TY - JOUR
T1 - Mutational analysis of uterine cervical cancer that survived multiple rounds of radiotherapy
AU - Nuryadi, Endang
AU - Sasaki, Yasushi
AU - Hagiwara, Yoshihiko
AU - Permata, Tiara Bunga Mayang
AU - Sato, Hiro
AU - Komatsu, Shuichiro
AU - Yoshimoto, Yuya
AU - Murata, Kazutoshi
AU - Ando, Ken
AU - Kubo, Nobuteru
AU - Okonogi, Noriyuki
AU - Takakusagi, Yosuke
AU - Adachi, Akiko
AU - Iwanaga, Mototaro
AU - Tsuchida, Keisuke
AU - Tamaki, Tomoaki
AU - Noda, Shin Ei
AU - Hirota, Yuka
AU - Shibata, Atsushi
AU - Ohno, Tatsuya
AU - Tokino, Takashi
AU - Oike, Takahiro
AU - Nakano, Takashi
N1 - Funding Information:
This work was supported by Grants-in-Aid from the Ministry of Education, Culture, Sports, Science, and Technology of Japan (programs for Leading Graduate Schools, Cultivating Global Leaders in Heavy Ion Therapeutics and Engineering). This work was also supported by Grants-in-Aid from the Japan Society for the Promotion of Science for KAKENHI, Grant Number 16H06279.
Publisher Copyright:
© Nuryadi et al.
PY - 2018/8/24
Y1 - 2018/8/24
N2 - Radiotherapy is an essential component of cancer therapy. Despite advances in cancer genomics, the mutation signatures of radioresistant tumors have not yet been fully elucidated. To address this issue, we analyzed a unique set of clinical specimens from a uterine cervical cancer that repeatedly locally recurred after multiple rounds of radiotherapy. Exon sequencing of 409 cancer-related genes in the treatment-naïve tumor and the tumors that recurred after initial and secondary radiotherapy identified (i) activating mutations in PIK3CA and KRAS, and putative inactivating mutations in SMAD4, as trunk mutation signatures that persisted over the clinical course; and (ii) mutations in KMT2A, TET1, and NLRP1 as acquired mutation signatures observed only in recurrent tumors after radiotherapy. Comprehensive mining of published in vitro genomics data pertaining to radiosensitivity revealed that simultaneous mutations in KRAS and SMAD4, which have not been described previously in uterine cervical cancer, are associated with cancer cell radioresistance. The association between this mutation signature and radioresistance was validated by isogenic cell-based experiments. These results provide proof-of-principle for the analytical pipeline employed in this study, which explores clinically relevant mutation signatures for radioresistance, and demonstrate that this approach is worth pursuing with larger cohorts in the future.
AB - Radiotherapy is an essential component of cancer therapy. Despite advances in cancer genomics, the mutation signatures of radioresistant tumors have not yet been fully elucidated. To address this issue, we analyzed a unique set of clinical specimens from a uterine cervical cancer that repeatedly locally recurred after multiple rounds of radiotherapy. Exon sequencing of 409 cancer-related genes in the treatment-naïve tumor and the tumors that recurred after initial and secondary radiotherapy identified (i) activating mutations in PIK3CA and KRAS, and putative inactivating mutations in SMAD4, as trunk mutation signatures that persisted over the clinical course; and (ii) mutations in KMT2A, TET1, and NLRP1 as acquired mutation signatures observed only in recurrent tumors after radiotherapy. Comprehensive mining of published in vitro genomics data pertaining to radiosensitivity revealed that simultaneous mutations in KRAS and SMAD4, which have not been described previously in uterine cervical cancer, are associated with cancer cell radioresistance. The association between this mutation signature and radioresistance was validated by isogenic cell-based experiments. These results provide proof-of-principle for the analytical pipeline employed in this study, which explores clinically relevant mutation signatures for radioresistance, and demonstrate that this approach is worth pursuing with larger cohorts in the future.
KW - KRAS
KW - Next-generation sequencing
KW - Radioresistance
KW - SMAD4
KW - Uterine cervical cancer
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U2 - 10.18632/oncotarget.25982
DO - 10.18632/oncotarget.25982
M3 - Article
C2 - 30220971
AN - SCOPUS:85052115417
SN - 1949-2553
VL - 9
SP - 32642
EP - 32652
JO - Oncotarget
JF - Oncotarget
IS - 66
ER -