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1. Modified FOLFOXIRI plus cetuximab versus bevacizumab in RAS wild-type metastatic colorectal cancer: a randomized phase II DEEPER trial

Author

Shiozawa, Manabu, Sunakawa, Yu, Watanabe, Takanori, Ota, Hirofumi, Yasui, Hisateru, Yabuno, Taichi, Tei, Mitsuyoshi, Kochi, Mitsugu, Manaka, Dai, Ohori, Hisatsugu, Yamaguchi, Tatsuro, Sagawa, Tamotsu, Kotaka, Masahito, Kubota, Yutaro, Sekikawa, Takashi, Nakamura, Masato, Takeuchi, Masahiro, Ichikawa, Wataru, Fujii, Masashi, and Tsuji, Akihito

Published
2024
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2. MYC acetylated lysine residues drive oncogenic cell transformation and regulate select genetic programs for cell adhesion-independent growth and survival

Author

Hurd, Matthew, Pino, Jeffrey, Jang, Kay, Allevato, Michael M, Vorontchikhina, Marina, Ichikawa, Wataru, Zhao, Yifan, Gates, Ryan, Villalpando, Emily, Hamilton, Michael J, Faiola, Francesco, Pan, Songqin, Qi, Yue, Hung, Yu-Wen, Girke, Thomas, Ann, David, Seewaldt, Victoria, and Martinez, Ernest

Subjects
Biochemistry and Cell Biology, Biological Sciences, Cancer, Genetics, Aetiology, 2.1 Biological and endogenous factors, Animals, Humans, Mice, Acetylation, Cell Adhesion, Cell Proliferation, Cell Transformation, Neoplastic, Histone Acetyltransferases, Lysine, MYC oncoprotein, lysine acetylation, malignant transformation, Medical and Health Sciences, Psychology and Cognitive Sciences, Developmental Biology, Biological sciences, Biomedical and clinical sciences, Psychology
Abstract

The MYC oncogenic transcription factor is acetylated by the p300 and GCN5 histone acetyltransferases. The significance of MYC acetylation and the functions of specific acetylated lysine (AcK) residues have remained unclear. Here, we show that the major p300-acetylated K148(149) and K157(158) sites in human (or mouse) MYC and the main GCN5-acetylated K323 residue are reversibly acetylated in various malignant and nonmalignant cells. Oncogenic overexpression of MYC enhances its acetylation and alters the regulation of site-specific acetylation by proteasome and deacetylase inhibitors. Acetylation of MYC at different K residues differentially affects its stability in a cell type-dependent manner. Lysine-to-arginine substitutions indicate that although none of the AcK residues is required for MYC stimulation of adherent cell proliferation, individual AcK sites have gene-specific functions controlling select MYC-regulated processes in cell adhesion, contact inhibition, apoptosis, and/or metabolism and are required for the malignant cell transformation activity of MYC. Each AcK site is required for anchorage-independent growth of MYC-overexpressing cells in vitro, and both the AcK148(149) and AcK157(158) residues are also important for the tumorigenic activity of MYC transformed cells in vivo. The MYC AcK site-specific signaling pathways identified may offer new avenues for selective therapeutic targeting of MYC oncogenic activities.

Published
2023

5. Three-year outcomes of a randomized phase III trial comparing adjuvant chemotherapy with S-1 plus docetaxel versus S-1 alone in stage III gastric cancer: JACCRO GC-07

Author

Kakeji, Yoshihiro, Yoshida, Kazuhiro, Kodera, Yasuhiro, Kochi, Mitsugu, Sano, Takeshi, Ichikawa, Wataru, Lee, Sang-Woong, Shibahara, Kazushige, Shikano, Toshio, Kataoka, Masato, Ishiguro, Atsushi, Ojima, Hitoshi, Sakai, Yoshinori, Musha, Nobuyuki, Takase, Tsunenobu, Kimura, Taisei, Takeuchi, Masahiro, and Fujii, Masashi

Published
2022
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6. Real-world effectiveness of nivolumab in advanced gastric cancer: the DELIVER trial (JACCRO GC-08)

Author

Takahashi, Yoshikazu, Sunakawa, Yu, Inoue, Eisuke, Kawabata, Ryohei, Ishiguro, Atsushi, Kito, Yosuke, Akamaru, Yusuke, Takahashi, Masazumi, Yabusaki, Hiroshi, Matsuyama, Jin, Makiyama, Akitaka, Tsuda, Masahiro, Suzuki, Takahisa, Yasui, Hisateru, Matoba, Ryo, Kawakami, Hisato, Nakajima, Takako Eguchi, Muro, Kei, Ichikawa, Wataru, and Fujii, Masashi

Published
2022
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8. Tumor Response Predicts Survival Time of Nivolumab Monotherapy for Advanced Gastric Cancer: A Subgroup Analysis of the DELIVER Trial (JACCRO GC-08).

Author

Sunakawa, Yu, Sakamoto, Yasuhiro, Kawabata, Ryohei, Ishiguro, Atsushi, Akamaru, Yusuke, Kito, Yosuke, Takahashi, Masazumi, Matsuyama, Jin, Yabusaki, Hiroshi, Makiyama, Akitaka, Suzuki, Takahisa, Tsuda, Masahiro, Yasui, Hisateru, Hihara, Jun, Takeno, Atsushi, Inoue, Eisuke, Ichikawa, Wataru, and Fujii, Masashi

Subjects
STOMACH tumors, DATA analysis, RESEARCH funding, SCIENTIFIC observation, DESCRIPTIVE statistics, LONGITUDINAL method, STATISTICS, NIVOLUMAB, PROGRESSION-free survival, CONFIDENCE intervals, OVERALL survival
Abstract

Background This prospective observational study evaluated the real-world effectiveness of nivolumab monotherapy in previously treated advanced gastric cancer (GC). A preplanned 2-year final analysis was performed to confirm survival and tumor behavior with nivolumab monotherapy. Patients and Methods The primary endpoint was overall survival (OS). The data regarding tumor size were prospectively collected and evaluated using the RECIST criteria. Exploratory analyses were performed for survival according to the tumor response and depth of response (DpR) in patients with measurable lesions who were receiving nivolumab monotherapy as third- or later-line therapy. Results In 487 patients, the median OS and progression-free survival (PFS) were 5.8 (95% CI 5.3-6.9) months and 1.8 (95% CI 1.7-2.0) months, respectively. The response rate (RR) was 14.5% in 282 patients with measurable lesions. In 234 patients treated with third- or later-line, the DpR was found to be associated with PFS and OS in the Spearman analysis (r  = 0.55 and 0.44, respectively) as well as using a discrete variable. When the DpR was divided into 5 groups (−20%≥DpR; −20%

Published
2024
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9. Phase 2 study of irinotecan plus cetuximab rechallenge as third-line treatment in KRAS wild-type metastatic colorectal cancer: JACCRO CC-08

Author

Masuishi, Toshiki, Tsuji, Akihito, Kotaka, Masahito, Nakamura, Masato, Kochi, Mitsugu, Takagane, Akinori, Shimada, Ken, Denda, Tadamichi, Segawa, Yoshihiko, Tanioka, Hiroaki, Hara, Hiroki, Sagawa, Tamotsu, Watanabe, Takanori, Takahashi, Takao, Negoro, Yuji, Manaka, Dai, Fujita, Hideto, Suto, Takeshi, Takeuchi, Masahiro, Ichikawa, Wataru, and Fujii, Masashi

Published
2020
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10. MYC interacts with the human STAGA coactivator complex via multivalent contacts with the GCN5 and TRRAP subunits

Author

Zhang, Na, Ichikawa, Wataru, Faiola, Francesco, Lo, Szu-Ying, Liu, Xiaohui, and Martinez, Ernest

Subjects
Biochemistry and Cell Biology, Biological Sciences, Genetics, Underpinning research, 2.1 Biological and endogenous factors, Aetiology, 1.1 Normal biological development and functioning, Generic health relevance, Cancer, Acetyltransferases, Adaptor Proteins, Signal Transducing, Amino Acid Sequence, Cell Line, Cell Line, Tumor, Chromatin, DNA-Binding Proteins, HEK293 Cells, HeLa Cells, Humans, Molecular Sequence Data, Nuclear Proteins, Promoter Regions, Genetic, Protein Binding, Protein Structure, Tertiary, Protein Subunits, Proto-Oncogene Proteins c-myc, TATA-Binding Protein Associated Factors, Trans-Activators, Transcription Factor TFIID, Transcription Factors, Transcriptional Activation, p300-CBP Transcription Factors, Coactivator, Histone acetyltransferase complex, MYC oncoprotein, Protein-protein interaction, Transcription, Hela Cells, Protein–protein interaction, Physical Sciences, Biological sciences, Physical sciences
Abstract

MYC is an oncogenic DNA-binding transcription activator of many genes and is often upregulated in human cancers. MYC has an N-terminal transcription activation domain (TAD) that is also required for cell transformation. Various MYC TAD-interacting coactivators have been identified, including the transcription/transformation-associated protein (TRRAP), a subunit of different histone acetyltransferase (HAT) complexes such as the human "SPT3-TAF9-GCN5 Acetyltransferase" (STAGA) complex involved in MYC transactivation of the TERT gene. However, it remains unclear whether TRRAP and/or other subunits are directly contacted by MYC within these macromolecular complexes. Here, we characterize the interactions of MYC TAD with the STAGA complex. By protein crosslinking we identify both TRRAP and the GCN5 acetyltransferase as MYC TAD-interacting subunits within native STAGA. We show that purified GCN5 binds to an N-terminal sub-domain of MYC TAD (residues 21-108) and that the interaction of GCN5 and STAGA with this sub-domain is dependent on two related sequence motifs: M2 within the conserved MYC homology box I (MBI), and M3 located between residues 100-106. Interestingly, specific substitutions within the M2/3 motifs that only moderately reduce the intracellular MYC-STAGA interaction and do not influence dimerization of MYC with its DNA-binding partner MAX, strongly inhibit MYC acetylation by GCN5 and reduce MYC binding and transactivation of the GCN5-dependent TERT promoter in vivo. Hence, we propose that MYC associates with STAGA through extended interactions of the TAD with both TRRAP and GCN5 and that the TAD-GCN5 interaction is important for MYC acetylation and MYC binding to certain chromatin loci.

Published
2014

11. Correlation of multiple endpoints in the first‐line chemotherapy of advanced gastric cancer: Pooled analysis of individual patient data from Japanese Phase III trials

Author

Arai, Hiroyuki, primary, Takeuchi, Madoka, additional, Ichikawa, Wataru, additional, Shitara, Kohei, additional, Sunakawa, Yu, additional, Oba, Koji, additional, Koizumi, Wasaburo, additional, Sakata, Yuh, additional, Furukawa, Hiroshi, additional, Yamada, Yasuhide, additional, Takeuchi, Masahiro, additional, and Fujii, Masashi, additional

Published
2023
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12. MO18-4 RAS status in ctDNA and efficacy of FOLFIRI plus ramucirumab in 2nd-line therapy for RAS wild-type mCRC: JACCRO CC-16AR

Author

Sunakawa, Yu, primary, Yasui, Hisateru, additional, Matsuura, Masato, additional, Mine, Takashi, additional, Yuasa, Yasuhiro, additional, Watanabe, Takanori, additional, Kinjo, Tatsuya, additional, Okita, Yoshihiro, additional, Okuyama, Hiroyuki, additional, Yuki, Satoshi, additional, Miyakawa, Koki, additional, Kobara, Ayana, additional, Ichikawa, Wataru, additional, Fujii, Masashi, additional, and Tsuji, Akihito, additional

Published
2023
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13. O4-3 An update analysis of the JACCRO CC-16: Ramucirumab plus FOLFIRI for RAS wild-type mCRC refractory to anti-EGFR antibody

Author

Manaka, Dai, primary, Tsuji, Akihito, additional, Shibutani, Masatsune, additional, Ishibashi, Keiichiro, additional, Yabuno, Taichi, additional, Okamura, Shu, additional, Furuya, Takumi, additional, Tanaka, Chihiro, additional, Nakamura, Masato, additional, Sagawa, Tamotsu, additional, Watanabe, Takanori, additional, Shiozawa, Manabu, additional, Sunakawa, Yu, additional, Ota, Hirofumi, additional, Kotaka, Masahito, additional, Okuyama, Hiroyuki, additional, Okita, Yoshihiro, additional, Cancer Research Organization, Japan Clinical, additional, Ichikawa, Wataru, additional, and Fujii, Masashi, additional

Published
2023
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14. PS4-3 Survival analysis of m-FOLFOXIRI plus cetuximab vs. bevacizumab in RAS wild-type mCRC: The DEEPER trial (JACCRO CC-13)

Author

Tsuji, Akihito, primary, Endo, Izuru, additional, Kobayashi, Kenji, additional, Miyamoto, Yuji, additional, Kusumoto, Tetsuya, additional, Yuasa, Yasuhiro, additional, Miwa, Keisuke, additional, Kochi, Mitsugu, additional, Sagawa, Tamotsu, additional, Kotaka, Masahito, additional, Kubota, Yutaro, additional, Sunakawa, Yu, additional, Sekikawa, Takashi, additional, Nakamura, Masato, additional, Takeuchi, Masahiro, additional, Ichikawa, Wataru, additional, and Fujii, Masashi, additional

Published
2023
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17. O7-4 Ramucirumab plus FOLFIRI for RAS wild-type mCRC refractory to 1st-line treatment with anti-EGFR antibody: JACCRO CC-16

Author

Sagawa, Tamotsu, primary, Tsuji, Akihito, additional, Satake, Hironaga, additional, Nakamura, Masato, additional, Sunakawa, Yu, additional, Korehisa, Shotaro, additional, Matsuura, Masato, additional, Yuasa, Yasuhiro, additional, Mine, Takashi, additional, Nagano, Hiroaki, additional, Shigeyasu, Kunitoshi, additional, Kinjo, Tatsuya, additional, Kotaka, Masahito, additional, Okuyama, Hiroyuki, additional, Kubota, Yutaro, additional, Kochi, Mitsugu, additional, Masuishi, Toshiki, additional, Takeuchi, Masahiro, additional, Ichikawa, Wataru, additional, and Fujii, Masashi, additional

Published
2022
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18. O7-2 FOLFOXIRI plus cetuximab versus bevacizumab in RAS wild-type mCRC: the subgroup-analysis of DEEPER trial (JACCRO CC-13)

Author

Yabuno, Taichi, primary, Tsuji, Akihito, additional, Tokunaga, Takuya, additional, Yuki, Satoshi, additional, Kudo, Toshihiro, additional, Mashita, Naoki, additional, Ando, Koji, additional, Takeuchi, Nobumichi, additional, Kashiwada, Tomomi, additional, Kataoka, Masato, additional, Kochi, Mitsugu, additional, Sagawa, Tamotsu, additional, Kotaka, Masahito, additional, Kubota, Yutaro, additional, Sunakawa, Yu, additional, Sekikawa, Takashi, additional, Nakamura, Masato, additional, Takeuchi, Masahiro, additional, Ichikawa, Wataru, additional, and Fujii, Masashi, additional

Published
2022
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20. The BEETS (JACCRO CC-18) trial: an observational and translational study of BRAF-mutated metastatic colorectal cancer.

Author

Inagaki, Chiaki, Matoba, Ryo, Yuki, Satoshi, Shiozawa, Manabu, Tsuji, Akihito, Inoue, Eisuke, Muro, Kei, Ichikawa, Wataru, Fujii, Masashi, and Sunakawa, Yu

Abstract

For BRAF V600E-mutated metastatic colorectal cancer (mCRC), the BEACON phase 3 trial showed survival benefit of triplet therapy with cetuximab (anti-EGFR antibody), encorafenib (BRAF inhibitor) and binimetinib (MEK inhibitor) as well as doublet therapy with cetuximab and encorafenib over irinotecan-based chemotherapy plus anti-EGFR antibody. Both regimens are standards of care in Japan, but definite biomarkers for predicting efficacy and selecting treatment remain lacking. The mechanisms underlying resistance to these regimens also warrant urgent exploration to further evolve treatment. This prospective observational/translational study evaluated real-word clinical outcomes with cetuximab and encorafenib with or without binimetinib for BRAF-mutated mCRC patients and investigated biomarkers for response and resistance by collecting blood samples before and after treatment. Clinical Trial Registration:UMIN000045530 (https://center6.umin.ac.jp/cgi-open-bin/ctr_e/ctr_view.cgi?recptno=R000051983) The BEETS trial is a study that looks at how well two combinations of targeted therapies (cetuximab + encorafenib with or without binimetinib) work and how safe they are for patients with advanced colorectal cancer that has a mutation (change) in the BRAF gene. In this trial, patients participate voluntarily instead of being assigned to one of the two therapy groups. When a patient has BRAF-mutated advanced colorectal cancer, it means that the cancer cells in their body have changes in a gene called BRAF. This gene normally produces a protein called BRAF, which is involved in the growth of cells. However, when there is a mutation in this gene, it can cause the production of an overactive BRAF protein, leading to fast and excessive cell growth and division. For patients with BRAF-mutated advanced colorectal cancer, combinations of targeted therapies have been found to be effective as a second- or third-line treatment, based on the results of a phase 3 clinical trial. The main goal of the BEETS trial is to evaluate how well these treatments work and how safe they are when used in real-world clinical practice. Additionally, the study will use laboratory tests (liquid biopsy) to explore new biomarkers that can help predict how well a treatment will work and assist in selecting the most suitable treatment plans. We hope that the findings of this study will contribute to improving the overall management of this specific type of cancer. The protocol paper of the BEETS (JACCRO CC-18) trial, a prospective observational/translational study of BEACON regimens for BRAF-mutated mCRC, is now available in Future Oncology. [ABSTRACT FROM AUTHOR]

Published
2023
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22. Abstract 5957: Molecular characteristics of gut microbiota in patients with gastric cancer: The DELIVER trial (JACCRO GC-08)

Author

Matoba, Ryo, primary, Iijima, Hiroshi, additional, Sakamoto, Yasuhiro, additional, Kawabata, Ryohei, additional, Ishiguro, Atsushi, additional, Akamaru, Yusuke, additional, Kito, Yosuke, additional, Yabusaki, Hiroshi, additional, Matsuyama, Jin, additional, Takahashi, Masazumi, additional, Makiyama, Akitaka, additional, Suzuki, Takahisa, additional, Tsuda, Masahiro, additional, Yasui, Hisateru, additional, Hihara, Jun, additional, Masuzawa, Toru, additional, Okuda, Hiroyuki, additional, Kawada, Junji, additional, Suzuki, Shuhei, additional, Kawakami, Hisato, additional, Nakajima, Takako Eguchi, additional, Muro, Kei, additional, Ichikawa, Wataru, additional, Fujii, Masashi, additional, and Sunakawa, Yu, additional

Published
2022
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26. Real-world effectiveness of nivolumab in advanced gastric cancer: the DELIVER trial (JACCRO GC-08)

Author

Takahashi, Yoshikazu, primary, Sunakawa, Yu, additional, Inoue, Eisuke, additional, Kawabata, Ryohei, additional, Ishiguro, Atsushi, additional, Kito, Yosuke, additional, Akamaru, Yusuke, additional, Takahashi, Masazumi, additional, Yabusaki, Hiroshi, additional, Matsuyama, Jin, additional, Makiyama, Akitaka, additional, Tsuda, Masahiro, additional, Suzuki, Takahisa, additional, Yasui, Hisateru, additional, Matoba, Ryo, additional, Kawakami, Hisato, additional, Nakajima, Takako Eguchi, additional, Muro, Kei, additional, Ichikawa, Wataru, additional, and Fujii, Masashi, additional

Published
2021
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27. Three-year outcomes of a randomized phase III trial comparing adjuvant chemotherapy with S-1 plus docetaxel versus S-1 alone in stage III gastric cancer: JACCRO GC-07

Author

Kakeji, Yoshihiro, primary, Yoshida, Kazuhiro, additional, Kodera, Yasuhiro, additional, Kochi, Mitsugu, additional, Sano, Takeshi, additional, Ichikawa, Wataru, additional, Lee, Sang-Woong, additional, Shibahara, Kazushige, additional, Shikano, Toshio, additional, Kataoka, Masato, additional, Ishiguro, Atsushi, additional, Ojima, Hitoshi, additional, Sakai, Yoshinori, additional, Musha, Nobuyuki, additional, Takase, Tsunenobu, additional, Kimura, Taisei, additional, Takeuchi, Masahiro, additional, and Fujii, Masashi, additional

Published
2021
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28. O1-4 Survival time of nivolumab treatment in advanced gastric cancer from real-world data of the DELIVER trial (JACCRO GC-08)

Author

Ishiguro, Atsushi, primary, Inoue, Eisuke, additional, Sakamoto, Yasuhiro, additional, Kawabata, Ryohei, additional, Akamaru, Yusuke, additional, Kito, Yosuke, additional, Takahashi, Masazumi, additional, Matsuyama, Jin, additional, Yabusaki, Hiroshi, additional, Makiyama, Akitaka, additional, Suzuki, Takahisa, additional, Tsuda, Masahiro, additional, Yasui, Hisateru, additional, Kawakami, Hisato, additional, Matoba, Ryo, additional, Muro, Kei, additional, Nakajima, Takako Eguchi, additional, Ichikawa, Wataru, additional, Fujii, Masashi, additional, and Sunakawa, Yu, additional

Published
2021
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32. Characterization of Physical and Functional Interactions Between the MYC Oncoprotein and the Acetyltransferase GCN5

Author

Ichikawa, Wataru

Subjects
Biochemistry, Molecular biology
Abstract

MYC is a transcription factor that is overexpressed in a wide range of human cancers, and MYC is known to play a role in many important biological processes such as cell death and cell proliferation. Heterodimerizing with the obligatory partner protein, MAX, the MYC and MAX dimer binds a specific DNA sequence, called an E box (CACGTG), through its basic helix-loop-helix zipper domain. MYC N-terminal transcription activation domain (TAD) has been shown to interact with proteins that are potential regulators of MYC transactivation and transformation activities. Among them, the TRRAP protein has been shown to contribute to the transformation activity of MYC through associations with the MYC box (MB) II and MBI-containing sequences. Importantly, TRRAP is also a subunit of several multiprotein complexes that possess histone acetyltransferase (HAT) activity, such as the STAGA (SPT-TAF-GCN5 Acetylase) coactivator complex. GCN5, another subunit of STAGA, is a HAT that acetylates lysine residues in histone H3 and non-histone proteins. MYC has been also identified as a target of GCN5, although the functional consequences of MYC acetylation by GCN5 remain to be investigated. In this work, we identify MYC K323 as the major site of acetylation by GCN5 and then demonstrate that GCN5 stabilizes MYC in a K323- and HAT domain-dependent manner. Interestingly, we also find that GCN5 enhances MYC ubiquitination in a HAT domain/activity-independent manner. Subsequently, we investigate which subunits of the STAGA complex directly interact with MYC, and then analyze the role of the MYC-STAGA interactions in the biological functions of MYC. We identify GCN5 as another STAGA subunit that directly associates with MYC. The direct interaction of MYC with GCN5 facilitates the interaction of MYC with the STAGA complex, acetylation of MYC, binding of MYC to the human TERT promoter, and activation of human TERT transcription. Lastly, we unexpectedly find a physical interaction between MYC and the tumor suppressor p53 that has not been reported previously, despite decades of intense research investigation on their functions. Based on our preliminary results, we suggest a prospective model in which MYC and p53 influence each other`s transcription regulatory activities via a direct physical interaction. These results further deepen our understanding of MYC biological functions and its role in cancer, and could eventually lead to the development of new therapeutic targets against cancer.

Published
2012

34. CYP2A6 and the plasma level of 5-chloro-2, 4-dihydroxypyridine are determinants of the pharmacokinetic variability of tegafur and 5-fluorouracil, respectively, in Japanese patients with cancer given S-1

Author

Fujita, Ken-ichi, Yamamoto, Wataru, Endo, Shoji, Endo, Hisashi, Nagashima, Fumio, Ichikawa, Wataru, Tanaka, Ryuhei, Miya, Toshimichi, Araki, Kazuhiro, Kodama, Keiji, Sunakawa, Yu, Narabayashi, Masaru, Miwa, Keisuke, Ando, Yuichi, Akiyama, Yuko, Kawara, Kaori, Kamataki, Tetsuya, and Sasaki, Yasutsuna

Published
2008

36. 18F-FDG-PET/CT as an imaging biomarker for regorafenib efficacy in metastatic colorectal cancer (JACCRO CC-12).

Author

Nakamura, Masato, Satake, Hironaga, Sagawa, Tamotsu, Takagane, Akinori, Sekikawa, Takashi, Oguchi, Kazuhiro, Kaji, Tomohito, Takeuchi, Masahiro, Ichikawa, Wataru, and Fujii, Masashi

Subjects
COLORECTAL cancer, BIOMARKERS, COMPUTED tomography, METASTASIS, REGORAFENIB, POSITRON emission tomography computed tomography
Abstract

Introduction: Regorafenib is a multikinase inhibitor approved for the treatment of metastatic colorectal cancer (mCRC). Despite providing a statistically significant survival benefit, a substantial number of patients fail to respond to or continue with treatment, which has resulted in an unmet clinical need for a biomarker of regorafenib efficacy. Methods: The JACCRO CC-12 study was a prospective, multicenter, single-arm phase II trial designed to evaluate the usefulness of [18F]fluorodeoxyglucose positron emission tomography (FDG-PET) as an imaging biomarker of regorafenib in patients with mCRC that progressed after standard chemotherapies. FDG-PET and contrast-enhanced computed tomography (CT) were performed before and after treatment with regorafenib 160 mg once daily 3 weeks on/1 week off. The primary end point was the change in the maximum standardized uptake value in the lesion with the highest uptake at pre-treatment FDG-PET. The secondary end points included overall survival (OS), progression-free survival (PFS), the objective response rate (ORR), safety, and the correlation between FDG-PET and CT. Results: Twenty patients were enrolled from November 2014 to March 2016, 17 of whom were evaluated for metabolic and morphological changes. Metabolic response with FDG-PET was partial response (PR) in one case (5.9%), stable disease (SD) in four (23.5%), and progressive disease (PD) in 12 (70.6%). The metabolic response rate was 5.9%. On CT imaging, no complete response or PR was observed, and the ORR was 0%. Median PFS and OS were 1.7 and 9.8 months, respectively. The median PFS of patients who achieved PR or SD by FDG-PET was 3.7 months, whereas that of those assessed as PD was 1 month (p = 0.13). The median OS of patients who achieved PR or SD by FDG-PET was 13.0 months, whereas that of patients assessed as PD was 10.6 months (p = 0.43). Frequent adverse events were palmar–plantar erythrodysesthesia syndrome, hypertension, loss of appetite, and fatigue. Conclusions: In this study, FDG-PET failed to demonstrate usefulness as an early imaging biomarker of regorafenib in patients with mCRC. [ABSTRACT FROM AUTHOR]

Published
2021
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39. Update on JACCRO CC-11 trial of 1st-line modified-FOLFOXIRI plus bevacizumab for RAS mutant metastatic colorectal cancer

Author

Nakamura, Masato, primary, Sunakawa, Yu, additional, Okuyama, Hiroyuki, additional, Matsuura, Masato, additional, Negoro, Yuji, additional, Yabuno, Taichi, additional, Takahashi, Takao, additional, Tamura, Takao, additional, Takeuchi, Nobumichi, additional, Satake, Hironaga, additional, Miyamoto, Yuji, additional, Kataoka, Masato, additional, Shiozawa, Manabu, additional, Makiyama, Akitaka, additional, Kobayashi, Kazuma, additional, Kubota, Yutaro, additional, Sekikawa, Takashi, additional, Takeuchi, Masahiro, additional, Ichikawa, Wataru, additional, and Fujii, Masashi, additional

Published
2019
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40. Update on phase II trial of cetuximab plus S-1/oxaliplatin (SOX) for metastatic colorectal cancer (mCRC): JACCRO CC-06

Author

Sunakawa, Yu, primary, Ichikawa, Wataru, additional, Hagiwara, Ken, additional, Tsuda, Masahiro, additional, Takagane, Akinori, additional, Yasui, Hisateru, additional, Satake, Hironaga, additional, Denda, Tadamichi, additional, Segawa, Yoshihiko, additional, Tanioka, Hiroaki, additional, Kotaka, Masahito, additional, Kochi, Mitsugu, additional, Watanabe, Takanori, additional, Nakamura, Masato, additional, Tsuji, Akihito, additional, Tani, Satoshi, additional, Negoro, Yuji, additional, Tobimatsu, Kazutoshi, additional, Takeuchi, Masahiro, additional, and Fujii, Masashi, additional

Published
2019
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43. Tumor Sidedness and Enriched Gene Groups for Efficacy of First-line Cetuximab Treatment in Metastatic Colorectal Cancer

Author

Sunakawa, Yu, primary, Mogushi, Kaoru, additional, Lenz, Heinz-Josef, additional, Zhang, Wu, additional, Tsuji, Akihito, additional, Takahashi, Takehiro, additional, Denda, Tadamichi, additional, Shimada, Ken, additional, Kochi, Mitsugu, additional, Nakamura, Masato, additional, Kotaka, Masahito, additional, Segawa, Yoshihiko, additional, Tanioka, Hiroaki, additional, Negoro, Yuji, additional, Moran, Miriana, additional, Astrow, Stephanie H., additional, Hsiang, Jack, additional, Stephens, Craig, additional, Fujii, Masashi, additional, and Ichikawa, Wataru, additional

Published
2018
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44. Correction: A phase II trial of 1st-line modified-FOLFOXIRI plus bevacizumab treatment for metastatic colorectal cancer harboring RAS mutation: JACCRO CC-11

Author

Satake, Hironaga, primary, Sunakawa, Yu, additional, Miyamoto, Yuji, additional, Nakamura, Masato, additional, Nakayama, Hiroshi, additional, Shiozawa, Manabu, additional, Makiyama, Akitaka, additional, Kobayashi, Kazuma, additional, Kubota, Yutaro, additional, Mori, Misuzu, additional, Kotaka, Masahito, additional, Takagane, Akinori, additional, Gotoh, Masahiro, additional, Takeuchi, Masahiro, additional, Fujii, Masashi, additional, Ichikawa, Wataru, additional, and Sekikawa, Takashi, additional

Published
2018
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47. MO1-16-1 - Update on JACCRO CC-11 trial of 1st-line modified-FOLFOXIRI plus bevacizumab for RAS mutant metastatic colorectal cancer

Author

Nakamura, Masato, Sunakawa, Yu, Okuyama, Hiroyuki, Matsuura, Masato, Negoro, Yuji, Yabuno, Taichi, Takahashi, Takao, Tamura, Takao, Takeuchi, Nobumichi, Satake, Hironaga, Miyamoto, Yuji, Kataoka, Masato, Shiozawa, Manabu, Makiyama, Akitaka, Kobayashi, Kazuma, Kubota, Yutaro, Sekikawa, Takashi, Takeuchi, Masahiro, Ichikawa, Wataru, and Fujii, Masashi

Published
2019
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48. MO1-16-2 - Update on phase II trial of cetuximab plus S-1/oxaliplatin (SOX) for metastatic colorectal cancer (mCRC): JACCRO CC-06

Author

Sunakawa, Yu, Ichikawa, Wataru, Hagiwara, Ken, Tsuda, Masahiro, Takagane, Akinori, Yasui, Hisateru, Satake, Hironaga, Denda, Tadamichi, Segawa, Yoshihiko, Tanioka, Hiroaki, Kotaka, Masahito, Kochi, Mitsugu, Watanabe, Takanori, Nakamura, Masato, Tsuji, Akihito, Tani, Satoshi, Negoro, Yuji, Tobimatsu, Kazutoshi, Takeuchi, Masahiro, and Fujii, Masashi

Published
2019
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50. Early tumor shrinkage as a predictor of favorable outcomes in patients with advanced pancreatic cancer treated with FOLFIRINOX

Author

Kaga, Yasuhiro, primary, Sunakawa, Yu, additional, Kubota, Yutaro, additional, Tagawa, Teppei, additional, Yamamoto, Taikan, additional, Ikusue, Toshikazu, additional, Uto, Yu, additional, Miyashita, Kouichirou, additional, Toshima, Hirokazu, additional, Kobayashi, Kouji, additional, Hisamatsu, Atsushi, additional, Ichikawa, Wataru, additional, Sekikawa, Takashi, additional, Shimada, Ken, additional, and Sasaki, Yasutsuna, additional

Published
2016
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