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Communication
Peer-Review Record

FGFR Signaling as a Candidate Therapeutic Target for Cancers Resistant to Carbon Ion Radiotherapy

Int. J. Mol. Sci. 2019, 20(18), 4563; https://doi.org/10.3390/ijms20184563
by Narisa Dewi Maulany Darwis 1,†, Ankita Nachankar 1,†, Yasushi Sasaki 2,†, Toshiaki Matsui 1, Shin-ei Noda 1, Kazutoshi Murata 1, Tomoaki Tamaki 1, Ken Ando 1, Noriyuki Okonogi 1, Shintaro Shiba 1, Daisuke Irie 1, Takuya Kaminuma 1, Takuya Kumazawa 1, Mai Anakura 1, Souichi Yamashita 3, Takashi Hirakawa 3, Sangeeta Kakoti 1, Yuka Hirota 1, Takashi Tokino 2, Akira Iwase 3, Tatsuya Ohno 4, Atsushi Shibata 5, Takahiro Oike 1,4,* and Takashi Nakano 1add Show full author list remove Hide full author list
Reviewer 1: Anonymous
Reviewer 2: Anonymous
Int. J. Mol. Sci. 2019, 20(18), 4563; https://doi.org/10.3390/ijms20184563
Submission received: 22 August 2019 / Revised: 10 September 2019 / Accepted: 12 September 2019 / Published: 14 September 2019
(This article belongs to the Special Issue Counteracting Radioresistance Using the Optimization of Radiotherapy)

Round 1

Reviewer 1 Report

I would like to make just one minor comment. The results shown on Fig. 3C have not been explained in the text. It is not clear whether the three cell lines were exposed to ionising radiation before LY2874455 treatment or the graph shows the effects of this drug on non-irradiated cells. This should be clarified.

Author Response

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Author Response File: Author Response.pdf

Reviewer 2 Report

This is an interesting study of carbon ion radiotherapy and suggesting that FGFR signaling is a target to understand resistance to carbon ion radiotherapy.

The central issue in the paper is why there is resistance. The increased RBE of carbon ion should result in a perfect situation for appropriate treatment planning, and prevent local recurrence. The issue with carbon ion radiotherapy as is the case with proton radiotherapy is the normal tissue tolerance. The authors should focus on normal tissue effects of carbon ion, rather than on cancer recurrence, which could be obviated by giving higher doses of irradiation.

The methodology is related to looking for genes possibly related to local recurrence. The studies should end with cell lines in culture and on Figure 4, the authors study A549, H1299, and H1703, which are cell lines. Studies with fresh tissue from patient biopsy specimens comparing pre-treatment and in-field recurrence would be appropriate for this study. In the absence of such data, the studies are theoretical and should be referred to as a potential therapeutic mechanism.

Author Response

Please see the attachment

Author Response File: Author Response.pdf

Round 2

Reviewer 2 Report

Accept as is.

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