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Yue Xu, PhD; Ming Zheng, PhD; Amanda Khuong, BS; Robert E. Merritt, MD; Joseph B. Shrager, MD; Heather A. Wakelee, MD; Robert A. Kratzke, MD; Chuong D. Hoang, MD
Author and Funding Information

From the Division of Thoracic Surgery, Department of Cardiothoracic Surgery (Drs Xu, Merritt, Shrager, and Hoang and Ms Khuong), Department of Anesthesia (Dr Zheng), and the Division of Oncology, Department of Medicine (Dr Wakelee), Stanford University School of Medicine; the Veterans Affairs Palo Alto Healthcare System (Drs Shrager and Hoang), Palo Alto, CA; and the Division of Hematology, Oncology, and Transplant, Department of Medicine (Dr Kratzke), University of Minnesota Medical School.

Correspondence to: Chuong D. Hoang, MD, Falk Bldg, 300 Pasteur Dr, Stanford, CA 94305-5407; e-mail: cdhoang@stanford.edu


Funding/Support: Dr Hoang is supported by funds from the Mesothelioma Applied Research Foundation. Funding to purchase dedicated research equipment for this project was provided by Kazan, McClain, Abrams, Fernandez, Lyons, Greenwood, Harley & Oberman Foundation, Inc.

Financial/nonfinancial disclosures: The authors have reported to CHEST that no potential conflicts of interest exist with any companies/organizations whose products or services may be discussed in this article.

Reproduction of this article is prohibited without written permission from the American College of Chest Physicians. See online for more details.


Chest. 2013;144(6):1971-1972. doi:10.1378/chest.13-1931
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To the Editor:

We appreciate the comments of Ms Wright and colleagues about our recent article.1 Unfortunately, we disagree with their conclusion that our study did not contribute to knowledge about the role of microRNA in mesothelioma.

We did not “cherry pick” our validation samples, but instead selected them because these tissue specimens were plentiful and would not be exhausted. Selected validation, using a subset of microRNA and tissue specimens, of array profiling data is the most reasonable, cost-effective design. This strategy is a well-accepted practice in current literature, including the article by Kubo et al.2

We selected miR-1 for functional analysis in mesothelioma because we have ongoing interests in this microRNA. We discussed this topic in the Results and Discussion sections of our study. We agree that other miR-1 family members and multiple other microRNAs identified from our list of most differentially expressed microRNAs are interesting, too. Further studies elucidating distinguished functions of other microRNAs are being conducted.

Polymerase chain reaction (PCR) analysis of known apoptotic genes was done to confirm the apoptotic phenotype of transfected cell lines. Correlation analysis of miR-1 and its gene targets is not highly useful, since specific functional information of those interactions cannot be discerned. Identifying and confirming microRNA direct gene targets were not in the scope of our investigation and were never the goal of this study.

In our experimental procedures, we described in great detail which company’s RNA products were used for microRNA overexpression, the transfection reagents used, the system used to run our real-time PCR, and the list of gene primer sequences used to perform PCR or the catalog number of the microRNA assay. We followed recommendations of the manufacturer where indicated. We searched PubMed, and as of August 15, 2013, many of the microRNAs we mentioned as examples of putative, novel mesothelioma-associated microRNAs remained consistent. In the Discussion section, we limited the context to prior microRNA profiling studies, not an encyclopedic review of every microRNA that has heretofore been mentioned with mesothelioma. The Kubo et al2 article is not a microarray profiling study, but details the methylation status of miR-34b and its functional implication.

In summary, we have identified a set of underexpressed and overexpressed microRNAs specific to mesothelioma based on a survey of human tissue specimens. We reported that overexpression of miR-1 in mesothelioma cell lines induces apoptosis. We welcome subsequent independent studies of miR-1 in mesothelioma. We anticipate the other microRNAs we have identified will contribute to ongoing research in mesothelioma.

Acknowledgments

Role of sponsors: The sponsor had no role in the design of the study, the collection and analysis of the data, or the preparation of the manuscript.

Xu Y, Zheng M, Merritt RE, et al. miR-1 induces growth arrest and apoptosis in malignant mesothelioma. Chest. 2013;144(5):1632-1643. [CrossRef] [PubMed]
 
Kubo T, Toyooka S, Tsukuda K, et al. Epigenetic silencing of microRNA-34b/c plays an important role in the pathogenesis of malignant pleural mesothelioma. Clin Cancer Res. 2011;17(15):4965-4974. [CrossRef] [PubMed]
 

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References

Xu Y, Zheng M, Merritt RE, et al. miR-1 induces growth arrest and apoptosis in malignant mesothelioma. Chest. 2013;144(5):1632-1643. [CrossRef] [PubMed]
 
Kubo T, Toyooka S, Tsukuda K, et al. Epigenetic silencing of microRNA-34b/c plays an important role in the pathogenesis of malignant pleural mesothelioma. Clin Cancer Res. 2011;17(15):4965-4974. [CrossRef] [PubMed]
 
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