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岡田泰行

徳島大学

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2024年12月20日更新

職名: 助教
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電子メール: yokada@tokushima-u.ac.jp
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学位: 博士
職歴・経歴: 2020/10: 徳島大学特任助教, 病院 (-2023.3.)
2023/4: 徳島大学助教, 病院

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2024年12月20日更新

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担当経験のある授業科目: 内科学第二 (学部)
消化器コース (学部)
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2024年12月20日更新

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論文

Kazuyoshi Noda, Yasushi Sato, Yasuyuki Okada, Kensei Nishida, Yutaka Kawano, Toshihito Tanahashi, Masahiro Bando, Koichi Okamoto, Masanori Takehara, Masahiro Sogabe, Hiroshi Miyamoto, Kei Daizumoto, Hiro-omi Kanayama and Tetsuji Takayama :
Exosomal miR-199a-3p Secreted From Cancer-Associated Adipocytes Promotes Pancreatic Cancer Progression.,
Cancer Medicine, Vol.13, No.20, e70265, 2024.

(要約): Pancreatic ductal adenocarcinoma (PDAC) is a highly aggressive cancer. Recent studies indicated that cancer-associated adipocytes (CAAs) play crucial roles in tumor progression; however, the precise mechanism remains unknown. Here, we analyzed specific exosomal microRNAs (miRNA) signatures derived from pancreatic CAAs to investigate their role in cancer progression. CAAs were generated by co-culturing human adipocytes with human pancreatic cancer cells, and exosomes were isolated from the CAA-conditioned medium (CAA-CM). Small RNA-seq analysis was used to identify differentially expressed miRNAs in these exosomes. The effects of miRNAs on cell proliferation, migration/invasion, and drug sensitivity were examined. Luciferase reporter assays, real-time polymerase chain reaction, and western blotting were performed to investigate the molecular mechanisms of the miRNAs. The clinical relevance of the miRNAs was investigated using publicly available data and our cohort of patients with PDAC. miR-199a-3p expression was significantly increased in CAA-CM-derived exosomes. CAA-derived exosomes transferred miR-199a-3p to pancreatic cancer cells. Transfection with miR-199a-3p increased the proliferation, invasion, migration, and drug resistance of pancreatic cancer cells by downregulating SOCS7, increasing STAT3 phosphorylation, and upregulating SAA1 expression. High tissue miR-199a-3p expression is correlated with poor prognosis in patients with PDAC. Liquid biopsies revealed that exosomal miR-199a-3p could accurately differentiate patients with PDAC from healthy controls. Multivariate survival analysis indicated that miR-199a is an independent prognostic factor for PDAC. miR-199a-3p in CAA-derived exosomes contributes to the malignant transformation of pancreatic cancer via the SOCS7/STAT3/SAA1 pathway, suggesting its potential as a biomarker and therapeutic target for PDAC.
(キーワード): Humans / MicroRNAs / Exosomes / Pancreatic Neoplasms / Disease Progression / Cell Proliferation / Carcinoma, Pancreatic Ductal / Adipocytes / Cell Line, Tumor / Gene Expression Regulation, Neoplastic / Cell Movement / STAT3 Transcription Factor / Prognosis / Biomarkers, Tumor / Female / Male / Drug Resistance, Neoplasm
(出版サイトへのリンク): ● Publication site (DOI): 10.1002/cam4.70265
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 39431622; ● Search Scopus @ Elsevier (PMID): 39431622; ● Search Scopus @ Elsevier (DOI): 10.1002/cam4.70265

(DOI: 10.1002/cam4.70265, PubMed: 39431622) Masahiro Sogabe, Toshiya Okahisa, Miwako Kagawa, Takanori Kashihara, Ryo Shinomiya, Takanori Miyake, Tomoyuki Kawaguchi, Reiko Yokoyama, Kaizo Kagemoto, Yoshifumi Kida, Yasuyuki Okada, Tetsu Tomonari, Yutaka Kawano, Yasushi Sato, Masahiko Nakasono and Tetsuji Takayama :
The association between alcohol consumption and cardiometabolic factors and liver fibrosis in metabolic dysfunction-associated steatotic liver disease and metabolic dysfunction and alcohol-associated liver disease.,
Alimentary Pharmacology & Therapeutics, Vol.60, No.11-12, 1587-1598, 2024.

(要約): The relationships between alcohol consumption, cardiometabolic factors, and liver fibrosis in patients with metabolic dysfunction-associated steatotic liver disease and those with metabolic dysfunction and alcohol-associated liver disease remain unclear. To investigate the longitudinal associations among alcohol consumption, cardiometabolic factors, and liver fibrosis in patients with these two liver diseases. This observational cohort study included 1866 patients with metabolic dysfunction-associated steatotic liver disease and 521 patients with metabolic dysfunction and alcohol-associated liver disease who underwent > two health checkups over >2 years. The associations of both liver diseases with worsening non-invasive liver fibrosis scores were assessed using the Cox regression analysis. Both liver diseases independently worsened liver fibrosis in both sexes. However, the hazard ratio for worsening liver fibrosis in females was significantly higher with metabolic dysfunction and alcohol-associated liver disease than with metabolic dysfunction-associated steatotic liver disease. Worsening liver fibrosis was not associated with alcohol consumption. Among males with metabolic dysfunction-associated steatotic liver disease, the hazard ratio for worsening liver fibrosis was significantly higher in those with multiple cardiometabolic factors compared to those with a single cardiometabolic factor. Although both metabolic steatotic liver disease and metabolic alcohol-associated liver disease were correlated with liver fibrosis progression in both sexes, the impact of alcohol consumption and cardiometabolic factors on fibrosis progression differed by sex. Cardiometabolic factors may have a stronger impact on liver fibrosis than alcohol consumption in males with metabolic dysfunction-associated steatotic liver disease.
(キーワード): Humans / Male / Female / Middle Aged / Alcohol Drinking / Liver Cirrhosis / Adult / Cohort Studies / Aged / Liver Diseases, Alcoholic / Fatty Liver / Risk Factors / Sex Factors
(出版サイトへのリンク): ● Publication site (DOI): 10.1111/apt.18280
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 39310953; ● Search Scopus @ Elsevier (PMID): 39310953; ● Search Scopus @ Elsevier (DOI): 10.1111/apt.18280

(DOI: 10.1111/apt.18280, PubMed: 39310953) Yuya Ueki, Hideki Otsuka, Tamaki Otani, Ryosuke Kasai, Youichi Otomi, Daiki Ikemitsu, Shota Azane, Yamato Kunikane, Takanori Bandoh, Noritake Matsuda, Yasuyuki Okada, Tetsuji Takayama and Masafumi Harada :
Combined visual and quantitative assessment of somatostatin receptor scintigraphy for staging and restaging of neuroendocrine tumors,
Japanese Journal of Radiology, Vol.42, No.5, 519-535, 2024.

(要約): Somatostatin receptor scintigraphy (SRS) using In-DTPA-DPhe-octreotide (pentetreotide) has become an integral part of neuroendocrine neoplasm management. The lack of precise quantification is a disadvantage of SRS. This study aimed to adapt the standardized uptake value (SUV) to SRS, establish the SUV range for physiological uptake in the liver, kidney, and spleen, and elucidate the utility of combined visual and quantitative SRS assessment for staging and restaging of neuroendocrine tumors (NETs). This study included 21 patients with NETs who underwent In-pentetreotide SRS. The SUV of physiological and pathological uptake was calculated using bone single-photon emission computed tomography (SPECT) quantitative analysis software (GI-BONE). For visual analysis, the primary and metastatic lesions were scored visually on planar and SPECT images using a five-point scale. We assessed the relationships between the SUVs of the liver, kidney, and spleen in the dual phase, and among quantitative indices, visual score, and pathological lesions classification. Sixty-three NEN lesions were evaluated. The mean ± standard deviation maximum SUVs (SUVmax) were liver: 4 h, 2.6 ± 1.0; 24 h, 2.2 ± 1.0; kidney: 4 h, 8.9 ± 1.8; 24 h, 7.0 ± 2.0; and spleen; 4 h, 11.3 ± 4.5; 24 h, 11.5 ± 7.6. Higher SUVmax was significantly associated with higher visual scores on dual-phase SPECT (4 h, p < 0.001; 24 h, p < 0.001) (4 h: scores 3 and 4, p < 0.05; scores 3 and 5: p < 0.01; scores 4 and 5: p < 0.01; 24 h: scores 3 and 4, p = 0.0748; scores 3 and 5: p < 0.01; scores 4 and 5: p < 0.01). We adapted the SUV to SRS and established the range of SUV for physiological uptake in the liver, kidney, and spleen. Combined visual and quantitative assessment is useful for imaging individual lesions in greater detail, and may serve as a new tumor marker of SRS for staging and restaging of NETs.
(キーワード): Humans / Neuroendocrine Tumors / Male / Female / Middle Aged / Neoplasm Staging / Aged / Adult / Receptors, Somatostatin / Radiopharmaceuticals / Tomography, Emission-Computed, Single-Photon / Somatostatin / Retrospective Studies / Aged, 80 and over
(徳島大学機関リポジトリ): ● Metadata: 118973
(出版サイトへのリンク): ● Publication site (DOI): 10.1007/s11604-024-01529-z
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 38345724; ● Search Scopus @ Elsevier (PMID): 38345724; ● Search Scopus @ Elsevier (DOI): 10.1007/s11604-024-01529-z

(徳島大学機関リポジトリ: 118973, DOI: 10.1007/s11604-024-01529-z, PubMed: 38345724) 岡田泰行, 岡本耕一, 谷直也, 和田浩典, 川口智之, 野田和克, 宮本佳彦, 春藤譲治, 上原久典, 高山哲治 :
胃神経内分泌腫瘍を合併した多腺性自己免疫症候群3 型の1 例,
Gastroenterological Endoscopy, Vol.66, No.3, 259-265, 2024年.

(キーワード): 多腺性自己免疫症候群 / 自己免疫性胃炎 / 胃神経内分泌腫瘍 / 1型糖尿病
(出版サイトへのリンク): ● Publication site (DOI): 10.11280/gee.66.259
(文献検索サイトへのリンク): ● CiNii @ 国立情報学研究所 (CRID): 1390299539243025536; ● Search Scopus @ Elsevier (DOI): 10.11280/gee.66.259

(DOI: 10.11280/gee.66.259, CiNii: 1390299539243025536) Yasuyuki Okada, Peng Fuduan, Perea Jose, Corchete Luis, Bujanda Luis, Li Wei and Goel Ajay :
Genome-wide methylation profiling identifies a novel gene signature for patients with synchronous colorectal cancer,
British Journal of Cancer, Vol.128, No.1, 112-120, 2023.

(要約): There are no robust tools for the diagnosis of synchronous colorectal cancer (SyCRC). Herein, we developed the first methylation signature to identify and characterise patients with SyCRC. For biomarker discovery, we analysed the genome-wide methylation profiles of 16 SyCRC and 18 solitary colorectal cancer (SoCRC) specimens. We thereafter established a methylation signature risk-scoring model to identify SyCRC in an independent cohort of 38 SyCRC and 42 SoCRC patients. In addition, we evaluated the prognostic value of the identified methylation profile. We identified six differentially methylated CpG probes/sites that distinguished SyCRC from SoCRC. In the validation cohort, we developed a methylation panel that identified patients with SyCRC from not only larger tumour (AUC = 0.91) but also the paired remaining tumour (AUC = 0.93). Moreover, high risk scores of our panel were associated with the development of metachronous CRC among patients with SyCRC (AUC = 0.87) and emerged as an independent predictor for relapse-free survival (hazard ratio = 2.72; 95% CI = 1.12-6.61). Furthermore, the risk stratification model which combined with clinical risk factors was a diagnostic predictor of recurrence (AUC = 0.90). Our novel six-gene methylation panel robustly identifies patients with SyCRC, which has the clinical potential to improve the diagnosis and management of patients with CRC.
(キーワード): Humans / DNA Methylation / Colorectal Neoplasms / Neoplasm Recurrence, Local / Prognosis / Protein Processing, Post-Translational / Biomarkers, Tumor / Gene Expression Regulation, Neoplastic
(徳島大学機関リポジトリ): ● Metadata: 118462
(出版サイトへのリンク): ● Publication site (DOI): 10.1038/s41416-022-02033-9
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 36319845; ● Search Scopus @ Elsevier (PMID): 36319845; ● Search Scopus @ Elsevier (DOI): 10.1038/s41416-022-02033-9

(徳島大学機関リポジトリ: 118462, DOI: 10.1038/s41416-022-02033-9, PubMed: 36319845) Yasushi Sato, Yasuyuki Okada, Yasuteru Fujino, Tomoyuki Kawaguchi, Yoshifumi Kida, Yasuhiro Mitsui, Hironori Tanaka, Tetsu Tomonari, Shinji Kitamura, Koichi Okamoto, Yutaka Kawano, Hiroshi Miyamoto, Masahiro Sogabe and Tetsuji Takayama :
Clinical Outcomes of Comprehensive Genomic Profiling Tests for Gastrointestinal Cancers: Experience from Tokushima University Hospital.,
The Journal of Medical Investigation : JMI, Vol.70, No.1.2, 154-159, 2023.

(要約): In Japan, cancer genome profiling (CGP) for cancer patients without standard treatment has been covered by public insurance since June 2019. This study analyzed data of 122 patients with gastrointestinal tumors who underwent CGP to clarify cancer genome medicine's current status and possible problems at the Tokushima University Hospital. The major types of cancer included pancreatic (n=30), colorectal (n=25), biliary tract (n=15), gastric (n=11), and hepatocellular carcinoma (n=8). CGP tests included F1CDx in 70 patients (57%), F1LCDx in 36 (30%), TSO500 in 14 (11%), and NCC Oncopanel in 2 (2%). Actionable gene alterations were identified in 72 patients (59%), but only 5 patients (4%) were treated for pancreatic (n=1), colorectal (n=3), and small bowel cancers (n=1). The main reasons for not receiving genotype-matched therapy included the lack of appropriate drugs or clinical trials that matched the actionable gene alterations (n=40) and the inability to participate in clinical trials (n=10). There is still not a sufficient number of patients receiving genotype-matched treatment for gastrointestinal cancers. To promote cancer genome medicine in regional areas, attempts to improve access to genotype-matched therapies are required, as well as to promote the development of new molecular-targeted drugs and clinical trials for these drugs. J. Med. Invest. 70 : 154-159, February, 2023.
(キーワード): Humans / Gastrointestinal Neoplasms / Neoplasms / Colorectal Neoplasms / Genomics / Hospitals / Japan
(徳島大学機関リポジトリ): ● Metadata: 118346
(出版サイトへのリンク): ● Publication site (DOI): 10.2152/jmi.70.154
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 37164713; ● Search Scopus @ Elsevier (PMID): 37164713; ● Search Scopus @ Elsevier (DOI): 10.2152/jmi.70.154

(徳島大学機関リポジトリ: 118346, DOI: 10.2152/jmi.70.154, PubMed: 37164713) 和田浩典, 藤野泰輝, 影本開三, 喜田慶史, 岡田泰行, 三井康裕, 岡本耕一, 佐藤康史, 坂東良美, 宮本弘志, 高山哲治 :
がん遺伝子パネル検査を契機にHER2陽性が判明しTrastuzumab投与により長期生存が得られた進行胃癌の1例.,
日本消化器病学会雑誌, Vol.119, No.10, 937-945, 2022年.

(要約): Intratumoral HER2 heterogeneity is a well-described gastric cancer feature and may explain many false-negative results related to this oncogene. An 81-year-old man was diagnosed at our hospital with stage IV gastric cancer with multiple lymph node metastases. Immunohistochemistry (IHC) analysis indicated that the primary tumor was HER2-negative. After a chemotherapy course, we submitted a pretreatment biopsy specimen for comprehensive cancer genome profiling (CGP) to determine the last-line therapy. This revealed HER2 amplification. The specimen was reevaluated using fluorescence in situ hybridization and IHC with deeper-cut specimens, which confirmed that the tumor was indeed HER2-positive. Therefore, the patient was treated with chemotherapy plus trastuzumab, which elicited tumor shrinkage and conferred long-term survival. Our current data underscore the CGP importance, which can provide more accurate tumor profilings and inform subsequent treatment decisions.
(キーワード): がん遺伝子パネル検査 / Trastuzumab / HER2陽性胃癌
(出版サイトへのリンク): ● Publication site (DOI): 10.11405/nisshoshi.119.937
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 36216544; ● CiNii @ 国立情報学研究所 (CRID): 1390293710918867840; ● Search Scopus @ Elsevier (PMID): 36216544; ● Search Scopus @ Elsevier (DOI): 10.11405/nisshoshi.119.937

(DOI: 10.11405/nisshoshi.119.937, PubMed: 36216544, CiNii: 1390293710918867840) Beibei Ma, Hiroyuki Ueda, Koichi Okamoto, Masahiro Bando, Shota Fujimoto, Yasuyuki Okada, Tomoyuki Kawaguchi, Hironori Wada, Hiroshi Miyamoto, Mitsuo Shimada, Yasushi Sato and Tetsuji Takayama :
TIMP1 promotes cell proliferation and invasion capability of right-sided colon cancers via the FAK/Akt signaling pathway.,
Cancer Science, Vol.113, No.12, 4244-4257, 2022.

(要約): Although right-sided colorectal cancer (CRC) shows a worse prognosis than left-sided CRC, the underlying mechanism remains unclear. We established patient-derived organoids (PDOs) from left- and right-sided CRCs and directly compared cell proliferation and invasion capability between them. We then analyzed the expression of numerous genes in signal transduction pathways to clarify the mechanism of the differential prognosis. Cell proliferation activity and invasion capability in right-sided cancer PDOs were significantly higher than in left-sided cancer PDOs and normal PDOs, as revealed by Cell Titer Glo and transwell assays, respectively. We then used quantitative RT-PCR to compare 184 genes in 30 pathways among right-sided and left-sided cancer and normal PDOs and found that the TIMP1 mRNA level was highest in right-sided PDOs. TIMP1 protein levels were upregulated in right-sided PDOs compared with normal PDOs but was downregulated in left-sided PDOs. TIMP1 knockdown with shRNA significantly decreased cell proliferation activity and invasion capability in right-sided PDOs but not in left-sided PDOs. Moreover, TIMP1 knockdown significantly decreased pFAK and pAkt expression levels in right-sided PDOs but not in left-sided PDOs. A database analysis of The Cancer Genome Atlas revealed that TIMP1 expression in right-sided CRCs was significantly higher than in left-sided CRCs. Kaplan-Meier survival analysis showed significantly shorter overall survival in high-TIMP1 patients versus low-TIMP1 patients with right-sided CRCs but not left-sided CRCs. Our data suggest that TIMP1 is overexpressed in right-sided CRCs and promotes cell proliferation and invasion capability through the TIMP1/FAK/Akt pathway, leading to a poor prognosis. The TIMP1/FAK/Akt pathway can be a target for therapeutic agents in right-sided CRCs.
(キーワード): Humans / Prognosis / Signal Transduction / Colorectal Neoplasms / Colonic Neoplasms / Cell Proliferation / Tissue Inhibitor of Metalloproteinase-1
(徳島大学機関リポジトリ): ● Metadata: 117615
(出版サイトへのリンク): ● Publication site (DOI): 10.1111/cas.15567
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 36073574; ● Search Scopus @ Elsevier (PMID): 36073574; ● Search Scopus @ Elsevier (DOI): 10.1111/cas.15567

(徳島大学機関リポジトリ: 117615, DOI: 10.1111/cas.15567, PubMed: 36073574) Jung Gerhard, Hernández-Illán Eva, Lozano J Juan, Sidorova Julia, Muñoz Jenifer, Yasuyuki Okada, Quintero Enrique, Hernandez Goretti, Jover Rodrigo, Carballal Sabela, Cuatrecasas Miriam, Moreno Lorena, Diaz Mireia, Ocaña Teresa, Sánchez Ariadna, Rivero Liseth, Ortiz Oswaldo, Llach Joan, Castells Antoni, Pellisé Maria, Goel Ajay, Batlle Eduard and Balaguer Francesc :
Epigenome-Wide DNA Methylation Profiling of Normal Mucosa Reveals HLA-F Hypermethylation as a Biomarker Candidate for Serrated Polyposis Syndrome,
The Journal of Molecular Diagnostics : JMD, Vol.24, No.6, 674-686, 2022.

(要約): Serrated polyposis syndrome (SPS) is associated with a high risk for colorectal cancer. Intense promoter hypermethylation is a frequent molecular finding in the serrated pathway and may be present in normal mucosa, predisposing to the formation of serrated lesions. To identify novel biomarkers for SPS, fresh-frozen samples of normal mucosa from 50 patients with SPS and 19 healthy individuals were analyzed by using the 850K BeadChip Technology (Infinium). Aberrant methylation levels were correlated with gene expression using a next-generation transcriptome profiling tool. Two validation steps were performed on independent cohorts: first, on formalin-fixed, paraffin-embedded tissue of the normal mucosa; and second, on 24 serrated lesions. The most frequently hypermethylated genes were HLA-F, SLFN12, HLA-DMA, and RARRES3; and the most frequently hypomethylated genes were PIWIL1 and ANK3 (Δβ = 10%; P < 0.05). Expression levels of HLA-F, SLFN12, and HLA-DMA were significantly different between SPS patients and healthy individuals and correlated well with the methylation status of the corresponding differentially methylated region (fold change, >20%; r > 0.55; P < 0.001). Significant hypermethylation of CpGs in the gene body of HLA-F was also found in serrated lesions (Δβ = 23%; false discovery rate = 0.01). Epigenome-wide methylation profiling has revealed numerous differentially methylated CpGs in normal mucosa from SPS patients. Significant hypermethylation of HLA-F is a novel biomarker candidate for SPS.
(キーワード): Adenomatous Polyposis Coli / Argonaute Proteins / Biomarkers / Colorectal Neoplasms / DNA Methylation / Epigenome / Histocompatibility Antigens Class I / Humans / Mucous Membrane
(徳島大学機関リポジトリ): ● Metadata: 118463
(出版サイトへのリンク): ● Publication site (DOI): 10.1016/j.jmoldx.2022.03.010
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 35447336; ● Search Scopus @ Elsevier (PMID): 35447336; ● Search Scopus @ Elsevier (DOI): 10.1016/j.jmoldx.2022.03.010

(徳島大学機関リポジトリ: 118463, DOI: 10.1016/j.jmoldx.2022.03.010, PubMed: 35447336) 藤野泰輝, 田中久美子, 中村文香, 喜田慶史, 平尾章博, 岡田泰行, 武原正典, 福家慧, 坂東良美, 高山哲治 :
関節リウマチの経過中に発生したリウマトイド血管炎に起因する多発大腸潰瘍の1例.,
Gastroenterological Endoscopy, Vol.63, No.7, 1358-1364, 2021年.

(キーワード): リウマトイド血管炎 / 大腸潰瘍
(出版サイトへのリンク): ● Publication site (DOI): 10.11280/gee.63.1358
(文献検索サイトへのリンク): ● CiNii @ 国立情報学研究所 (CRID): 1390007282525435264; ● Search Scopus @ Elsevier (DOI): 10.11280/gee.63.1358

(DOI: 10.11280/gee.63.1358, CiNii: 1390007282525435264) Yasuyuki Okada, Naoki Takahashi, Tetsuji Takayama and Ajay Goel :
LAMC2 promotes cancer progression and gemcitabine resistance through modulation of EMT and ATP-binding cassette transporters in pancreatic ductal adenocarcinoma.,
Carcinogenesis, Vol.42, No.4, 546-556, 2021.

(要約): Pancreatic ductal adenocarcinoma (PDAC) is an aggressive disease with poor prognosis. Gemcitabine remains an effective option for the majority of PDAC patients. Unfortunately, currently no reliable prognostic and predictive biomarkers of therapeutic response are available for the patients with PDAC. Laminin γ2 (LAMC2) is overexpressed in several cancers, and its high expression facilitates cancer development and chemoresistance. However, its functional role in PDAC remains unclear, and a better understanding of this will likely help improve the prognosis of PDAC patients. This study aimed to elucidate the clinical and biological role of LAMC2 in PDAC. We first analyzed the expression levels of LAMC2 by real-time reverse transcription PCR in a cohort of 114 PDAC patients. Interestingly, higher expression of LAMC2 significantly correlated with poor survival in PDAC cohort. In addition, elevated LAMC2 expression served as a potential prognostic marker for survival. Subsequently, functional characterization for the role of LAMC2 in PDAC was performed by small interfering RNA knockdown in pancreatic cancer (PC) cell lines. Interestingly, inhibition of LAMC2 in PC cells enhanced the gemcitabine sensitivity and induction of apoptosis. Moreover, it inhibited colony formation ability, migration and invasion potential. Furthermore, LAMC2 regulated the expression of epithelial-mesenchymal transition (EMT) phenotype. In addition, LAMC2 significantly correlated with genes associated with the expression of ATP-binding cassette (ABC) transporters in PC cells and PDAC patients. In conclusion, these results suggest that LAMC2 regulates gemcitabine sensitivity through EMT and ABC transporters in PDAC and may be a novel therapeutic target in PDAC patients.
(徳島大学機関リポジトリ): ● Metadata: 118465
(出版サイトへのリンク): ● Publication site (DOI): 10.1093/carcin/bgab011
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 33624791; ● Search Scopus @ Elsevier (PMID): 33624791; ● Search Scopus @ Elsevier (DOI): 10.1093/carcin/bgab011

(徳島大学機関リポジトリ: 118465, DOI: 10.1093/carcin/bgab011, PubMed: 33624791) Yasuyuki Okada, Satoshi Nisiwada, Kensuke Yamamura, Masayuki Sho, Hideo Baba, Tetsuji Takayama and Ajay Goel :
Identification of laminin γ2 as a prognostic and predictive biomarker for determining response to gemcitabine-based therapy in pancreatic ductal adenocarcinoma.,
European Journal of Cancer, Vol.146, 125-134, 2021.

(要約): Pancreatic ductal adenocarcinoma (PDAC) is one of the most lethal malignancies. While the extracellular matrix component plays an integral role in PDAC pathogenesis and mediating chemoresistance, its role in predicting response to chemotherapy in patients with PDAC remains unclear. We performed a systematic biomarker discovery by analysing genome-wide transcriptomic profiling data from 423 patients (GSE71729, GSE21501 and The Cancer Genome Atlas [TCGA]) for predicting overall survival (OS). This was subsequently validated in two independent clinical cohorts of 270 patients with PDAC (training cohort, n = 121, and validation cohort, n = 149). In addition, we investigated endoscopic ultrasound-fine needle aspiration biopsy specimens from 51 patients with PDAC with an unresectable cancer for predicting therapeutic response to gemcitabine-based therapy. After rigorous bioinformatic analysis, we identified laminin γ2 (LAMC2) to be a significant prognostic factor in all three PDAC data sets (GSE71729: hazard ratio [HR] = 2.04, P = 0.002; GSE21501: HR = 2.17, P = 0.031; TCGA: HR = 2.57, P < 0.001). High LAMC2 expression in patients with PDAC was associated with a significantly poor OS and relapse-free survival in both the training (P < 0.001, P < 0.001) and validation cohorts (P = 0.001, P = 0.026). More importantly, LAMC2 expression robustly identified patients with PDAC and unresectable disease and those who responded to gemcitabine-based therapy (area under the curve = 0.79; 95% confidence interval [CI], 0.65-0.89). The univariate logistic regression analysis revealed that high LAMC2 expression was the only factor that predicted poor response to gemcitabine in patients with PDAC (odds ratio = 4.90; 95% CI, 1.45-16.6; P = 0.011). We conclude that LAMC2 is a novel prognostic and predictive biomarker for gemcitabine-based therapy in both the adjuvant and palliative setting; which could have significant impact on precision and individualised treatment of patients with PDAC.
(徳島大学機関リポジトリ): ● Metadata: 118464
(出版サイトへのリンク): ● Publication site (DOI): 10.1016/j.ejca.2020.12.031
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 33607476; ● Search Scopus @ Elsevier (PMID): 33607476; ● Search Scopus @ Elsevier (DOI): 10.1016/j.ejca.2020.12.031

(徳島大学機関リポジトリ: 118464, DOI: 10.1016/j.ejca.2020.12.031, PubMed: 33607476)

MISC

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講演・発表: Yasushi Sato, Kazuyoshi Noda, Yasuyuki Okada, Kensei Nishida, Yutaka Kawano, Toshihito Tanahashi, Masanori Takehara, Yasuteru Fujino, Koichi Okamoto, Hiroshi Miyamoto and Tetsuji Takayama :
Exosomal miR-199a-3p secreted from cancer-associated adipocytes promote pancreatic cancer progression.,
DDW2023, Chicago, May 2023. Yasuyuki Okada, Fuduan Peng, Jose Perea, Luis Bujanda, Tetsuji Takayama, Wei Li and Ajay Goel :
Identification of a Novel Epigenetic Signature for the Identification of Patients with Synchronous Colorectal Cancers.,
Digestive Disease Week2021, May 2021. Yasuyuki Okada, Ya Cui, Satoshi Nishiwada, Eunsung Jun, Fuminori Sonohara, SongCheol Kim, Yasuhiro Koreda, Masayuki Sho, Wei Li, Tetsuji Takayama and Ajay Goel :
Expression Profiling Identifies a Novel miRNA-based Signature for Predicting Local Recurrence in Patients with Pancreatic Ductal Adenocarcinoma.,
Digestive Disease Week2021, May 2021. Yasuyuki Okada, Goel Ajay, Nishiwada Satoshi, Takahashi Naoki and Tetsuji Takayama :
LAMC2 promotes progression and gemcitabine resistance through modulation of EMT and ATP-binding transporters in pancreatic ductal adenocarcinoma,
AACR annual meeting 2021, Apr. 2021. 宮本弘志, 上田浩之, 三宅孝典, 髙橋拓, 横山怜子, 岡田泰行, 曽我部正弘, 佐藤康史, 高山哲治 :
膵癌における相同組換え修復欠損とプラチナ製剤を含む化学療法の関連.,
JDDW2024, 2024年11月. 岡田泰行, 上田浩之, 高山哲治 :
<ワークショップ>膵癌の早期診断を目的とした血清microRNAパネルの開発.,
JDDW2024, 2024年11月. Hiroshi Miyamoto, Ayuka Mineda, Sawaka Yukishige, Soichiroh Sasa, Kei Daizumoto, Tomoya Fukawa, Yasuyuki Okada, Yasuhiro Mitsui, Koichi Okamoto, Yasushi Sato, Hiroyuki Morino and Tetsuji Takayama :
Management of patients with presumed germline pathogenic variant from comprehensive genomic profiling tests.,
日本人類遺伝学会第69回大会, Oct. 2024. 福家慧, 佐藤康史, 岡田泰行, 岡本耕一, 河野豊, 宮本弘志, 高山哲治, 影本開三, 喜田慶史 :
UBR4 は EGFR の内在化を制御することで，大腸癌患者における抗 EGFR 抗体の新規バイオマーカーとなる.,
第21回日本臨床腫瘍学会学術集会, 2024年2月. 岡田泰行, 宮本弘志, 高山哲治 :
膵腫瘍に対するがん遺伝子パネル検査を念頭に置いたEUS-FNAの至適な方法についての検討.,
JDDW2023, 2023年11月. 岡田泰行, Goel Ajay, 高山哲治 :
膵癌の術後局所再発を予測するmicroRNAパネルの開発.,
JDDW2023, 2023年11月. 平田圭市郎, 上田浩之, 三宅孝典, 樫原孝典, 岡田泰行, 田中宏典, 和田浩典, 藤野泰輝, 友成哲, 谷口達哉, 岡本耕一, 宮本弘志, 川中崇, 生島仁史, 坂東良美, 佐藤康史, 高山哲治 :
切除不能・再発膵神経内分泌腫瘍(pancreatic neruoendocrine neoplasm:P-NEN)に対する集学的治療による治療成績の向上.,
第109回日本消化器病学会総会, 2023年4月. 和田浩典, 岡田泰行, 谷口達哉, 田中宏典, 岡本耕一, 高山哲治 :
Wntシグナル伝達経路を標的とした大腸癌の化学予防.,
第81回日本癌学会学術総会, 2022年10月. Beibei Ma, Hiroyuki Ueda, Koichi Okamoto, Masahiro Bando, Yasuyuki Okada, Mitsuo Shimada, Yasushi Sato and Tetsuji Takayama :
TIMP1 Promotes Cell Proliferation and Invasion Capability of Right-sided Colon Cancers.,
第81回日本癌学会学術総会, Sep. 2022. Yasuyuki Okada, Yasuhiro Mitsui, Shinji Kitamura, Koichi Okamoto, Hiroshi Miyamoto, Yasushi Sato, Naoki Muguruma and Tetsuji Takayama :
LAMC2 is a novel predictive biomarker for gemcitabine-based therapy in pancreatic ductal adenocarcinoma.,
第19回日本臨床腫瘍学会学術集会, Feb. 2022. 田中宏典, 友成哲, 影本開三, 岡田泰行, 和田浩典, 中村文香, 北村晋志, 岡本耕一, 宮本弘志, 佐藤康史, 六車直樹, 高山哲治 :
免疫チェックポイント阻害薬投与中の肝障害.,
第59回日本癌治療学会学術集会, 2021年10月. Beibei Ma, Hiroyuki Ueda, Naoki Muguruma, Koichi Okamoto, Tomoyuki Kawaguchi, Akira Fukuya, Yoshifumi Kida, Yasuyuki Okada, Tatsuya Taniguchi, Yasushi Sato and Tetsuji Takayama :
Activation of EGFR signaling pathway in the left-side colorectal cancerLeft-side vs. right-side cancer organoids.,
第80回日本癌学会学術総会, Sep. 2021.

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補助金・競争的資金: 膵癌の診断マーカーとなるexosome内のmiRNAモデルの開発 (研究課題/領域番号: 24K18918 )
Exosomeエンジニアリングによる膵癌とその微小環境の改変を標的とする治療法の開発 (研究課題/領域番号: 23K27588 )
AIを用いた切除可能膵癌に対する化学療法最適化を予測するためのmiRNAモデルの開発 (研究課題/領域番号: 23K07396 )
染色体不安定性に着目した大腸癌の抗癌剤耐性機序の解析 (研究課題/領域番号: 23K24321 )
AIを用いた膵癌の化学療法の治療効果を予測するmiRNAモデルの開発 (研究課題/領域番号: 22K16045 )
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