@article{TEXTUAL,
      recid = {9827},
      author = {Asada, Hajime and Tani, Akiyoshi and Sakuma, Hiroki and  Hirabayashi, Miyuki and Matsumoto, Yuki and Watanabe, Kei  and Tsuboi, Masaya and Yoshida, Shino and Harada, Kei and  Uchikai, Takao and Goto-Koshino, Yuko  and Chambers, James  K. and Ishihara, Genki and Kobayashi, Tetsuya and Irie,  Mitsuhiro and Uchida, Kazuyuki and Ohno, Koichi and  Bonkobara, Makoto and Tsujimoto, Hajime and Tomiyasu,  Hirotaka},
      title = {Whole exome and transcriptome analysis revealed the  activation of ERK and Akt signaling pathway in canine  histiocytic sarcoma},
      journal = {Scientific Reports},
      address = {2023-05-25},
      number = {TEXTUAL},
      abstract = {Histiocytic sarcoma (HS) is an incurable aggressive tumor,  and no consensus has been made on the treatment due to its  rare occurrence. Since dogs spontaneously develop the  disease and several cell lines are available, they have  been advocated as translational animal models. In the  present study, therefore, we explored gene mutations and  aberrant molecular pathways in canine HS by next generation  sequencing to identify molecular targets for treatment.  Whole exome sequencing and RNA-sequencing revealed gene  mutations related to receptor tyrosine kinase pathways and  activation of ERK1/2, PI3K-AKT, and STAT3 pathways.  Analysis by quantitative PCR and immunohistochemistry  revealed that fibroblast growth factor receptor 1 (FGFR1)  is over-expressed. Moreover, activation of ERK and Akt  signaling were confirmed in all HS cell lines, and FGFR1  inhibitors showed dose-dependent growth inhibitory effects  in two of the twelve canine HS cell lines. The findings  obtained in the present study indicated that ERK and Akt  signaling were activated in canine HS and drugs targeting  FGFR1 might be effective in part of the cases. The present  study provides translational evidence that leads to  establishment of novel therapeutic strategies targeting ERK  and Akt signaling in HS patients.},
      url = {http://knowledge.uchicago.edu/record/9827},
}