Differential shotgun analysis of mesenchymal stem cells from osteoarthritis patients

Comunicaciones a congreso

Identification of non-small cell lung cancer biomarkers using mass spectrometry

Comunicaciones a congreso

An anti-ICAM-2 (CD102) monoclonal antibody induces immune-mediated regressions of transplanted ICAM-2-negative colon carcinomas

Monoclonal antibodies (mAbs) can mediate antitumor effects by indirect mechanisms involving antiangiogenesis and up-regulation of the cellular immune response rather than by direct tumor cell destruction. From mAbs raised by immunization of rats with transformed murine endothelial cells, a mAb (EOL4G8) was selected for its ability to eradicate a fraction of established colon carcinomas that did not express the EOL4G8-recognized antigen. The antigen was found to be ICAM-2 (CD102). Antitumor effects of EOL4G8, which required a functional T-cell compartment, were abrogated by depletion of CD8(+) cells and correlated with antitumor CTL activity, whereas only a mild inhibition of angiogenesis was observed. Interestingly, we found that EOL4G8 acting on endothelial ICAM-2 markedly enhances leukotactic factor activity-1-independent adhesion of immature dendritic cells to endothelium-an effect that is at least in part mediated by DC-SIGN (CD209)

The impact of new research technologies on our understanding of environmental causes of disease: the concept of clinical vulnerability

In spite of decades of epidemiological research, the etiology and causal patterns for many common diseases, such as breast and colon cancer or neurodegenerative diseases, are still largely unknown. Such chronic diseases are likely to have an environmental origin. However, "environmental" risks have been often elusive in epidemiological studies. This is a conundrum for current epidemiological research. On the other side, the relative contribution of genes to chronic diseases, as emerging from GWAS, seems to be modest (15-50% increase in disease risk). What is yet to be explored extensively is a model of disease based on long-term effects of low doses of environmental exposures, incorporating both genetic and acquired susceptibility ("clinical vulnerability"), and the cumulative effects of different exposures. Such a disease model would be compatible with the weak associations found by GWAS and the still elusive role of many (low-level) environmental exposures. We also propose that the introduction of "-omic" high-throughput technologies, such as transcriptomics, proteomics and metabolomics, may provide, in the next years, powerful tools to investigate early effects of environmental exposures and understand the etiology of common diseases better, according to the "clinical vulnerability model". The development of "-omics", in spite of current limitations and lack of sound validation, could greatly contribute to the elucidation of the disease model we propose

PTRF/Cavin-1 and MIF Proteins Are Identified as Non-Small Cell Lung Cancer Biomarkers by Label-Free Proteomics

With the completion of the human genome sequence, biomedical sciences have entered in the “omics” era, mainly due to high-throughput genomics techniques and the recent application of mass spectrometry to proteomics analyses. However, there is still a time lag between these technological advances and their application in the clinical setting. Our work is designed to build bridges between high-performance proteomics and clinical routine. Protein extracts were obtained from fresh frozen normal lung and non-small cell lung cancer samples. We applied a phosphopeptide enrichment followed by LC-MS/MS. Subsequent label-free quantification and bioinformatics analyses were performed. We assessed protein patterns on these samples, showing dozens of differential markers between normal and tumor tissue. Gene ontology and interactome analyses identified signaling pathways altered on tumor tissue. We have identified two proteins, PTRF/cavin-1 and MIF, which are differentially expressed between normal lung and non-small cell lung cancer. These potential biomarkers were validated using western blot and immunohistochemistry. The application of discovery-based proteomics analyses in clinical samples allowed us to identify new potential biomarkers and therapeutic targets in non-small cell lung cancer

Proteomic analysis from haploid and diploid embryos of Quercus suber L. identifies qualitative and quantitative differential expression patterns

Quercus suber L. is a Mediterranean forest species with ecological, social and economic value. Clonal propagation of Q. suber elite trees has been successfully obtained from in vitro-derived somatic and gametic embryos. These clonal lines play a main role in breeding and genetic studies of Q. suber. To aid in unravelling diverse genetic and biological unknowns, a proteomic approach is proposed. The proteomic analysis of Q. suber somatic and gametic in vitro culture-derived embryos, based on DIGE and MALDI-MS, has produced for the first time proteomic data on this species. Seventeen differentially expressed proteins have been identified which display significantly altered levels between gametic and somatic embryos. These proteins are involved in a variety of cellular processes, most of which had been neither previously associated with embryo development nor identified in the genus Quercus. Some of these proteins are involved in stress and pollen development and others play a role in the metabolism of tannins and phenylpropanoids, which represent two of the major pathways for the synthesis of cork chemical components. Furthermore, the augmented expression levels found for specific proteins are probably related to the homozygous state of a doubled-haploid sample. Proteins involved in synthesis of cork components can be detected at such early stages of development, showing the potential of the method to be useful in searching for biomarkers related to cork quality. © 2009 Wiley-VCH Verlag GmbH & Co. KGaA