撤回:Notch-1参与结肠癌细胞对瑞非尼的耐药

IF 4 2区 生物学 Q2 CELL BIOLOGY
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引用次数: 0

摘要

引用本文:G. Mirone, S. Perna, A. Shukla, G. Marfe,“Notch-1在结肠癌细胞对瑞非尼耐药中的作用”,《细胞生理学杂志》,第31期,no。5 (2015): 1097-1105, https://doi.org/10.1002/jcp.25206.The上述文章于2015年9月30日在线发表在Wiley online Library (wileyonlinelibrary.com)上,经主编Robert Heath同意撤回;和Wiley期刊有限责任公司。由于第三方提出的担忧,已经同意撤回图5B和图7D,图5B和图7D是由不同的作者在不同的文章中不适当的重复。此外,图2B中也存在不一致的地方。通讯作者根据关注的问题做出了回应,并提供了图5B的western blots原件和图2B的解释。然而,在最后一位作者的其他文章中发现了数据问题,主编现在对文章中提供的全部数据的完整性和可靠性失去了信心,并认为该手稿的结论在很大程度上受到了损害。作者被告知撤稿。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
RETRACTION: Involvement of Notch-1 in Resistance to Regorafenib in Colon Cancer Cells

RETRACTION: G. Mirone, S. Perna, A. Shukla, G. Marfe, “Involvement of Notch-1 in Resistance to Regorafenib in Colon Cancer Cells,” Journal of Cellular Physiology 231, no. 5 (2015): 1097-1105, https://doi.org/10.1002/jcp.25206.

The above article, published online on 30 September 2015 in Wiley Online Library (wileyonlinelibrary.com), has been retracted by agreement between the journal Editor-in-Chief, Robert Heath; and Wiley Periodicals LLC. The retraction has been agreed due to concerns raised by the third party, which revealed inappropriate figure duplications in Figure 5B and Figure 7D, by different groups of authors in different articles. In addition, there are inconsistencies in Figure 2B. The corresponding author has responded in accordance with the concerns and provided the original western blots for Figure 5B and explanation for Figure 2B. However, data issues were found in the last authors' other articles and the Editor-in-Chief now has lost confidence in the integrity and reliability of the full body of data presented in the article and consider the conclusions of this manuscript substantially compromised. The authors were informed of the retraction.

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来源期刊
CiteScore
14.70
自引率
0.00%
发文量
256
审稿时长
1 months
期刊介绍: The Journal of Cellular Physiology publishes reports of high biological significance in areas of eukaryotic cell biology and physiology, focusing on those articles that adopt a molecular mechanistic approach to investigate cell structure and function. There is appreciation for the application of cellular, biochemical, molecular and in vivo genetic approaches, as well as the power of genomics, proteomics, bioinformatics and systems biology. In particular, the Journal encourages submission of high-interest papers investigating the genetic and epigenetic regulation of proliferation and phenotype as well as cell fate and lineage commitment by growth factors, cytokines and their cognate receptors and signal transduction pathways that influence the expression, integration and activities of these physiological mediators. Similarly, the Journal encourages submission of manuscripts exploring the regulation of growth and differentiation by cell adhesion molecules in addition to the interplay between these processes and those induced by growth factors and cytokines. Studies on the genes and processes that regulate cell cycle progression and phase transition in eukaryotic cells, and the mechanisms that determine whether cells enter quiescence, proliferate or undergo apoptosis are also welcomed. Submission of papers that address contributions of the extracellular matrix to cellular phenotypes and physiological control as well as regulatory mechanisms governing fertilization, embryogenesis, gametogenesis, cell fate, lineage commitment, differentiation, development and dynamic parameters of cell motility are encouraged. Finally, the investigation of stem cells and changes that differentiate cancer cells from normal cells including studies on the properties and functions of oncogenes and tumor suppressor genes will remain as one of the major interests of the Journal.
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