 years old. The high-risk age ranged from 50 to 70 years old. The ratio of male and female was 1.4:1. The lesions located in rectum accounted for 46.2% and those for 22.0% in sigmoid. Patients under age 40 had a higher percentage of poor differentiation (33.5%) and mucinous carcinoma (16.7%). The cases with confirmed stage I, II, III and IV were 5.8%, 42.9%, 31.0% and 20.3% respectively. For all cases, the 1-, 3-, 5- and 10-year survival rates were 92.3%, 73.9%, 65.1% and 57.5% respectively. The independent risk factors for patient prognosis were age, gross type, differentiation, TNM staging and surgical type. Adjuvant chemotherapy was a protective factor. As compared with phase I (1995 - 2001), phase II (2002 - 2007) had a higher proportions of employing stapler, Dixon operation and adjuvant chemotherapy. The 1-, 3- and 5-year survival rates of phase II were higher than phase I (93.4%, 78.0% and 73.2% vs 90.6%, 69.2% and 58.8%).The prognostic factors of patients with colorectal cancer are age, gross type, differentiation, TNM staging, surgical type and adjuvant chemotherapy.

Benign multicystic peritoneal mesothelioma (BMPM) is a rare cystic mesothelial lesion that occurs predominantly in reproductive aged women. A 56-year-old Caucasian male was admitted to our surgical department with a chief complaint of a painful mass in his right lower abdomen for almost 2 years. The physical examination revealed a palpable painful mass. Computed tomography demonstrated an irregular, cystic tumor in his right lower abdomen. There was no obvious capsule or internal septations. No enhancement after intravenous administration of contrast was noted. An exploratory laparotomy was performed, and a multicystic tumor and adherent to the caecum was noted. The walls of the cysts were thin and smooth, filled with clear fluid, and very friable. An en bloc resection of the tumor, including appendix and caecum, was performed. Histological examination revealed multiple cysts lined with flattened simple epithelial cells, and the capsule walls of the cysts were composed of fibrous tissue. Immunohistochemical analysis documented positive expression of mesothelial cells and calretinin. The final diagnosis was BMPM. The patient was well at 6-mo follow-up. BMPM is exceedingly rare lesion. A complete resection of the tumor is required. The diagnosis of BMPM is based on pathological analysis.

To investigate a therapeutic method for gastrointestinal stromal tumor (GIST) based on KIT RNA interference (RNAi) with AdMax adenovirus.KIT short hairpin RNA (shRNA), whose lateral sides were decorated with restriction endonuclease sequences, was designed. T(4) DNA ligase catalyzed the joint of the KIT shRNA and the green fluorescent protein-containing PDC316-EGFP-U6 to form PDC316-EGFP-U6-KIT. Homologous recombination of AdEGFP-U6-KIT was performed with the AdMax system. Heterotopically transplanted GISTs were established in nude mice. AdEGFP-U6-KIT was intratumorally injected. The volume, inhibition ratio of tumor and CD117 expression of GIST graft tumor in nude mice were compared between test and control groups.The length of KIT shRNA was determined to be about 50bp by agarose electrophoresis. Gene sequencing detected the designed KIT RNAi sequence in PDC316-EGFP-U6-KIT. After transfection with AdEGFP-U6-KIT, 293 cells displayed green fluorescence. The physical and infective titers of AdEGFP-U6-KIT were 5 × 10(11) viral particles/mL and 5.67 × 10(7) plaque forming units/mL, respectively. The mean volume of the grafted tumor was significantly smaller in test mice than in control mice (75.3 ± 22.9 mm(3) vs 988.6 ± 30.5 mm(3), t = -18.132, P0.05). The inhibition ratio of the tumors was 59.6% in the test group. CD117 positive expression was evident in two cases (20%) in the test group and 10 cases (100%) in the control group (χ(2) = 10.2083, P0.005).AdEGFP-U6-KIT is successfully constructed, and KIT RNAi mediated with Admax vector system can effectively inhibit the expression of the KIT gene and the growth of GIST in nude mice.