The acquisition of the capacity to invade surrounding tissues confers a more malignant phenotype to tumor cells and is necessary for the establishment of metastases. The understanding of the molecular mechanisms underlying cell invasion in human solid tumors such as colorectal cancers could provide not only more sensitive prognostic analyses but also novel molecular targets for cancer therapy.We report in this article that K ؉ ion channels belonging to the HERG family are important determinants for the acquisition of an invasive phenotype in colorectal cancers. The herg1 gene and HERG1 protein are expressed in many colon cancer cell lines, and the activity of HERG channels modulates colon cancer cell invasiveness. Moreover, the amount of HERG1 protein expressed on the plasma membrane is directly related to the invasive phenotype of colon cancer cells.Finally, both the herg1 gene and HERG1 protein were expressed in a high percentage of primary human colorectal cancers, with the highest incidence occurring in metastatic cancers, whereas no expression could be detected either in normal colonic mucosa or in adenomas.

More robust prognostic and predictive markers, supplementing standard clinical and pathologic staging, are needed for node-negative patients.

Our results suggest that host genetic factors (such as the IL1RN and the IL1B-31 polymorphisms) interact in the complex process of gastric carcinogenesis in this high-risk Italian population. Overall, this effect appears more modest than previously reported in other populations, supporting the hypothesis that other still-to-be-defined factors are important in gastric carcinogenesis. These findings might be due to a haplotype effect.

Risk factors for gastric cancer (GC) include inter-individual variability in the inflammatory response to Helicobacter pylori infection, in the ability of detoxifying DNA reactive species and repairing DNA damage generated by oxidative stress and dietary carcinogens. To evaluate the association between polymorphic DNA repair genes and GC risk, a case-control study including 314 histologically confirmed GC patients and 548 healthy controls was conducted in a GC high-risk area in Tuscany, Italy. Polymorphic variants of base excision repair (APE1-D148E, XRCC1-R194W, XRCC1-R399Q and OGG1-S326C), nucleotide excision repair (XPC-PAT, XPA-23G>A, ERCC1-19007T>C and XPD-L751Q), recombination (XRCC3-T241M) and alkylation damage reversal (MGMT-L84F) were tested for their potential role in the development of GC by using logistic regression models. The same population was also characterised for GSTT1 and GSTM1 variant alleles to search for possible functional interactions between metabolic and DNA repair genotypes by two-way interactions using multivariate logistic models. No significant association between any single DNA repair genotype and GC risk was detected with a borderline association with the XPC-PAT homozygous genotype [odds ratio (OR) =1.42; 95% confidence interval (CI) 0.94-2.17]. Gene-gene interaction analysis revealed combinations of unfavourable genotypes involving either multiple DNA repair polymorphisms or DNA repair and GST-specific genotypes. The combination of the XPC-PAT and the XPA variant alleles significantly increased GC risk (OR=2.15; 95% CI 1.17-3.93, P=0.0092). A significant interaction was also found between the APE1 wild-type genotype and either the single GSTT1 (OR=4.90; 95% CI 2.38-10.11, P=0.0079) or double GSTM1-GSTT1 null (OR=7.84; 95% CI 3.19-19.22, P=0.0169) genotypes or the XPA-mutant allele (OR=3.56; 95% CI 1.53-8.25, P=0.0012). These findings indicate that a complex interaction between host factors such as oxidative stress, antioxidant capacity and efficiency of multiple DNA repair pathways underlies the inter-individual variability in GC risk.

A 15 years old patient was taken to the operative room for an explorative laparotomy due to abdominal pain and a pelvic spleen at preoperative computed tomography: was pointed out the absence of all splenic ligamentous attachments and short gastric vessels with a consequently dislocation of a bigger and congested spleen in the pelvis. This organ, wrapped in the omentum, was in a serious ischemic suffering due to a 720 degrees clock torsion around its exceptionally long pedicle (about 20 cm); besides was confirmed pancreatic body and tail ectopy. Following the derotation, the volume of the organ has decreased but became fixed in above norm dimensions. A total splenectomy was executed. Case presentationA 15 year old otherwise healthy Caucasian male student (52 kilograms of weight, 170 centimeters of height, no smoker, no drinking alcohol, not assuming medications with no significative family history) presented to the Emergency Department with a 24 hours abdominal pain and increase of his abdominal girth. The pain was noncontinuous, poorly localized, and was non-colicky and non-radiating in nature. There was no history of vomiting, bowel or urinary symptoms. Over the prior 2 months, he reported one other similar episode that had resolved spontaneously. He was afebrile and his vital signs were stable. Abdominal examination revealed marked diffuse abdominal tenderness and guarding. A large hypogastric abdominal mass was palpable. Urinalysis and urine culture were normal; he had a white cell count of 19.4 × 10 9 / L, hemoglobin 11.0 g/dL and platelets 410 × 10 9 /L). On abdominal sonography, no spleen could be demonstrated in the normal position; the left upper quadrant was filled with bowel loops. An enlarged spleen extending from lower-polar region of the left kidney to the pelvis was seen. A large hypoechoic area was seen, suggestive of infarction, with a streak of perisplenic fluid. Ultrasonography demonstrated no blood flow in the splenic vein and in the splenic artery. Subsequent contrast-enhanced CT scan also showed absence of the spleen in the left upper quadrant as well as an enlarged spleen in the left lumbar and iliac region. The splenic parenchyma showed poorly, inhomogenous enhancing areas suggestive of infarction. The splenic vein was dilatated and showed a non-enhancing filling defect near the hilum, indicating the presence of a thrombosis. The splenic vessels, pancreatic tail, and the surrounding fat formed a whorled appearance, supermedial to the splenic hilum, that was suggestive of torsion.The patient underwent exploratory laparotomy through a midline incision. This revealed the absence of all splenic ligamentous attachments and short gastric vessels with a consequently dislocation of a bigger and congested spleen in the pelvis. This organ, wrapped in the omentum, was in