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Research marketplace Science Exchange is now $25 million richer. The startup hooking researchers up with service providers just added the Series B funding round to its coffers, putting its total raised at $30.5 million. Maverick Capital led the round, with participation from Union Square Ventures, Index Ventures, OATV, Collaborative Fund, YC Continuity Fund, TEDMED CEO Jose Suarez, Sam Altman, Steve Case, Paul Buchheit, and other angel investors. Science Exchange came out of Y Combinator in 2011 to help academic and government researchers find the right lab services. The idea is similar to Emerald Cloud Therapeutics or another YC company, Transcriptic in that customers can order services needed through an online platform. However, Science Exchange is more of a marketplace and both Emerald and Transcriptic would be considered cloud-based service providers for the needed lab research. The startup claims to work with more than 2,500 of these types of institutions now on the demand side. Many research institutions don’t have the full resources to conduct research needed and research is often costly and takes a long time to get results. Science Exchange offers a marketplace of outsourcing services to conduct the research for these institutions and in theory lower the cost and time it takes. But most of this was for smaller organizations held within government and academia. Science Exchange started moving beyond smaller academic research institutions and into big pharma over the last year, including work with the France-based pharmaceutical conglomerate Sanofi. According to Science Exchange, the foray into larger organizations has helped the startup grow by 500 percent in the last year – it now claims eight out of the top 10 pharmaceutical companies use the startup for outsourced research. Larger pharmaceutical companies are also helping to spur the growth with a higher volume of more complex orders compared to academic and government institutions. “And so the dollar value of those types of orders are much bigger, almost an order of magnitude than other users,” Science Exchange co-founder Dan Knox told TechCrunch. Researchers from Harvard or Stanford might order research costing around $3,000 to 5,000 on average, whereas a big pharmaceutical company will be spending 10 times that for multiple tests, for example. The startup plans to use the new funding to hire in several areas including product, engineering, sales, marketing, and customer success. Knox also told us Science Exchange plans to expand to more of the top research institutions in the U.S. and Europe and that it would like to get into food tech and cosmetics research in the future.


Experimental results that don’t hold up to replication have caused consternation among scientists for years, especially in the life and social sciences (SN: 1/24/15, p. 20). In 2015 several research groups examining the issue reported on the magnitude of the irreproducibility problem. The news was not good. Results from only 35 of 97 psychology experiments published in three major journals in 2008 could be replicated, researchers reported in August (SN: 10/3/15, p. 8). The tumor-shrinking ability of the cancer drug sunitinib was overestimated by 45 percent on average, an analysis published in October showed (SN: 11/14/15, p. 17). And a report in June found that, in the United States alone, an estimated $28 billion is spent annually on life sciences research that can’t be reproduced (SN: 7/11/15, p. 5). Estimated annual U.S. spending on preclinical research that is irreproducible There are many possible reasons for the problem, including pressure to publish, data omission and contamination of cell cultures (SN Online: 7/2/15; SN: 2/7/15, p. 22). Faulty statistics are another major source of irreproducibility, and several prominent scientific journals have set guidelines for how statistical analyses should be conducted. Very large datasets, which have become common in genetics and other fields, present their own challenges: Different analytic methods can produce widely different results, and the sheer size of big data studies makes replication difficult. Perfect reproductions might never be possible in biology and psychology, where variability among and between people, lab animals and cells, as well as unknown variables, influences the results. But several groups, including the Science Exchange and the Center for Open Science, are leading efforts to replicate psychology and cancer studies to pinpoint major sources of irreproducibility. Although there is no consensus on how to solve the problem, suggestions include improving training for young scientists, describing methods more completely in published papers and making all data and reagents available for repeat experiments.


Vanden Heuvel J.P.,INDIGO Biosciences | Vanden Heuvel J.P.,Pennsylvania State University | Bullenkamp J.,Kings College London | Iorns E.,Science Exchange | And 5 more authors.
eLife | Year: 2016

The Reproducibility Project: Cancer Biology seeks to address growing concerns about the reproducibility in scientific research by conducting replications of selected experiments from a number of high-profile papers in the field of cancer biology. The papers, which were published between 2010 and 2012, were selected on the basis of citations and Altmetric scores (Errington et al., 2014). This Registered Report describes the proposed replication plan of key experiments from “Systematic identification of genomic markers of drug sensitivity in cancer cells” by Garnett and colleagues, published in Nature in 2012 (Garnett et al., 2012). The experiments to be replicated are those reported in Figures 4C, 4E, 4F, and Supplemental Figures 16 and 20. Garnett and colleagues performed a high throughput screen assessing the effect of 130 drugs on 639 cancer-derived cell lines in order to identify novel interactions for possible therapeutic approaches. They then tested this approach by exploring in more detail a novel interaction they identified in which Ewing’s sarcoma cell lines showed an increased sensitivity to PARP inhibitors (Figure 4C). Mesenchymal progenitor cells (MPCs) transformed with the signature EWS-FLI1 translocation, the hallmark of Ewing’s sarcoma family tumors, exhibited increased sensitivity to the PARP inhibitor olaparib as compared to MPCs transformed with a different translocation (Figure 4E). Knockdown mediated by siRNA of EWS-FLI1 abrogated this sensitivity to olaparib (Figure 4F). The Reproducibility Project: Cancer Biology is a collaboration between the Center for Open Science and Science Exchange, and the results of the replications will be published by eLife. © Vanden Heuvel and Bullenkamp.


Drews-Elger K.,University of Miami | Iorns E.,Science Exchange | Dias A.,University of Miami | Miller P.,University of Miami | And 11 more authors.
Breast Cancer Research and Treatment | Year: 2014

The mechanisms by which breast cancer (BrC) can successfully metastasize are complex and not yet fully understood. Our goal was to identify tumor-induced stromal changes that influence metastatic cell behavior, and may serve as better targets for therapy. To identify stromal changes in cancer-bearing tissue, dual-species gene expression analysis was performed for three different metastatic BrC xenograft models. Results were confirmed by immunohistochemistry, flow cytometry, and protein knockdown. These results were validated in human clinical samples at the mRNA and protein level by retrospective analysis of cohorts of human BrC specimens. In pre-clinical models of BrC, systemic recruitment of S100A8+ myeloid cells—including myeloid-derived suppressor cells (MDSCs)—was promoted by tumor-derived factors. Recruitment of S100A8+ myeloid cells was diminished by inhibition of tumor-derived factors or depletion of MDSCs, resulting in fewer metastases and smaller primary tumors. Importantly, these MDSCs retain their ability to suppress T cell proliferation upon co-culture. Secretion of macrophage inhibitory factor (MIF) activated the recruitment of S100A8+ myeloid cells systemically. Inhibition of MIF, or depletion of MDSCs resulted in delayed tumor growth and lower metastatic burden. In human BrC specimens, increased mRNA and protein levels of S100A8+ infiltrating cells are highly associated with poor overall survival and shorter metastasis free survival of BrC patients, respectively. Furthermore, analysis of nine different human gene expression datasets confirms the association of increased levels of S100A8 transcripts with an increased risk of death. Recruitment of S100A8+ myeloid cells to primary tumors and secondary sites in xenograft models of BrC enhances cancer progression independent of their suppressive activity on T cells. In clinical samples, infiltrating S100A8+ cells are associated with poor overall survival. Targeting these molecules or associated pathways in cells of the tumor microenvironment may translate into novel therapeutic interventions and benefit patient outcome. © 2014, Springer Science+Business Media New York.


Chroscinski D.,Noble Life Sciences | Sampey D.,BioFactura | Maherali N.,Harvard Stem Cell Institute | Iorns E.,Science Exchange | And 4 more authors.
eLife | Year: 2015

The Reproducibility Project: Cancer Biology seeks to address growing concerns about reproducibility in scientific research by conducting replications of 50 papers in the field of cancer biology published between 2010 and 2012. This Registered report describes the proposed replication plan of key experiments from ‘Tumour vascularization via endothelial differentiation of glioblastoma stem-like cells’ by Ricci-Vitiani and colleagues, published in Nature in 2010 (Ricci-Vitiani et al., 2010). The experiments that will be replicated are those reported in Figure 4B and Supplementary Figure 10B (Ricci-Vitiani et al., 2010), which demonstrate that glioblastoma stem-like cells can derive into endothelial cells, and can be selectively ablated to reduce tumor progression in vivo, and Supplementary Figures S10C and S10D (Ricci-Vitiani et al., 2010), which demonstrate that fully differentiated glioblastoma cells cannot form functionally relevant endothelium. The Reproducibility Project: Cancer Biology is a collaboration between the Center for Open Science and Science Exchange, and the results of the replications will be published by eLife. © Copyright Chroscinski et al.

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