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Mantis C.,Northwestern University | Kandela I.,Northwestern University | Aird F.,Northwestern University | Iorns E.,Science Exchange | And 4 more authors.
eLife | Year: 2017

In 2015, as part of the Reproducibility Project: Cancer Biology, we published a Registered Report (Kandela et al., 2015) that described how we intended to replicate selected experiments from the paper "Coadministration of a tumor-penetrating peptide enhances the efficacy of cancer drugs" (Sugahara et al., 2010). Here we report the results of those experiments. We found that coadministration with iRGD peptide did not have an impact on permeability of the chemotherapeutic agent doxorubicin (DOX) in a xenograft model of prostate cancer, whereas the original study reported that it increased the penetrance of this cancer drug (Figure 2B; Sugahara et al., 2010). Further, in mice bearing orthotopic 22Rv1 human prostate tumors, we did not find a statistically significant difference in tumor weight for mice treated with DOX and iRGD compared to DOX alone, whereas the original study reported a decrease in tumor weight when DOX was coadministered with iRGD (Figure 2C; Sugahara et al., 2010). In addition, we did not find a statistically significant difference in TUNEL staining in tumor tissue between mice treated with DOX and iRGD compared to DOX alone, while the original study reported an increase in TUNEL positive staining with iRGD coadministration (Figure 2D; Sugahara et al., 2010). Similar to the original study (Supplemental Figure 9A; Sugahara et al., 2010), we did not observe an impact on mouse body weight with DOX and iRGD treatment. Finally, we report meta-analyses for each result. © Mantis et al.


Kandela I.,Northwestern University | Aird F.,Northwestern University | Iorns E.,Science Exchange | Williams S.R.,Center for Open Science | And 2 more authors.
eLife | Year: 2017

In 2015, as part of the Reproducibility Project: Cancer Biology, we published a Registered Report (Kandela et al., 2015) that described how we intended to replicate selected experiments from the paper "Discovery and Preclinical Validation of Drug Indications Using Compendia of Public Gene Expression Data" (Sirota et al., 2011). Here we report the results of those experiments. We found that cimetidine treatment in a xenograft model using A549 lung adenocarcinoma cells resulted in decreased tumor volume compared to vehicle control; however, while the effect was in the same direction as the original study (Figure 4C; Sirota et al., 2011), it was not statistically significant. Cimetidine treatment in a xenograft model using ACHN renal cell carcinoma cells did not differ from vehicle control treatment, similar to the original study (Supplemental Figure 1; Sirota et al., 2011). Doxorubicin treatment in a xenograft model using A549 lung adenocarcinoma cells did not result in a statistically significant difference compared to vehicle control despite tumor volume being reduced to levels similar to those reported in the original study (Figure 4C; Sirota et al., 2011). Finally, we report a random effects meta-analysis for each result. These meta-analyses show that the inhibition of A549 derived tumors by cimetidine resulted in a statistically significant effect, as did the inhibition of A549 derived tumors by doxorubicin. The effect of cimetidine on ACHN derived tumors was not statistically significant, as predicted. © Kandela and Aird.


Aird F.,Northwestern University | Kandela I.,Northwestern University | Mantis C.,Northwestern University | Iorns E.,Science Exchange | And 4 more authors.
eLife | Year: 2017

In 2015, as part of the Reproducibility Project: Cancer Biology, we published a Registered Report (Kandela et al., 2015) that described how we intended to replicate selected experiments from the paper “BET bromodomain inhibition as a therapeutic strategy to target c-Myc” (Delmore et al., 2011). Here we report the results of those experiments. We found that treatment of human multiple myeloma (MM) cells with the small-molecular inhibitor of BET bromodomains, (+)-JQ1, selectively downregulated MYC transcription, which is similar to what was reported in the original study (Figure 3B; Delmore et al., 2011). Efficacy of (+)-JQ1 was evaluated in an orthotopically xenografted model of MM. Overall survival was increased in (+)-JQ1 treated mice compared to vehicle control, similar to the original study (Figure 7E; Delmore et al., 2011). Tumor burden, as determined by bioluminescence, was decreased in (+)-JQ1 treated mice compared to vehicle control; however, while the effect was in the same direction as the original study (Figure 7CD; Delmore et al., 2011), it was not statistically significant. The opportunity to detect a statistically significant difference was limited though, due to the higher rate of early death in the control group, and increased overall survival in (+)-JQ1 treated mice before the pre-specified tumor burden analysis endpoint. Additionally, we evaluated the (-)-JQ1 enantiomer that is structurally incapable of inhibiting BET bromodomains, which resulted in a minimal impact on MYC transcription, but did not result in a statistically significant difference in tumor burden or survival distributions compared to treatment with (+)-JQ1. Finally, we report meta-analyses for each result. © Aird et al.


Horrigan S.K.,Noble Life Sciences | Iorns E.,Science Exchange | Williams S.R.,Center for Open Science | Perfito N.,Science Exchange | Errington T.M.,Center for Open Science
eLife | Year: 2017

In 2015, as part of the Reproducibility Project: Cancer Biology, we published a Registered Report (Chroscinski et al., 2015) that described how we intended to replicate selected experiments from the paper “The CD47-signal regulatory protein alpha (SIRPa) interaction is a therapeutic target for human solid tumors “(Willingham et al., 2012). Here we report the results of those experiments. We found that treatment of immune competent mice bearing orthotopic breast tumors with anti-mouse CD47 antibodies resulted in short-term anemia compared to controls, consistent with the previously described function of CD47 in normal phagocytosis of aging red blood cells and results reported in the original study (Table S4; Willingham et al., 2012). The weight of tumors after 30 days administration of anti-CD47 antibodies or IgG isotype control were not found to be statistically different, whereas the original study reported inhibition of tumor growth with anti-CD47 treatment (Figure 6A,B; Willingham et al., 2012). However, our efforts to replicate this experiment were confounded because spontaneous regression of tumors occurred in several of the mice. Additionally, the excised tumors were scored for inflammatory cell infiltrates. We found IgG and anti-CD47 treated tumors resulted in minimal to moderate lymphocytic infiltrate, while the original study observed sparse lymphocytic infiltrate in IgG-treated tumors and increased inflammatory cell infiltrates in anti-CD47 treated tumors (Figure 6C; Willingham et al., 2012). Furthermore, we observed neutrophilic infiltration was slightly increased in anti-CD47 treated tumors compared to IgG control. Finally, we report a meta-analysis of the result. © Horrigan.


Elizabeth Iorns, Ph.D., Founder and CEO of Science Exchange, joins panel to discuss how today's young entrepreneurs are reshaping the biopharma business model


News Article | February 23, 2017
Site: www.prnewswire.com

PALO ALTO, Calif. and LANCASTER, Pa., Feb. 23, 2017 /PRNewswire/ -- Science Exchange and Eurofins are excited to announce that Eurofins Central Laboratory is now a service provider listed on the Science Exchange marketplace for outsourced research services. This means that pharmaceutical a...


News Article | March 23, 2016
Site: techcrunch.com

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.


PALO ALTO, Calif. and FARMERS BRANCH, Texas, Feb. 22, 2017 /PRNewswire/ -- Science Exchange and Apollo Laboratories are excited to announce that drug development services from Apollo Laboratories will now be available from the Science Exchange marketplace. As a result, pharmaceutical and...


News Article | December 15, 2015
Site: www.sciencenews.org

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.


News Article | November 9, 2016
Site: www.chromatographytechniques.com

What is there to stop someone publishing scientific research that is based on no actual research or uses fake evidence to support their claims? If the risk to reputation and all that follows isn’t enough to deter someone from such scientific fraud, then what other steps can science take to maintain the integrity of any published research? The criminal prosecution of Dr Caroline Barwood should serve as a warning to researchers who might be tempted to engage in such actions. She was convicted last month of fraudulently applying for research grants. The criminal charges for fraud and attempted fraud that were brought against Barwood were based mainly on her attempts to obtain funding for research investigating a treatment for Parkinson’s disease. The research was allegedly conducted with Professor Bruce Murdoch through the Centre for Neurogenic Communication Disorders Research at the University of Queensland. In 2012, an unidentified whistleblower contacted the University of Queensland about Murdoch and Barwood’s Parkinson’s study. After an internal investigation the university discovered multiple irregularities, no primary data from the research and no evidence that the research had actually been conducted. Publications based on the research had appeared in several prominent journals. The university informed the journals and four papers have now been retracted. Both Barwood and Murdoch resigned from the university. But the university referred the matter to Queensland’s Crime and Corruption Commission. After a lengthy investigation, the Commission recommended that criminal charges be laid against both researchers. In March 2016 Murdoch pleaded guilty to 17 fraud-related charges. He was given a two year suspended sentence. The sentencing magistrate found that there was no evidence Murdoch had conducted the clinical trials on which his findings, and some of his publications, were allegedly based. A critical feature of the prosecution was that both public and private research money had funded the research. Barwood’s conviction followed later in 2016. She was convicted of five charges and sentenced to two years imprisonment, also suspended. She may face a further trial because the jury couldn’t reach agreement on another two charges. These cases may be rare but mark a willingness to use criminal prosecutions to deal with researchers who engage in fraud. But is hitting researchers for fraud over their applications for funds enough to deter the scientific fraud itself? In a hard-hitting editorial in 2013, the journal Nature said: Several prominent commentators, including a former editor of the British Medical Journal have joined the call for scientific fraud to be recognised as a criminal offence. The re-framing of some forms of scientific misconduct as criminal fraud recognises that scientific fraud involving the fabrication of research and/or results in circumstances where private or public funding has been sought or obtained is similar to other forms of fraud. It involves dishonesty and deception for the purpose of obtaining money or other financial advantage. It is immaterial that the benefit may not have been for the direct, personal benefit of the researcher. It also recognizes that like other forms of fraud, scientific fraud requires careful, detailed investigation and the obtaining of evidence. Police and other prosecuting authorities (such as the Crime and Corruption Commission) are best able to conduct this sort of investigation and gather this information. The first prosecution for scientific fraud appears to have been in the United States in 2006. Eric Poehlman was found guilty of fraud and sentenced to prison for a year and a day after he falsified results from his obesity research. Poehlman had received significant amounts of research funding. Perhaps the most famous case in recent years involved Dong-Pyou Han, a biomedical scientist at Iowa State University. Han falsified the results of several experiments involving the development of a vaccine for HIV. He eventually pleaded guilty to making false statements to obtain research grants. He was sentenced to 57 months in prison and ordered to pay back $7.2 million in grant funds that he had fraudulently obtained. All these cases involved intentional deception. They were not simply lapses in scientific standards or based on disputes about appropriate methodology or analysis. A further troubling feature is that many cases involved eminent or promising researchers from leading institutions and universities, including now the University of Queensland. Run them out of town Criminal prosecutions for academic fraud are rare. A researcher who is found to have engaged in fraud will more likely lose their job, suffer reputational damage, be de-registered (if they are a registered health care professional), have publications retracted and find it difficult to obtain further research funding. But these traditional strategies for dealing with scientific fraud have significant limitations. The potential lack of institutional integrity is foremost. Universities and other institutions are sometimes more concerned with protecting their own reputations rather than properly investigating potential fraud. That said, the decisive action taken by the University of Queensland demonstrates a commitment to high research standards. The retraction of published papers based on fraudulent research is fraught with problems. In an editorial published in 2013 the journal Nature Medicine noted a lack of co-operation by the researcher’s institution in investigating cases of alleged fraud and threats of legal action by the suspect researcher made retractions difficult. It said: There are now promising alternatives to criminal prosecution and traditional sanctions. They have potentially broader impact because they are not restricted to research which has been funded and they come from within the scientific community itself. These initiatives include some journals now requiring authors to submit their raw data before publication is considered, and the website Retraction Watch which monitors fraud by identifying scientific articles that have been retracted. Also, a reproducibility initiative by Science Exchange encourages researchers to submit their experiments and results and have them replicated by independent researchers. This provides another means for ensuring research integrity. Criminal prosecutions are certainly an appropriate strategy for dealing with some forms of scientific fraud. But they are not a panacea. At best, they function as an additional mechanism for pursuing egregious cases where researchers have obtained, or tried to obtain, research funding based on non-existent studies or results that has been altered. In these cases the scientific fraud clearly constitutes criminal conduct and should be prosecuted as such. But in many instances the traditional regulatory mechanisms and sanctions, in conjunction with newer initiatives to more closely monitor research, will still be the primary mechanisms for ensuring the integrity of scientific research. This article was originally published on The Conversation and written by Marilyn McMahon, associate professor in Law, Deakin University.

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