Zobrazeno 1 - 10
of 28
pro vyhledávání: '"Chihiro Ando"'
Autor:
Kazuya Nishii, Kadoaki Ohashi, Shuta Tomida, Takamasa Nakasuka, Atsuko Hirabae, Sachi Okawa, Jun Nishimura, Hisao Higo, Hiromi Watanabe, Hirohisa Kano, Chihiro Ando, Go Makimoto, Kiichiro Ninomiya, Yuka Kato, Toshio Kubo, Eiki Ichihara, Katsuyuki Hotta, Masahiro Tabata, Shinichi Toyooka, Heiichiro Udono, Yoshinobu Maeda, Katsuyuki Kiura
Publikováno v:
Cancer Immunology Research. 10:1111-1126
Epidermal growth factor receptor (EGFR) is the most frequently mutated driver oncogene in nonsmoking-related, non–small cell lung cancer (NSCLC). EGFR-mutant NSCLC has a noninflamed tumor microenvironment (TME), with low infiltration by CD8+ T cell
Autor:
Katsuyuki Kiura, Yoshinobu Maeda, Heiichiro Udono, Shinichi Toyooka, Masahiro Tabata, Katsuyuki Hotta, Eiki Ichihara, Toshio Kubo, Yuka Kato, Kiichiro Ninomiya, Go Makimoto, Chihiro Ando, Hirohisa Kano, Hiromi Watanabe, Hisao Higo, Jun Nishimura, Sachi Okawa, Atsuko Hirabae, Takamasa Nakasuka, Shuta Tomida, Kadoaki Ohashi, Kazuya Nishii
Supplementary Figure from CD8+ T-cell Responses Are Boosted by Dual PD-1/VEGFR2 Blockade after EGFR Inhibition in Egfr-Mutant Lung Cancer
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::2334d452502440a0d62f9426fd9125e4
https://doi.org/10.1158/2326-6066.22545329.v1
https://doi.org/10.1158/2326-6066.22545329.v1
Autor:
Katsuyuki Kiura, Yoshinobu Maeda, Heiichiro Udono, Shinichi Toyooka, Masahiro Tabata, Katsuyuki Hotta, Eiki Ichihara, Toshio Kubo, Yuka Kato, Kiichiro Ninomiya, Go Makimoto, Chihiro Ando, Hirohisa Kano, Hiromi Watanabe, Hisao Higo, Jun Nishimura, Sachi Okawa, Atsuko Hirabae, Takamasa Nakasuka, Shuta Tomida, Kadoaki Ohashi, Kazuya Nishii
Epidermal growth factor receptor (EGFR) is the most frequently mutated driver oncogene in nonsmoking-related, non–small cell lung cancer (NSCLC). EGFR-mutant NSCLC has a noninflamed tumor microenvironment (TME), with low infiltration by CD8+ T cell
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::2545f28bebbe52ae229d98e350c440b3
https://doi.org/10.1158/2326-6066.c.6550913
https://doi.org/10.1158/2326-6066.c.6550913
Autor:
Katsuyuki Kiura, Yoshinobu Maeda, Masahiro Tabata, Katsuyuki Hotta, Kadoaki Ohashi, Kammei Rai, Toshio Kubo, Yuka Kato, Kiichiro Ninomiya, Takamasa Nakasuka, Chihiro Ando, Kazuya Nishii, Hiromi Watanabe, Eiki Ichihara, Hirohisa Kano
Supplementary Figure 6. Body weight changes in a xenograft mouse model. Of the mice bearing H3122 tumors, those in the vehicle and SHP099 groups were euthanized on days 14 and 21 respectively, as they had reached the humanitarian endpoint due to tumo
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::12603e752a26ffae7f7705be3030f5c7
https://doi.org/10.1158/1535-7163.22522915.v1
https://doi.org/10.1158/1535-7163.22522915.v1
Autor:
Katsuyuki Kiura, Yoshinobu Maeda, Masahiro Tabata, Katsuyuki Hotta, Kadoaki Ohashi, Kammei Rai, Toshio Kubo, Yuka Kato, Kiichiro Ninomiya, Takamasa Nakasuka, Chihiro Ando, Kazuya Nishii, Hiromi Watanabe, Eiki Ichihara, Hirohisa Kano
Supplementary Figure 2. ROS1 TKI in combination with SHP099 (A) Immunoblots of the indicated proteins in HCC78 and ABC-20 cells treated for 24 h with DS-6051b (Ds, 100 nM) with or without SHP099 (SHP, 5 µM). Comb, combination. (B) RAS-GTP assay in H
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::158aec9b14ac8d37722555a44c6c7d80
https://doi.org/10.1158/1535-7163.22522927.v1
https://doi.org/10.1158/1535-7163.22522927.v1
Autor:
Katsuyuki Kiura, Yoshinobu Maeda, Masahiro Tabata, Katsuyuki Hotta, Kadoaki Ohashi, Kammei Rai, Toshio Kubo, Yuka Kato, Kiichiro Ninomiya, Takamasa Nakasuka, Chihiro Ando, Kazuya Nishii, Hiromi Watanabe, Eiki Ichihara, Hirohisa Kano
Supplementary Figure 1. phospho-RTK array in PC-9 cells phospho-RTK array in PC-9 cells treated with 100 nM of the EGFR TKI erlotinib for up to 96 h. Multiple RTKs were gradually activated over time.
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::2a182931610fc833ea5bed5d3df9468a
https://doi.org/10.1158/1535-7163.22522930
https://doi.org/10.1158/1535-7163.22522930
Autor:
Katsuyuki Kiura, Yoshinobu Maeda, Masahiro Tabata, Katsuyuki Hotta, Kadoaki Ohashi, Kammei Rai, Toshio Kubo, Yuka Kato, Kiichiro Ninomiya, Takamasa Nakasuka, Chihiro Ando, Kazuya Nishii, Hiromi Watanabe, Eiki Ichihara, Hirohisa Kano
After molecular-targeted therapy, some cancer cells may remain that are resistant to therapies targeting oncogene alterations, such as those in the genes encoding the EGFR and anaplastic lymphoma kinase (ALK) as well as c-ros oncogene 1 (ROS1). The m
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::358fb0eb8c9db74ac20506606b035d89
https://doi.org/10.1158/1535-7163.c.6543526
https://doi.org/10.1158/1535-7163.c.6543526
Autor:
Katsuyuki Kiura, Yoshinobu Maeda, Masahiro Tabata, Katsuyuki Hotta, Kadoaki Ohashi, Kammei Rai, Toshio Kubo, Yuka Kato, Kiichiro Ninomiya, Takamasa Nakasuka, Chihiro Ando, Kazuya Nishii, Hiromi Watanabe, Eiki Ichihara, Hirohisa Kano
Supplementary Figure 7. SHP2 compared to selumetinib in a xenograft mouse model. (A) Immunoblots of the PC-9 xenograft tumors treated with the indicated agents for 7 days. (B) Body weight changes after combination therapy with osimertinib and SHP099
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::4d8a4b04610d70855df0b34cb190f233
https://doi.org/10.1158/1535-7163.22522912
https://doi.org/10.1158/1535-7163.22522912
Autor:
Katsuyuki Kiura, Yoshinobu Maeda, Masahiro Tabata, Katsuyuki Hotta, Kadoaki Ohashi, Kammei Rai, Toshio Kubo, Yuka Kato, Kiichiro Ninomiya, Takamasa Nakasuka, Chihiro Ando, Kazuya Nishii, Hiromi Watanabe, Eiki Ichihara, Hirohisa Kano
Supplementary Figure 5. Combined use of RMC4550 with alectinib, crizotinib or osimertinib Immunoblots of the indicated proteins in H3122 and ABC-19 cells treated with alectinib (Alec, 100 nM), HCC78 and ABC-20 cells treated with crizotinib (Cri, 1 µ
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::303e2de6f7cd76455fbf75cb0c01bbf5
https://doi.org/10.1158/1535-7163.22522918
https://doi.org/10.1158/1535-7163.22522918
Autor:
Takamasa Nakasuka, Hirohisa Kano, Chihiro Ando, Yoshinobu Maeda, Katsuyuki Hotta, Kammei Rai, Kadoaki Ohashi, Kazuya Nishii, Eiki Ichihara, Kiichiro Ninomiya, Hiromi Watanabe, Masahiro Tabata, Toshio Kubo, Katsuyuki Kiura, Yuka Kato
Publikováno v:
Molecular Cancer Therapeutics. 20:1653-1662
After molecular-targeted therapy, some cancer cells may remain that are resistant to therapies targeting oncogene alterations, such as those in the genes encoding the EGFR and anaplastic lymphoma kinase (ALK) as well as c-ros oncogene 1 (ROS1). The m