Published May 29, 2018 - More info
Platinum compounds display clinical activity against a wide variety of solid tumors; however, resistance to these agents is a major limitation in cancer therapy. Reduced platinum uptake and increased platinum export are examples of resistance mechanisms that limit the extent of DNA damage. Here, we report the discovery and characterization of the role of ATP11B, a P-type ATPase membrane protein, in cisplatin resistance. We found that
Myrthala Moreno-Smith, J.B. Halder, Paul S. Meltzer, Tamas A. Gonda, Lingegowda S. Mangala, Rajesha Rupaimoole, Chunhua Lu, Archana S. Nagaraja, Kshipra M. Gharpure, Yu Kang, Cristian Rodriguez-Aguayo, Pablo E. Vivas-Mejia, Behrouz Zand, Rosemarie Schmandt, Hua Wang, Robert R. Langley, Nicholas B. Jennings, Cristina Ivan, Jeremy E. Coffin, Guillermo N. Armaiz, Justin Bottsford-Miller, Sang Bae Kim, Margaret S. Halleck, Mary J.C. Hendrix, William Bornman, Menashe Bar-Eli, Ju-Seog Lee, Zahid H. Siddik, Gabriel Lopez-Berestein, Anil K. Sood
Original citation: J Clin Invest. 2013;123(5):2119–2130. https://doi.org/10.1172/JCI65425
Citation for this expression of concern: J Clin Invest. 2018;128(7):3199. https://doi.org/10.1172/JCI122301
The Editors recently became aware that Figure 3B appears to use a set of images that were previously published in a 2009 Clinical Cancer Research paper with different sample labels (doi: 10.1158/1078-0432.CCR-08-2306). Additionally, the empty liposome and control siRNA PCNA–stained panels appear to be the same. The Editorial Board is pursuing further investigation of this matter, and we will inform our readers of the outcome when the investigation is complete.
See the related article at ATP11B mediates platinum resistance in ovarian cancer.