Recent studies have shown that cancer cells can deceive phagocytosing macrophage cells through the CD47 protein which gives the message “don’t eat me” or “don’t kill me” to immune components. The efficacy of anti-CD47 treatment approach was shown in cancers such as, non-small cell lung cancer, non-Hodgkin lymphoma, ovarian cancer, and breast cancer. The studies on the immunobiology of neuroblastoma has increased as monoclonal antibody based immunotherapy has shown to be effective in high-risk patients such as anti disialoganglioside. Therefore, the aim of this study was to evaluate the levels of CD47 protein expression among neuroblastoma patients with different risk groups and genetic alterations. This study included paraffin-embedded tumor tissues of 66 neuroblastoma patients (28 girls, 38 boys) with an age range of 0.5 to 108 months with a mean value of 24.9 (±23.5). According to risk classifications 21 were at low risk (31, 8%), 24 were at intermediate risk (36, 4%) and 19 were at high-risk (28, 8%) groups. These samples were evaluated for MYCN amplification, 1p36 LOH, 11q23 deletion and 17q25 gain by real-time PCR. In addition, CD47 expression status (positive or negative) was detected by immunohistochemical analysis. All data was analyzed with Chi-Square and Mann-Whitney U non-parametric tests within SPSS program, version 22.0. p value lower than 0, 5 was found statistically significant. According to the results, patients at low risk did not express CD47, while patients at high-risk group were mostly expressing CD47 (p = 0.049). MYCN amplification positive patients were expressing CD47 protein (p = 0.046). Patients without 17q25 gain were found to be expressing CD47 protein (p = 0.006). In addition, CD47 expression was increasing as age was getting higher in terms of months (p = 0.018). The findings of this study suggest that positive expression pattern of CD47 may be a poor prognostic biomarker especially in high risk 17q gain negative neuroblastoma patients.

Relationship between the tilt angle of bipolar radial head prostheses and radiological radiocapitellar instability

ConclusionIn conclusion, exerts an important antitumor effect by inhibiting c-Src and up-regulating PTEN with the subsequent reduction in FAK phosphorylation required to establish appropriate focal adhesions for migration, proliferation and survival. This inhibition is mediated by the recruitment of the c-Src intrinsic inhibitors, PTEN and Csk. All together, these results reinforce the relevance of this sequence of Cx43 that interacts with c-Src for the development of new therapies against glioblastoma. PO-292BREAST CANCER STEM CELL REPROGRAMMING: DECIPHERING THE IMPACT OF GLUCOSE AND THE CONTRIBUTE OF TUMOUR MICROENVIRONMENT Introduction Diabetes-associated hyperglycemia is linked to poorer prognosis and survival in breast cancer (BC). Indeed, glucose can affect both tumour and tumour-surrounding cells. BC cells are embedded in an adipocyte-rich microenvironment, which, beside adipocytes, contains Stromal-Vascular Fraction Cells (SVFCs). In this scenario, epithelial and stromal compartments communicate through the release of soluble factors and establish an intricate crosstalk. Here, we analysed whether glucose could directly affect the phenotype of ER + MCF7 BC cells and interfere with their interaction with adipose-derived SVFCs, thereby promoting tumour progression. Material and methods MCF7 cell stemness markers were measured by qReal-Time PCR. Adipose-derived (Ad-)SVFCs were obtained by mammary adipose tissue specimens of women undergoing plastic surgery. The trascriptome of MCF7 exposed to either low (LG-5.5 mM) or high glucose concentration (HG-25 mM) was obtained by RNA-Sequencing (Illumina HiSeq3000). Results and discussions HG exposure of MCF7 determined a significant increase of SOX2 mRNA levels as compared to LG, suggesting the induction of stemness programming. Coculture with Ad-SVFCs in HG increased SOX2, NANOG and OCT4 mRNA levels in MCF7, as compared to isolated culture, indicating the involvement of SVF-produced soluble factors in BC stem cell reprogramming. Moreover, in presence of Ad-SVFCs and HG, MCF7 produced a higher number of mammospheres, which also displayed larger size. However, both in LG and in HG, conditioned media (CM) obtained from Ad-SVFCs produced no relevant effect on MCF7 stemness. Nevertheless, when Ad-SVFCs were pre-incubated with CM obtained from HG-treated MCF7, their CM very effectively increased OCT4, NANOG and SOX2 mRNA levels in MCF7. Thus, HG likely perturbs MCF7, which produce soluble factors leading Ad-SVFCs to release, in turn, reprogramming factors for BC cell stemness. In this regard, we have observed that HG modification of MCF7 transcriptome includes deregulation of 17 genes (pval=0.05) encoding for secreted proteins involved in cancer progression-related pathways, which may potentially play a role in tumour-stroma interactions.