The aim of the present study was to evaluate the involvement of the right ventricle (RV) in reperfused anterior ST-elevation myocardial infarction (STEMI). Left anterior descending (LAD)-perfused area (using thioflavin-S staining after selective infusion in proximal LAD artery, %), infarct size (using triphenyltetrazolium chloride staining, %), and salvaged myocardium (% of LAD-perfused area) in the right and left ventricle (LV) were quantified in a 90-min LAD occlusion 3-day reperfusion model in swine (n = 8). Additionally, we studied, using cardiovascular magnetic resonance, 20 patients with a first STEMI due to proximal LAD occlusion treated with primary angioplasty. Area at risk (T2-weighted sequence, %), infarct size (late enhancement imaging, %), and salvaged myocardium (% of area at risk) in the right and LV were quantified. In swine, a large LAD-perfused area was detected both in the right and LV (30 ± 5 vs. 62 ± 15%, P< 0.001) but more salvaged myocardium (94 ± 6 vs. 73 ± 11%, P< 0.001) resulted in a smaller right ventricular infarct size (2 ± 1 vs. 16 ± 5%, P< 0.001). Similarly, in patients a large area at risk was detected both in the right and LV (34 ± 13 vs. 43 ± 12%, P = 0.02). More salvaged myocardium (94 ± 10 vs. 33 ± 26%, P < 0.001) resulted in a smaller infarct size (2 ± 3 vs. 30 ± 16%, P< 0.001) in the RV. In reperfused extensive anterior STEMI, a large area of the RV is at risk but the resultant infarct size is small.

BACKGROUND: TNM stage has been identified as an independent variable for local recurrence and survival after colon cancer resection. It is still unclear whether peritoneal invasion (pT4a) is a risk factor for adverse oncologic outcome or whether these patients have better results compared with contiguous organs infiltration (pT4b), independent from nodal status (pN). OBJECTIVE: The purpose of this study was to analyze whether peritoneal invasion is an independent risk factor for worse oncologic outcome after curative colon cancer resection. DESIGN: This was a retrospective analysis with multivariate regression of a prospective database, according to Strengthening the Reporting of Observational Studies in Epidemiology Statement. SETTINGS: The study was conducted in a specialized colorectal unit of a tertiary hospital. PATIENTS: A consecutive series of pT3-pT4a-pT4b patients with colon cancer who underwent curative surgery (1993–2010) were included, and patients with metastasis were excluded. MAIN OUTCOME MEASURES: A multivariate Cox regression analysis was performed to assess independent risk factors for 5-year local recurrence, peritoneal carcinomatosis-like recurrence, disease-free survival, and cancer-specific survival. RESULTS: A total of 1010 patients were analyzed (79.3% pT3, 9.9% pT4a, and 10.8% pT4b). At diagnosis, 22.0% had obstructive symptoms, and 10.5% had bowel perforation. A total of 72.2% of the surgeries were elective, and in 15.6% en bloc resection of contiguous organs was performed. Median follow-up was 62 months (38–100 mo). For the whole group, 5-year actuarial rates were 8.8% for local recurrence, 2.5% for peritoneal carcinomatosis, 75.5% for disease-free survival, and 81.8% for cancer-specific survival. At multivariate analysis, pT4a stage was an independent risk factor for local recurrence (p = 0.002; HR = 3.1), peritoneal carcinomatosis (p = 0.02; HR = 4.9), worse disease-free survival (p = 0.002; HR = 1.9), and cancer-specific survival (p = 0.001; HR = 2.2). When considering only the 566 patients with ≥12 nodes identified, T stage was still associated with higher local recurrence (p = 0.04) and carcinomatosis rate (p = 0.04), as well as worse disease-free (p = 0.009) and cancer-specific survival (p = 0.014). LIMITATIONS: This was a retrospective, single-center study. CONCLUSIONS: pT4a stage is an independent risk factor for worse oncologic outcome after curative colon cancer resection compared with pT3 and pT4b stages. The current pT4a-pT4b classification should be reconsidered. Of note, even in pT4a patients, 5-year carcinomatosis rate does not exceed 6%. See Video Abstract at http://links.lww.com/DCR/A926.

Background Osteosarcomas (OS) are aggressive neoplasms with a wide range of morphologic patterns. Materials and Methods OS cases (primary and xenotransplanted) with paraffin blocks available were collected and included in tissue microarrays (TMAs). A morphologic evaluation including the different passages in mice was carried out according to the new WHO criteria. In addition, TMAs were analyzed with a wide panel of immunohistochemical (IHC) markers (osteonectin, osteocalcin,cytokeratin, S100, Sox-9, Ki-67, Bcl-2, p53, p16, survivin, CD99, and caveolin-1). Results A total of 61 cases were collected. The distribution of the cases according to the histopathologic pattern was: 38 osteogenic OS, 8 primary chondrogenic OS, 2 primary telangiectatic OS, 6 parosteal OS, 2 primary small cell OS, 2 primary poorly differentiated OS, 1 primary dedifferentiated OS, and 3 primary pleomorphic MFH-like OS. The tumor morphology in xenotransplants was similar to the primary or metastatic tumor of origin and was generally maintained over the passages. The IHC results were heterogeneous and osteonectin and osteocalcin were the most expressed in original tumor and xenografts. S100 and Sox-9 were expressed in chondrogenic areas. Caveolin and survivin showed significant IHC variation between the subsequent passages. p16 displayed heterogenic expression. p53 expression increased over the passages, and Ki-67 expression was not associated with a more undifferentiated pattern, but increased over the passages. Conclusions An accurate morphologic evaluation using TMAs in original tumor is essential for the OS diagnosis; hence there is no IHC marker that alone distinguishes the OS subtypes. Xenografts in OS allow the study of tumor progression in this type of aggressive neoplasm.

Preclinical evidence has shown increased expression of mu opioid receptor 1 (MOR-1) in colorectal cancer although its association with disease-free and overall survival (DFS and OS) has not been investigated. We hypothesized that MOR-1 was overexpressed in tumor samples compared to normal tissue and this was associated with decreased DFS and OS. We carried out a retrospective study assessing the association of MOR-1 tumor expression with long-term outcomes by immunohistochemistry in normal and tumor samples from 174 colorectal cancer patients. The primary endpoint was five years of DFS. Secondary endpoints were five years of OS, the difference in MOR-1 expression between normal and tumor tissue and the occurrence of postoperative complications. Multivariable Cox regression showed no significant association between MOR-1 expression and DFS (HR 0.791, 95% CI 0.603–1.039, p = 0.092). MOR-1 expression was higher in tumor tissue compared to non-tumor tissue. No associations were found between MOR-1 expression and OS or postoperative complications. These findings suggest that although MOR-1 is over-expressed in colorectal cancer samples there is no association to increased risk of recurrence or mortality. Future studies are warranted to elucidate the role of cancer stage, genetic polymorphism, and quantitative assessment of MOR-1 over-expression on long-term outcomes in colorectal cancer.