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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.

Aim: To investigate whether serum vascular endothelial growth factor-C (SVEGF-C) and multi-detector computed tomography (MDCT) can predict lymph node metastasis (LNM) in gastric cancer (GC). Methods: The SVEGF-C level of 80 patients with GC was examined by enzyme linked immunosorbent assay. An MDCT scan of the abdomen was performed. Kaplan – Meier survival analysis was used to analyse survival. Results: In patients with GC, a higher level of SVEGF-C was found in the LNM group (650.9 ± 198.6 vs 451.0 ± 115.5 pg/mL, P = 0.000) and in patients with distant metastases (834.3 ± 80.0 pg/mL vs 557.9 ± 187.0 pg/mL, P = 0.000). With a cut-off value of 542.5 pg/mL, the sensitivity, specificity, accuracy, positive predictive value and negative predictive value of SVEGF-C for predicating LNM were 82.8, 81.8, 82.5, 92.3 and 64.3%, respectively. MDCT could not be employed to detect the LNM. When SVEGF-C associated with MDCT was employed to determine LNM in GC, the sensitivity, specificity, accuracy, positive predictive value and negative predictive value were 91.4, 86.4, 90.0, 94.6 and 79.2%, respectively. No difference of SVEGF-C level was found among N1, N2 and N3 groups (P > 0.05). The 5-year overall survival was 47.5%. A shorter mean survival time were found in patients with SVEGF-C >834.3 pg/ml (43.3 ± 2.8 months vs 67.4 ± 2.5 months, P = 0.000) and in patients who were MDCT-positive (42.7 ± 3.8 months vs 60.8 ± 2.2 months, P = 0.0034). Conclusion: SVEGF-C may be a biomarker for a preoperative diagnosis of LNM. In conjunction with MDCT, SVEGF-C can improve the accuracy of a diagnosis of LNM in GC. A higher SVEGF-C level and an MDCT-positive finding could predict the poorer prognosis of GC.

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

Background: The study aims to investigate the relationship among serum vascular endothelial growth factor (SVEGF-C), VEGF-C expression and lymph vessel density (LVD) in tumour tissue, and their influence to colorectal carcinoma (CRC). Methods: The SVEGF-C concentration of 110 patients with CRC and 40 healthy donors was examined by ELISA. The 110 tumour tissues and 40 normal colorectal specimens were examined by immunohistochemical staining (SP method) with VEGF-C and podoplanin (lymphatic vessel specific antibody). Kaplan–Meier survival analysis determined the influence on CRC prognosis. Results: CRC SVEGF-C level (889.0 ± 264.0 pg/mL) significantly exceeded (P= 0.000) the control level (373.2 ± 97.3 ng/L), and was significantly higher in T3, lymph node metastasis (LNM), distant metastasis, and pTNM groups III and IV. LNM prediction sensitivity, specificity, and accuracy of SVEGF-C were 85.7, 80.0 and 83.6%, respectively (875 pg/mL cut-off). VEGF-C expression was elevated in CRC versus control patients (P= 0.000), and was significantly related to LNM and pTNM stages III and IV. Mean LVD in CRC (6.3 ± 0.7/200 HP) significantly exceeded control mean (3.0 ± 0.7/200 HP) (P= 0.000). LVD was significantly higher in LNM and pTNM stages III and IV. SVEGF-C level was significantly higher in VEGF-C positive versus negative patients (P= 0.000), and was related to LVD (P= 0.009). Kaplan–Meier ranking of prognostic factors was SVEGF-C level (P= 0.000), VEGF-C expression (P= 0.001) and LVD (P= 0.012). Conclusion: SVEGF-C level, VEGF-C and LVD are related to LNM and poor prognosis in patients with CRC. SVEGF-C may be a biomarker for LNM in CRC.

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.