Natural selection of academic papers

Academic papers, like genes, code for ideas or technological innovations that structure and transform the scientific organism and consequently the society at large. Genes are subject to the process of natural selection which ensures that only the fittest survive and contribute to the phenotype of the organism. The process of selection of academic papers, however, is far from natural. Commercial for-profit publishing houses have taken control over the evaluation and access to scientific information with serious consequences for the dissemination and advancement of knowledge. Academic authors and librarians are reacting by developing an alternative publishing system based on free-access journals and self-archiving in institutional repositories and global disciplinary libraries. Despite the emergence of such trends, the journal monopoly, rather than the scientific community, is still in control of selecting papers and setting academic standards. Here we propose a dynamical and transparent peer review process, which we believe will accelerate the transition to a fully open and free-for-all science that will allow the natural selection of the fittest ideas.     

Understanding the role of open peer review and dynamic academic articles

We welcome the commentary by L. Egghe (Scientometrics, this issue) stimulating discussion on our recent article “Natural selection of academic papers” (NSAP) (Scientometrics, 85(2):553–559, 2010) that focuses on an important modern issue at the heart of the scientific enterprise—the open and continuous evaluation and evolution of research. We are also grateful to the editor of Scientometrics for giving us the opportunity to respond to some of the arguments by L. Egghe that we believe are inaccurate or require further comment.     

Angiogenesis-Related Pathways in the Pathogenesis of Ovarian Cancer

Ovarian Cancer represents the most fatal type of gynecological malignancies. A number of processes are involved in the pathogenesis of ovarian cancer, especially within the tumor microenvironment. Angiogenesis represents a hallmark phenomenon in cancer, and it is responsible for tumor spread and metastasis in ovarian cancer, among other tumor types, as it leads to new blood vessel formation. In recent years angiogenesis has been given considerable attention in order to identify targets for developing effective anti-tumor therapies. Growth factors have been identified to play key roles in driving angiogenesis and, thus, the formation of new blood vessels that assist in “feeding” cancer. Such molecules include the vascular endothelial growth factor (VEGF), the platelet derived growth factor (PDGF), the fibroblast growth factor (FGF), and the angiopoietin/Tie2 receptor complex. These proteins are key players in complex molecular pathways within the tumor cell and they have been in the spotlight of the development of anti-angiogenic molecules that may act as stand-alone therapeutics, or in concert with standard treatment regimes such as chemotherapy. The pathways involved in angiogenesis and molecules that have been developed in order to combat angiogenesis are described in this paper.