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Your search keyword '"Masuda, Takaaki"' showing total 11 results
Start Over Author "Masuda, Takaaki" Publisher american association for cancer research
11 results on '"Masuda, Takaaki"'

2. Abstract 5238: Clinical significance of GET4 expression in colorectal cancer

Author

Koike, Kensuke, primary, Masuda, Takaaki, additional, Sato, Kuniaki, additional, Motomura, Yuushi, additional, Takahashi, Jyunnichi, additional, Shimizu, Dai, additional, Kuramitsu, Shotaro, additional, Fujii, Atsushi, additional, Kitagawa, Akihiro, additional, Noda, Miwa, additional, tsuruda, Yusuke, additional, Ootu, Hajime, additional, Kuroda, Yousuke, additional, Eguchi, Hidetoshi, additional, Nakagawa, Takashi, additional, and Mimori, Koushi, additional

Published
2019
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3. Abstract 3173: Clinical significance of Fanconi anemia complementation group E(FANCE)DNA repair-related gene expression in hepatocellular carcinoma

Author

Takahashi, Junichi, primary, Masuda, Takaaki, additional, Kuroda, Yosuke, additional, Kitagawa, Akihiro, additional, Motomura, Yushi, additional, Koike, Kensuke, additional, Shimizu, Dai, additional, Kuramitsu, Shotaro, additional, Fujii, Atsushi, additional, Noda, Miwa, additional, Sato, Kuniaki, additional, Tsuruda, Yusuke, additional, Otsu, Hajime, additional, Eguchi, Hidetoshi, additional, Sugimachi, Keishi, additional, Mori, Masaki, additional, and Mimori, Koshi, additional

Published
2019
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4. Abstract 475: Clinical significance of eif5-mimic protein 1 in pancreatic cancer

Author

Motomura, Yushi, primary, Masuda, Takaaki, additional, Sato, Kuniaki, additional, Fujii, Atsushi, additional, Kitagawa, Akihiro, additional, Wakiyama, Hiroaki, additional, Koike, Kensuke, additional, Takahashi, Junichi, additional, Shimizu, Dai, additional, Kuramitsu, Shotaro, additional, Noda, Miwa, additional, Tsuruda, Yusuke, additional, Otsu, Hajime, additional, Kuroda, Yosuke, additional, Eguchi, Hidetoshi, additional, Sakamoto, Katsumi, additional, Hirakawa, Masakazu, additional, Honda, Hiroshi, additional, and Mimori, Koshi, additional

Published
2019
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6. Abstract 3908: The mechanism of premetastatic niche formation through FBXW7/NOTCH/CCL2 pathway and clinical trial using CCL2 inhibitor “SK-818” for breast cancer patients

Author

Noda, Miwa, primary, Masuda, Takaaki, additional, Hayashi, Naoki, additional, Kogawa, Takahiro, additional, Ohno, Shinji, additional, Nakayama, Keiichi, additional, Kuroda, Yohsuke, additional, Eguchi, Hidetoshi, additional, Ito, Shuhei, additional, Inomata, Masafumi, additional, and Mimori, Koshi, additional

Published
2017
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7. Abstract 4411: Loss of fructose-1,6-bisphosphatase expression induces altering glucose metabolism and tumor progression in hepatocellular carcinoma

Author

Wakiyama, Hiroaki, primary, Hirata, Hidenari, additional, Sugimachi, Keishi, additional, Masuda, Takaaki, additional, Hayashi, Naoki, additional, Kuroda, Yohsuke, additional, Ito, Shuhei, additional, Eguchi, Hidetoshi, additional, Terashima, Kotaro, additional, Sakamoto, Katsumi, additional, Hirakawa, Masakazu, additional, Honda, Hiroshi, additional, and Mimori, Koshi, additional

Published
2017
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8. Abstract 5439: The chronological analysis of previously-reported serum microRNA expression in colorectal cancer

Author

Yoshikawa, Yukihiro, primary, Fukunaga, Mitsuko, additional, Masuda, Takaaki, additional, Noda, Miwa, additional, Wakiyama, Hiroaki, additional, Koyama, Yuta, additional, Kidogami, Shinya, additional, Sato, Kuniaki, additional, Hu, Qingjiang, additional, Nambara, Sho, additional, Saito, Tomoko, additional, Sakimura, Shotaro, additional, Hayashi, Naoki, additional, Kuroda, Yohsuke, additional, Ito, Shuhei, additional, Doki, Yuichiro, additional, Mori, Masaki, additional, and Mimori, Koshi, additional

Published
2017
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9. Abstract 4927: Identification of novel candidate of driver genes on chromosome 7 in colorectal cancer

Author

Sato, Kuniaki, primary, Hu, Qingjiang, additional, Kidogami, Shinya, additional, Ogawa, Yushi, additional, Saito, Tomoko, additional, Nambara, Sho, additional, Komatsu, Hisateru, additional, Hirata, Hidenari, additional, Sakimura, Shotaro, additional, Uchi, Ryutaro, additional, Hayashi, Naoki, additional, Iguchi, Tomohiro, additional, Eguchi, Hidetoshi, additional, Ito, Shuhei, additional, Masuda, Takaaki, additional, Nakagawa, Takashi, additional, and Mimori, Koshi, additional

Published
2016
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10. The Evolving Genomic Landscape of Esophageal Squamous Cell Carcinoma Under Chemoradiotherapy.

Author

Hirata H, Niida A, Kakiuchi N, Uchi R, Sugimachi K, Masuda T, Saito T, Kageyama SI, Motomura Y, Ito S, Yoshitake T, Tsurumaru D, Nishimuta Y, Yokoyama A, Hasegawa T, Chiba K, Shiraishi Y, Du J, Miura F, Morita M, Toh Y, Hirakawa M, Shioyama Y, Ito T, Akimoto T, Miyano S, Shibata T, Mori M, Suzuki Y, Ogawa S, Ishigami K, and Mimori K

Subjects
Chemoradiotherapy, Clonal Evolution drug effects, Clonal Evolution genetics, Clonal Evolution radiation effects, Computational Biology methods, Databases, Genetic, Disease Management, Drug Resistance, Neoplasm genetics, Esophageal Squamous Cell Carcinoma diagnosis, Esophageal Squamous Cell Carcinoma therapy, Genetic Predisposition to Disease, Humans, INDEL Mutation, Mutation, Neoplasm Recurrence, Local, Neoplasm Staging, Polymorphism, Single Nucleotide, Prognosis, Radiation Tolerance genetics, Tumor Burden, Exome Sequencing, Biomarkers, Tumor, Esophageal Squamous Cell Carcinoma genetics, Evolution, Molecular, Genomics methods
Abstract

Esophageal squamous cell carcinoma (ESCC) often recurs after chemoradiotherapy, and the prognosis of ESCC after chemoradiotherapy has not improved over the past few decades. The mutation process in chemoradiotherapy-resistant clones and the functional relevance of genetic alterations remain unclear. To address these problems, we performed whole-exome sequencing of 52 tumor samples from 33 patients with ESCC who received radiotherapy combined with 5-fluorouracil/platinum. In multiregion analyses of pretreatment and locally recurrent lesions from five cases, most driver gene-altered clones remained under chemoradiotherapy selection pressure, while few driver gene alterations were acquired at recurrence. The mutation signatures of recurrent ESCC, including increased deletion frequency and platinum dose-dependent base substitution signatures, were substantially different from those of primary ESCC and reflected the iatrogenic impacts of chemoradiotherapy. Single-region analysis of 28 pretreatment tumors indicated that focal copy-number gain at the MYC locus was significantly associated with poor progression-free survival and overall survival after chemoradiotherapy. MYC gain remained throughout the chemoradiotherapy course and potentially contributes to intrinsic resistance to chemoradiotherapy. Consistent with these findings, MYC copy number and mRNA and protein levels in ESCC cell lines correlated positively with resistance to radiotherapy, and MYC knockdown improved sensitivity to radiotherapy. Overall, these data characterize the clonal evolution process induced by chemoradiotherapy and clinically relevant associations for genetic alterations in ESCC. These findings increase our understanding of therapeutic resistance and support the rationale for precision chemoradiotherapy. SIGNIFICANCE: Whole-exome sequencing reveals the genetic evolution of ESCC during chemoradiotherapy, highlighting MYC gain in pretreatment tumors as a potential marker of therapy resistance., (©2021 American Association for Cancer Research.)

Published
2021
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11. Decreased Expression of Fructose-1,6-bisphosphatase Associates with Glucose Metabolism and Tumor Progression in Hepatocellular Carcinoma.

Author

Hirata H, Sugimachi K, Komatsu H, Ueda M, Masuda T, Uchi R, Sakimura S, Nambara S, Saito T, Shinden Y, Iguchi T, Eguchi H, Ito S, Terashima K, Sakamoto K, Hirakawa M, Honda H, and Mimori K

Subjects
Animals, Apoptosis, Biomarkers, Tumor genetics, Biomarkers, Tumor metabolism, Blotting, Western, Carcinoma, Hepatocellular genetics, Carcinoma, Hepatocellular metabolism, Case-Control Studies, Cell Proliferation, DNA Helicases genetics, DNA-Binding Proteins genetics, Female, Follow-Up Studies, Humans, Immunoenzyme Techniques, Liver metabolism, Liver pathology, Liver Neoplasms genetics, Liver Neoplasms metabolism, Mice, Mice, Inbred BALB C, Mice, Nude, Neoplasm Recurrence, Local genetics, Neoplasm Recurrence, Local metabolism, Neoplasm Staging, Prognosis, Promoter Regions, Genetic genetics, RNA, Messenger genetics, RNA-Binding Proteins, Real-Time Polymerase Chain Reaction, Reverse Transcriptase Polymerase Chain Reaction, Survival Rate, Tumor Cells, Cultured, Xenograft Model Antitumor Assays, Carcinoma, Hepatocellular pathology, DNA Helicases metabolism, DNA-Binding Proteins metabolism, Gene Expression Regulation, Neoplastic, Gluconeogenesis physiology, Glucose metabolism, Liver Neoplasms pathology, Neoplasm Recurrence, Local pathology
Abstract

Fructose-1,6-bisphosphatase (FBP1), the rate-limiting enzyme in gluconeogenesis, is reduced in expression in certain cancers where it has been hypothesized to act as a tumor suppressor, including in hepatocellular carcinoma (HCC). Here, we report functional evidence supporting this hypothesis, providing a preclinical rationale to develop FBP1 as a therapeutic target for HCC treatment. Three independent cohorts totaling 594 cases of HCC were analyzed to address clinical significance. Lower FBP1 expression associated with advanced tumor stage, poor overall survival, and higher tumor recurrence rates. In HCC cell lines, where endogenous FBP1 expression is low, engineering its ectopic overexpression inhibited tumor growth and intracellular glucose uptake by reducing aerobic glycolysis. In patient specimens, promoter methylation and copy-number loss of FBP1 were independently associated with decreased FBP1 expression. Similarly, FBP1 downregulation in HCC cell lines was also associated with copy-number loss. HCC specimens exhibiting low expression of FBP1 had a highly malignant phenotype, including large tumor size, poor differentiation, impaired gluconeogenesis, and enhanced aerobic glycolysis. The effects of FBP1 expression on prognosis and glucose metabolism were confirmed by gene set enrichment analysis. Overall, our findings established that FBP1 downregulation in HCC contributed to tumor progression and poor prognosis by altering glucose metabolism, and they rationalize further study of FBP1 as a prognostic biomarker and therapeutic target in HCC patients. Cancer Res; 76(11); 3265-76. ©2016 AACR., (©2016 American Association for Cancer Research.)

Published
2016
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