MEDICAL SCIENCES Correction for “Protective role of miR-155 in breast cancer through RAD51 targeting impairs homologous recombination after irradiation,” by Pierluigi Gasparini, Francesca Lovat, Matteo Fassan, Lucia Casadei, Luciano Cascione, Naduparambil K. Jacob, Stefania Carasi, Dario Palmieri, Stefan Costinean, Charles L. Shapiro, Kay Huebner, and Carlo M. Croce, which appeared in issue 12, March 25, 2014, of Proc Natl Acad Sci USA (111:4536–4541; first published March 10, 2014; 10.1073/pnas.1402604111).
The editors wish to note that, after this article was published, a reader noticed that some fragments of text and some sentences in the abstract, significance statement, introduction, and discussion overlap with text from other articles and were reproduced without quotation marks. No concerns have been raised about the originality of the research or about the results and conclusions.
Some text in the abstract and the significance statement overlaps with text from ref. 19.
19. Wang Y, Huang JW, Calses P, Kemp CJ, Taniguchi T (2012) MiR-96 downregulates REV1 and RAD51 to promote cellular sensitivity to cisplatin and PARP inhibition. Cancer Res 72(16):4037–4046.
Some text in the introduction overlaps with text from the following references:
4. Nogueira A, Catarino R, Medeiros R (2011) DNA damage repair and cancer: The role of RAD51 protein and its genetic variants, DNA Repair and Human Health, ed Vengrova S (InTech, Rijeka, Croatia).
19. Wang Y, Huang JW, Calses P, Kemp CJ, Taniguchi T (2012) MiR-96 downregulates REV1 and RAD51 to promote cellular sensitivity to cisplatin and PARP inhibition. Cancer Res 72(16):4037–4046.
21. Le Calvez-Kelm F, et al. (2012) RAD51 and breast cancer susceptibility: No evidence for rare variant association in the Breast Cancer Family Registry study. PLoS ONE 7(12):e52374.
25. Bartel DP (2009) MicroRNAs: Target recognition and regulatory functions. Cell 136(2):215–233.
In the discussion, paragraph 5 overlaps substantially with text from ref. 44 and is now shown with quotation marks below.
“The DNA damage response process is frequently impaired in aggressive breast cancers, as a consequence of either mutation or deregulation of critical components, such as BRCA1, ataxia telangiectasia mutated (ATM), and p53. Whereas p53 mutations have high frequency, mutations in genes coding for ATM or BRCA1 represent rare events in sporadic breast cancers. Functional impairment of BRCA (‘BRCAness’ phenotype) has been frequently observed in sporadic breast cancers [40, 41]. Existence of alternative mechanisms limiting the expression and functions of either BRCA1 or its regulators, such as ATM, characterize this phenomenon. Among these mechanisms, aberrant activity of miRNAs plays a critical role, as reported for miR-146 and miR-182, which directly target BRCA1 [42, 43] or miR-181a/b targeting ATM [44].” (44)
44. Bisso A, et al. (2013) Oncogenic miR-181a/b affect the DNA damage response in aggressive breast cancer. Cell Cycle 12(11):1679–1687.