These findings suggest that, through expression of CXCL5, eosinophils can recruit and activate CXC receptor 2 (CXCR2)-bearing cells such as neutrophils at sites of inflammation. Eosinophils may also promote connective tissue remodelling through release of this peptide.

Our results confirm that, in cases in which biopsies or surgical specimens are not available, IC (with either cell block or ThinPrep techniques) is a reliable method for the determination of the ER and PgR status performed under strict conditions using primary breast carcinomas, and is therefore potentially useful in metastatic settings.

ObjectivesAmong patients who underwent primary surgery for non-small cell lung cancer (NSCLC), recurrent disease is frequent and cannot be accurately predicted solely from TNM stage and histopathological features. The aim of this study was to examine the association of tumor markers in pre-operative serum with recurrent disease.Material and methodsBlood samples were collected prior to lung cancer surgery from 107 patients with stage I-III lung adenocarcinoma surgically treated at Lund University hospital, Lund, Sweden, between 2005 and 2011. The serum tumor markers Carcinoembryonic antigen (CEA), Neuron-specific enolase (NSE), Cancer antigen 125 (CA 125), Human epididymis protein 4 (HE4) and Carbohydrate antigen (CA 19–9) were analyzed retrospectively and clinical follow-up data were collected from patient charts. Forty (37%) patients were diagnosed with recurrent disease.ResultsSixty-eight (64%) patients had at least one elevated tumor marker prior to surgery. In analysis of disease-free survival (DFS), CA 125 and/or CA 19–9 were significantly associated with recurrent disease adjusted to stage and adjuvant treatment (hazard ratio 2.8, 95% confidence interval 1.4–5.7, p = 0.006).ConclusionHigh pre-operative serum CA 19–9 and/or CA 125 might indicate an increased incidence of recurrent disease in resectable lung adenocarcinomas.

showed no or extremely low levels of HIF-2α mRNA and no HIF-2α protein at hypoxia. HIF-1α was stabilized after 4 h at hypoxia and the accumulation increased up to 96 h. SCLC cells survived well and showed net proliferation and low cell death at modest (1% oxygen) and severe hypoxia (0.1% oxygen). HIF-1α repression did virtually not influence cell death or viability despite reduced levels of hypoxia-inducible genes, such as BNIP3 and BNIP3L. At 1% oxygen no increased autophagy (LC3B-II activation) or NF-κB signaling were detected, while unfolded protein response was activated at severe hypoxia. Our data indicate that HIFs are not exclusively required for SCLC cell survival at modest or severe hypoxia and thatadditional, yet uncharacterized hypoxia-driven adaptation pathways may become activated.4

Our results indicate that only the cytoplasmic isoform 2 of Oct 3/4 is present in prostate cancer and benign prostate hyperplasia. The malignant and benign prostate cells, which are immunopositive for variant 2 of Oct 3/4, lack other stem cell markers supporting previously published data that variant 2 of Oct 3/4 is not a pluripotency marker.