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Pancreatic Neoplasms: HELP
Articles by Akihiro Funakoshi
Based on 12 articles published since 2009
(Why 12 articles?)
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Between 2009 and 2019, A. Funakoshi wrote the following 12 articles about Pancreatic Neoplasms.
 
+ Citations + Abstracts
1 Clinical Trial Updated results from GEST study: a randomized, three-arm phase III study for advanced pancreatic cancer. 2017

Okusaka, Takuji / Miyakawa, H / Fujii, H / Nakamori, S / Satoh, T / Hamamoto, Y / Ito, T / Maguchi, H / Matsumoto, S / Ueno, H / Ioka, T / Boku, N / Egawa, S / Hatori, T / Furuse, J / Mizumoto, K / Ohkawa, S / Yamaguchi, T / Yamao, K / Funakoshi, A / Chen, J S / Cheng, A L / Sato, A / Ohashi, Y / Tanaka, M / Anonymous450897. ·Department of Hepatobiliary and Pancreatic Oncology, National Cancer Center Hospital, 5-1-1 Tsukiji, Chuo-ku, Tokyo, 104-0045, Japan. tokusaka@ncc.go.jp. · Division of Biliopancreatology, Sapporo Kosei General Hospital, Sapporo, Japan. · Division of Clinical Oncology, Jichi Medical University, Tochigi, Japan. · Hepato-Biliary-Pancreatic Surgery, Osaka National Hospital, Osaka, Japan. · Department of Frontier Science for Cancer and Chemotherapy, Osaka University Graduate School of Medicine, Suita, Japan. · Keio Cancer Center, Keio University Hospital, Tokyo, Japan. · Department of Medicine and Bioreguratory Science, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan. · Center for Gastroenterology, Teine-Keijinkai Hospital, Sapporo, Japan. · Department of Medical Oncology, Kyoto University Hospital, Kyoto, Japan. · Department of Hepatobiliary and Pancreatic Oncology, National Cancer Center Hospital, 5-1-1 Tsukiji, Chuo-ku, Tokyo, 104-0045, Japan. · Department of Hepatobiliary and Pancreatic Oncology, Osaka Medical Center for Cancer and Cardiovascular Diseases, Osaka, Japan. · Gastrointestinal Medical Oncology Division, National Cancer Center Hospital, Tokyo, Japan. · Department of Surgery, Tohoku University, Sendai, Japan. · Department of Surgery and Digestive Diseases Center, International University of Health and Welfare Mita Hospital, Tokyo, Japan. · Department of Medical Oncology, Kyorin University School of Medicine, Tokyo, Japan. · Kyushu University Hospital Cancer Center, Fukuoka, Japan. · Division of Hepatobiliary and Pancreatic Oncology, Kanagawa Cancer Center, Yokohama, Japan. · Department of Gastroenterology, Chiba Cancer Center, Chiba, Japan. · Department of Gastroenterology, Aichi Cancer Center Hospital, Nagoya, Japan. · Division of Pancreatology, Fukuoka Sanno Hospital, Fukuoka, Japan. · Division of Hematology-Oncology, Linkou Chang Gung Memorial Hospital and Chang Gung University, Tao-Yuan, Taiwan, Republic of China. · Department of Oncology, National Taiwan University Hospital, and National Taiwan University Cancer Center, Taipei, Taiwan, Republic of China. · Department of Medical Oncology, Hirosaki University Graduate School of Medicine, Aomori, Japan. · Department of Integrated Science and Engineering for Sustainable Society, Chuo University, Tokyo, Japan. · Department of Surgery, Shimonoseki City Hospital, Shimonoseki, Japan. ·J Cancer Res Clin Oncol · Pubmed #28210843.

ABSTRACT: PURPOSE: The GEST study showed non-inferiority of S-1 but not superiority of gemcitabine plus S-1 (GS) to gemcitabine alone for overall survival with the data by the cut-off date of 31st July in 2010 for chemo-naïve patients with advanced pancreatic cancer. We considered it important to determine whether S-1 maintains non-inferiority after a long-term follow-up in the GEST study and to obtain a firm positive conclusion. In addition, it may be an interesting challenge to explore the efficacious profile of GS in the long-term follow-up study. Using the data from the follow-up period, background and efficacy in patients from Taiwan and Japan, as well as the rates of tumor shrinkage in locally advanced and metastatic patients (Waterfall plot) were also analyzed. METHODS: The results of the primary analysis were reconfirmed, and subset analysis of overall survival and progression-free survival was performed based on the overall survival data updated by the cut-off date of 31st July in 2011. RESULTS: The median follow-up period was 29.8 months, and 795 deaths occurred (95.6%). The median overall survival was 8.8 months for gemcitabine, 9.7 months for S-1 (hazard ratio [HR], 0.96; 97.5% confidence interval [CI], 0.79-1.17), and 9.9 months for GS (HR 0.91; 97.5% CI 0.75-1.11). In patients with performance status (PS) 0, the median overall survival was 9.8 months for gemcitabine, 10.9 months for S-1, and 10.5 months for GS. In patients with PS 1, the median overall survival was 6.2 months for gemcitabine, 6.3 months for S-1, and 9.6 months for GS. CONCLUSION: Our survey reconfirmed the non-inferiority of S-1 to gemcitabine and showed S-1 can be used as one of the standard treatment options for advanced pancreatic cancer. TRIAL REGISTRATION: ClinicalTrials.gov: NCT00498225.

2 Clinical Trial Randomised phase II trial of S-1 plus oxaliplatin vs S-1 in patients with gemcitabine-refractory pancreatic cancer. 2015

Ohkawa, S / Okusaka, T / Isayama, H / Fukutomi, A / Yamaguchi, K / Ikeda, M / Funakoshi, A / Nagase, M / Hamamoto, Y / Nakamori, S / Tsuchiya, Y / Baba, H / Ishii, H / Omuro, Y / Sho, M / Matsumoto, S / Yamada, N / Yanagimoto, H / Unno, M / Ichikawa, Y / Takahashi, S / Watanabe, G / Wakabayashi, G / Egawa, N / Tsuda, M / Hosotani, R / Hamada, C / Hyodo, I. ·Department of Hepatobiliary and Pancreatic Oncology, Kanagawa Cancer Center, 2-3-2, Nakao, Asahi-ku, Yokohama, Kanagawa 241-8515, Japan. · Department of Hepatobiliary and Pancreatic Oncology, National Cancer Center Hospital, 5-1-1, Tsukiji, Chuo-ku, Tokyo 104-0045, Japan. · Department of Gastroenterology, Graduate School of Medicine, University of Tokyo Hospital, 7-3-1, Hongo, Bunkyo-ku, Tokyo 113-8655, Japan. · Department of Gastrointestinal Oncology, Shizuoka Cancer Center, 1007, Shimonagakubo, Nagaizumi-cho Sunto-gun, Shizuoka 411-8777, Japan. · Department of Gastroenterology, Saitama Cancer Center, 780, Komuro, Inamachi, Kitaadachi-gun, Saitama 362-0806, Japan. · Department of Hepatobiliary and Pancreatic Oncology, National Cancer Center Hospital East, 6-5-1, Kashiwanoha, Kashiwa, Chiba 277-8577, Japan. · Department of Gastroenterology, National Hospital Organization Kyushu Cancer Center, 3-1-1, Notame, Minami-ku, Fukuoka 811-1395, Japan. · Department of Chemotherapy, Japanese Red Cross Nagoya Daiichi Hospital, 15-1, Michishita-cho, Nakamura-ku, Nagoya, Aichi 453-8511, Japan. · Department of Internal Medicine, Keio University Hospital, 35, Shinanomachi, Shinjuku-ku, Tokyo 160-8582, Japan. · Department of Hepatobiliary-Pancreatic Surgery, Osaka National Hospital, 2-1-14, Hoenzaka, Chuo-ku, Osaka 540-0006, Japan. · Department of Surgery, Niigata Cancer Center, 2-15-3, Kawagishi-cho, Chuo-ku, Niigata 951-8566, Japan. · Department of Digestive Surgery, Kumamoto University Hospital, 1-1-1, Honjo, Chuo-ku, Kumamoto 860-8556, Japan. · Department of Gastroenterology, Cancer Institute Hospital of JFCR, 3-8-31, Ariake, Koto-ku, Tokyo 135-8550, Japan. · Department of Chemotherapy, Tokyo Metropolitan Cancer and Infectious Diseases Center Komagome Hospital, 3-18-22, Honkomagome, Bunkyo-ku, Tokyo 113-8677, Japan. · Department of Surgery, Nara Medical University Hospital, 840, Shijo-cho, Kashihara, Nara 634-8522, Japan. · Department of Clinical Oncology, Kyoto University Hospital, 54, Kawahara-cho, Shogoin, Sakyo-ku Kyoto 606-8507, Japan. · Department of Surgical Oncology, Osaka City University Graduate School of Medicine, 1-4-3, Asahimachi, Abeno-ku, Osaka 545-8585, Japan. · Department of Surgery, Kansai Medical University Hirakata Hospital, 2-3-1, Shinmachi, Hirakata, Osaka 573-1191, Japan. · Department of Hepatobiliary-Pancreatic Surgery, Tohoku University Hospital, 1-1, Seiryomachi, Aoba-ku, Sendai, Miyagi 980-8574, Japan. · Department of Gastroenterological Surgery, Yokohama City University Hospital, 3-9, Fukuura, Kanazawa-ku, Yokohama, Kanagawa 236-0004, Japan. · Department of Clinical Oncology, Tohoku University Hospital, 1-1, Seiryo-machi, Aoba-ku, Sendai, Miyagi 980-8574, Japan. · Department of Digestive Surgery, Toranomon Hospital, 2-2-2, Toranomon, Minato-ku, Tokyo 105-8470, Japan. · Department of Surgery, Iwate Medical University Hospital, 19-1, Uchimaru, Morioka, Iwate 020-8505, Japan. · Department of Internal Medicine, Tokyo Metropolitan Matsuzawa Hospital, 2-1-1, Kamikitazawa, Setagaya-ku, Tokyo 156-0057, Japan. · Department of Gastroenterological Oncology, Hyogo Cancer Center, 13-70, Kitaoji-cho, Akashi, Hyogo, 673-8558, Japan. · Department of Surgery, Kobe City Medical Center General Hospital, 2-1-1, Minatojimanakamachi, Chuo-ku, Kobe, Hyogo 650-0047, Japan. · Department of Management Science, Tokyo University of Science, 1-3, Kagurazaka, Shinjuku-ku, Tokyo, 162-8601, Japan. · Department of Gastroenterology, University of Tsukuba, 1-1-1, Tennodai, Tsukuba, Ibaraki 305-8577, Japan. ·Br J Cancer · Pubmed #25880004.

ABSTRACT: BACKGROUND: This randomised, open-label, multicenter phase II study compared progression-free survival (PFS) of S-1 plus oxaliplatin (SOX) with that of S-1 alone in patients with gemcitabine-refractory pancreatic cancer. METHODS: Patients with confirmed progressive disease following the first-line treatment with a gemcitabine-based regimen were randomised to receive either S-1 (80/100/120 mg day(-1) based on body surface area (BSA), orally, days 1-28, every 6 weeks) or SOX (S-1 80/100/120 mg day(-1) based on BSA, orally, days 1-14, plus oxaliplatin 100 mg m(-2), intravenously, day 1, every 3 weeks). The primary end point was PFS. RESULTS: Between January 2009 and July 2010, 271 patients were randomly allocated to either S-1 (n=135) or SOX (n=136). Median PFS for S-1 and SOX were 2.8 and 3.0 months, respectively (hazard ratio (HR)=0.84; 95% confidence interval (CI), 0.65-1.08; stratified log-rank test P=0.18). Median overall survival (OS) was 6.9 vs 7.4 months (HR=1.03; 95% CI, 0.79-1.34; stratified log-rank test P=0.82). The response rate (RR) was 11.5% vs 20.9% (P=0.04). The major grade 3/4 toxicities (S-1 and SOX) were neutropenia (11.4% and 8.1%), thrombocytopenia (4.5% and 10.3%) and anorexia (12.9% and 14.7%). CONCLUSIONS: Although SOX showed an advantage in RR, it provided no significant improvement in PFS or OS compared with S-1 alone.

3 Clinical Trial Randomized phase III study of gemcitabine plus S-1, S-1 alone, or gemcitabine alone in patients with locally advanced and metastatic pancreatic cancer in Japan and Taiwan: GEST study. 2013

Ueno, Hideki / Ioka, Tatsuya / Ikeda, Masafumi / Ohkawa, Shinichi / Yanagimoto, Hiroaki / Boku, Narikazu / Fukutomi, Akira / Sugimori, Kazuya / Baba, Hideo / Yamao, Kenji / Shimamura, Tomotaka / Sho, Masayuki / Kitano, Masayuki / Cheng, Ann-Lii / Mizumoto, Kazuhiro / Chen, Jen-Shi / Furuse, Junji / Funakoshi, Akihiro / Hatori, Takashi / Yamaguchi, Taketo / Egawa, Shinichi / Sato, Atsushi / Ohashi, Yasuo / Okusaka, Takuji / Tanaka, Masao. ·Taiho Pharmaceutical, Tokyo, Japan. ·J Clin Oncol · Pubmed #23547081.

ABSTRACT: PURPOSE: The present phase III study was designed to investigate the noninferiority of S-1 alone and superiority of gemcitabine plus S-1 compared with gemcitabine alone with respect to overall survival. PATIENTS AND METHODS: The participants were chemotherapy-naive patients with locally advanced or metastatic pancreatic cancer. Patients were randomly assigned to receive only gemcitabine (1,000 mg/m(2) on days 1, 8, and 15 of a 28-day cycle), only S-1 (80, 100, or 120 mg/d according to body-surface area on days 1 through 28 of a 42-day cycle), or gemcitabine plus S-1 (gemcitabine 1,000 mg/m(2) on days 1 and 8 plus S-1 60, 80, or 100 mg/d according to body-surface area on days 1 through 14 of a 21-day cycle). RESULTS: In the total of 834 enrolled patients, median overall survival was 8.8 months in the gemcitabine group, 9.7 months in the S-1 group, and 10.1 months in the gemcitabine plus S-1 group. The noninferiority of S-1 to gemcitabine was demonstrated (hazard ratio, 0.96; 97.5% CI, 0.78 to 1.18; P < .001 for noninferiority), whereas the superiority of gemcitabine plus S-1 was not (hazard ratio, 0.88; 97.5% CI, 0.71 to 1.08; P = .15). All treatments were generally well tolerated, although hematologic and GI toxicities were more severe in the gemcitabine plus S-1 group than in the gemcitabine group. CONCLUSION: Monotherapy with S-1 demonstrated noninferiority to gemcitabine in overall survival with good tolerability and presents a convenient oral alternative for locally advanced and metastatic pancreatic cancer.

4 Clinical Trial Multicenter phase II study of gemcitabine and S-1 combination therapy (GS Therapy) in patients with metastatic pancreatic cancer. 2011

Ueno, Hideki / Okusaka, Takuji / Furuse, Junji / Yamao, Kenji / Funakoshi, Akihiro / Boku, Narikazu / Ohkawa, Shinichi / Yokosuka, Osamu / Tanaka, Katsuaki / Moriyasu, Fuminori / Nakamori, Shoji / Sato, Tosiya. ·Hepatobiliary and Pancreatic Oncology Division, National Cancer Center Hospital, 5-1-1 Tsukiji, Chuo-ku, Tokyo 104-0045, Japan. hiueno@ncc.go.jp ·Jpn J Clin Oncol · Pubmed #21715364.

ABSTRACT: OBJECTIVE: The aim of this multicenter Phase II study was to assess the efficacy and toxicity of gemcitabine and S-1 combination therapy for metastatic pancreatic cancer. METHODS: Chemotherapy-naïve patients with histologically or cytologically proven metastatic pancreatic adenocarcinoma were eligible for this study. Gemcitabine was administered at a dose of 1000 mg/m(2) over 30 min on days 1 and 8, and oral S-1 at a dose of 40 mg/m(2) twice daily from days 1 to 14, repeated every 3 weeks. RESULTS: A total of 55 patients were included and the efficacy and toxicity were analyzed in 54 patients who received at least one dose of gemcitabine and S-1 combination therapy. Although no complete response was seen, a partial response was achieved in 24 patients, resulting in an overall response rate of 44.4% (95% confidence interval: 30.9-58.6%). The median progression-free survival was 5.9 months (95% confidence interval: 4.1-6.9 months) and the median overall survival was 10.1 months (95% confidence interval: 8.5-10.8 months) with a 1-year survival rate of 33.0%. The major Grade 3-4 toxicities were neutropenia (80%), leucopenia (59%), thrombocytopenia (22%), anorexia (17%) and rash (7%). Hematological toxicity was mostly transient and there was only one episode of febrile neutropenia ≥Grade 3. CONCLUSIONS: Gemcitabine and S-1 combination therapy produced a high response rate with good survival in patients with metastatic pancreatic cancer. A randomized Phase III study to confirm the efficacy of gemcitabine and S-1 combination therapy is ongoing.

5 Clinical Trial Axitinib plus gemcitabine versus placebo plus gemcitabine in patients with advanced pancreatic adenocarcinoma: a double-blind randomised phase 3 study. 2011

Kindler, Hedy L / Ioka, Tatsuya / Richel, Dirk J / Bennouna, Jaafar / Létourneau, Richard / Okusaka, Takuji / Funakoshi, Akihiro / Furuse, Junji / Park, Young Suk / Ohkawa, Shinichi / Springett, Gregory M / Wasan, Harpreet S / Trask, Peter C / Bycott, Paul / Ricart, Alejandro D / Kim, Sinil / Van Cutsem, Eric. ·University of Chicago Comprehensive Cancer Center, Chicago, IL 60637, USA. hkindler@medicine.bsd.uchicago.edu ·Lancet Oncol · Pubmed #21306953.

ABSTRACT: BACKGROUND: Axitinib is a potent, selective inhibitor of vascular endothelial growth factor (VEGF) receptors 1, 2, and 3. A randomised phase 2 trial of gemcitabine with or without axitinib in advanced pancreatic cancer suggested increased overall survival in axitinib-treated patients. On the basis of these results, we aimed to assess the effect of treatment with gemcitabine plus axitinib on overall survival in a phase 3 trial. METHODS: In this double-blind, placebo-controlled, phase 3 study, eligible patients had metastatic or locally advanced pancreatic adenocarcinoma, no uncontrolled hypertension or venous thrombosis, and Eastern Cooperative Oncology Group performance status 0 or 1. Patients, stratified by disease extent (metastatic vs locally advanced), were randomly assigned (1:1) to receive gemcitabine 1000 mg/m(2) intravenously on days 1, 8, and 15 every 28 days plus either axitinib or placebo. Axitinib or placebo were administered orally with food at a starting dose of 5 mg twice a day, which could be dose-titrated up to 10 mg twice daily if well tolerated. A centralised randomisation procedure was used to assign patients to each treatment group, with randomised permuted blocks within strata. Patients, investigators, and the trial sponsor were masked to treatment assignments. The primary endpoint was overall survival. All efficacy analyses were done in all patients assigned to treatment groups for whom data were available; safety and treatment administration and compliance assessments were based on treatment received. This study is registered at ClinicalTrials.gov, number NCT00471146. FINDINGS: Between July 27, 2007, and Oct 31, 2008, 632 patients were enrolled and assigned to treatment groups (316 axitinib, 316 placebo). At an interim analysis in January, 2009, the independent data monitoring committee concluded that the futility boundary had been crossed. Median overall survival was 8·5 months (95% CI 6·9-9·5) for gemcitabine plus axitinib (n=314, data missing for two patients) and 8·3 months (6·9-10·3) for gemcitabine plus placebo (n=316; hazard ratio 1·014, 95% CI 0·786-1·309; one-sided p=0·5436). The most common grade 3 or higher adverse events for gemcitabine plus axitinib and gemcitabine plus placebo were hypertension (20 [7%] and 5 [2%] events, respectively), abdominal pain (20 [7%] and 17 [6%]), fatigue (27 [9%] and 21 [7%]), and anorexia (19 [6%] and 11 [4%]). INTERPRETATION: The addition of axitinib to gemcitabine does not improve overall survival in advanced pancreatic cancer. These results add to increasing evidence that targeting of VEGF signalling is an ineffective strategy in this disease. FUNDING: Pfizer.

6 Clinical Trial Phase II study of erlotinib plus gemcitabine in Japanese patients with unresectable pancreatic cancer. 2011

Okusaka, Takuji / Furuse, Junji / Funakoshi, Akihiro / Ioka, Tatsuya / Yamao, Kenji / Ohkawa, Shinichi / Boku, Narikazu / Komatsu, Yoshito / Nakamori, Shoji / Iguchi, Haruo / Ito, Tetsuhide / Nakagawa, Kazuhiko / Nakachi, Kohei. ·National Cancer Center Hospital, Tokyo, Japan. tokusaka@ncc.go.jp ·Cancer Sci · Pubmed #21175992.

ABSTRACT: Erlotinib combined with gemcitabine has not been evaluated in Japanese patients with unresectable pancreatic cancer. This two-step phase II study assessed the safety and pharmacokinetics of erlotinib 100 mg/day (oral) plus gemcitabine 1000 mg/m(2) (i.v. days 1, 8, 15) in a 28-day cycle in the first step, and efficacy and safety in the second step. The primary end-point was safety. One hundred and seven patients were enrolled (first step, n = 6; second step, n = 101). The most common adverse event was RASH (compiled using the preferred terms rash, acne, exfoliative rash, dermatitis acneiform, erythema, eczema, dermatitis and pustular rash) in 93.4% of patients. One treatment-related death occurred. While interstitial lung disease-like events were reported in nine patients (8.5%; grade 1/2/3, 3.8/2.8/1.9%), all patients recovered or improved. The median overall survival, the 1-year survival rate and median progression-free survival were 9.23 months, 33.0% and 3.48 months, respectively. The overall response and disease control rates were 20.3% and 50.0%, respectively. In Japanese patients with unresectable pancreatic cancer, erlotinib plus gemcitabine had acceptable toxicity and efficacy that was not inferior to that seen in Western patients.

7 Article [Various cancers related type 2 diabetes mellitus: Pancreatic cancer]. 2016

Funakoshi, Akihiro. · ·Nihon Rinsho · Pubmed #27266128.

ABSTRACT: -- No abstract --

8 Article A humanized anti-IGF-1R monoclonal antibody (R1507) and/or metformin enhance gemcitabine-induced apoptosis in pancreatic cancer cells. 2012

Kawanami, Takako / Takiguchi, Soichi / Ikeda, Noriko / Funakoshi, Akihiro. ·Institute for Clinical Research, National Kyushu Cancer Center, Fukuoka, Japan. ·Oncol Rep · Pubmed #22200743.

ABSTRACT: Pancreatic cancer is a disease with a dismal prognosis and treatment options are limited. This study investigated the interaction of gemcitabine with R1507 and/or metformin and the induction of an inhibitor of apoptosis protein by this com-bination. Pancreatic cancer cells were treated with gemcitabine, R1507 and metformin alone or in combination. The effects of treatments were evaluated for cell proliferation, apoptosis, and the expression of genes related to inhibition of apoptosis and chemotherapy resistance. Combination of gemcitabine with R1507 and/or metformin additively interacted with the inhibition of cell proliferation in human pancreatic ductal adenocarcinoma cell lines, SUIT-2 and MIAPaCa-2 with differential gemcitabine resistance, and assessment of apoptosis demonstrated that drug associations increased the apoptotic index in both cell lines. Treatment with gemcitabine induced the expression of survivin and XIAP in both cell lines, indicating the induction of chemoresistance. In conclusion, these data demonstrate that the combination of gemcitabine with R1507 and/or metformin has an additive effect in pancreatic cancer cell lines with differential sensitivity to gemcitabine; however, gemcitabine may induce chemotherapy resistance.

9 Article [A case of pancreatic well-differentiated neuroendocrine carcinoma surviving 8 years and 5 months with treatments for multiple liver tumors diagnosed as carcinoid tumor]. 2011

Okumura, Yukihiko / Sugimoto, Rie / Taguchi, Kenichi / Lee, Lingaku / Ueda, Keijiro / Furukawa, Masayuki / Funakoshi, Akihiro. ·Dept. of Gastroenterology, National Kyushu Cancer Center. ·Gan To Kagaku Ryoho · Pubmed #21677505.

ABSTRACT: The case was a 58-year-old woman who visited our hospital for a thorough examination after multiple liver tumors were found in her at a nearby hospital. By liver tumor biopsy, we diagnosed them as carcinoid. Bone scintigraphy showed an abnormal accumulation in the external left scapula and in both of her hip joints, but the primary lesion was unclear. She died 8 years and 5 months after disease onset from deterioration of liver lesions, inspite of our treatments, such as gemcitabine administration of systemic chemotherapy, transcatheter arterial chemoembolization for liver lesions, and radiation therapy for bone lesions. Pathological anatomy suggested a pancreatic, well-differentiated neuroendocrine carcinoma.

10 Article Amphiregulin regulates the activation of ERK and Akt through epidermal growth factor receptor and HER3 signals involved in the progression of pancreatic cancer. 2010

Yotsumoto, Fusanori / Fukami, Tatsuya / Yagi, Hiroshi / Funakoshi, Akihiro / Yoshizato, Toshiyuki / Kuroki, Masahide / Miyamoto, Shingo. ·Department of Biochemistry, School of Medicine Center for Advanced Molecular Medicine Department of Obstetrics & Gynecology, School of Medicine, Fukuoka University, Fukuoka, Japan. ·Cancer Sci · Pubmed #20726858.

ABSTRACT: Pancreatic cancer is one of the most lethal malignancies. Epidermal growth factor receptor (EGFR), HER3, Akt, and amphiregulin have been recognized as targets for pancreatic cancer therapy. Although gemcitabine + erlotinib has been the recommended chemotherapy for pancreatic cancer, the prognosis is extremely poor. The development of molecularly targeted therapies has been required for patients with pancreatic cancer. To assess the validation of amphiregulin as a target for pancreatic cancer therapy, we examined its expression in pancreatic cancer using real-time PCR analyses and ELISA. We also measured the apoptotic cell rate using TUNEL assays. In addition, alterations in signaling pathways were detected by immunoblotting analyses. Treatment with gemcitabine, which reduced the cell viability and augmented the cell apoptotic rate, activated and subsequently attenuated ERK and EGFR signals. However, gemcitabine, paclitaxel, or cisplatin treatment enhanced the Akt activation, heterodimer formation of EGFR with HER3, and secretion of amphiregulin, indicating that the presence of gemcitabine promoted the activity of targeted molecules including amphiregulin, Akt, and HER3 for pancreatic cancer therapy. Combined treatment with an inhibitor for amphiregulin and gemcitabine, paclitaxel, or cisplatin induced synergistic antitumor effects, accompanied by the suppression of Akt and ERK activation. Blockade of amphiregulin suppressed the activities of EGFR, HER3, and Akt and the expression of amphiregulin itself. According to this evidence, combination chemotherapy of conventional anticancer drugs plus an inhibitor for amphiregulin would allow us to provide more favorable clinical outcomes for patients with pancreatic cancer.

11 Article Association of aldehyde dehydrogenase 2 gene polymorphism with pancreatic cancer but not colon cancer. 2010

Miyasaka, Kyoko / Hosoya, Hiroko / Tanaka, Yasuo / Uegaki, Satoko / Kino, Kenji / Shimokata, Hiroshi / Kawanami, Takako / Funakoshi, Akihiro. ·Department of Clinical Physiology, Tokyo Metropolitan Institute of Gerontology, Tokyo Metropolitan Geriatric Hospital, Tokyo, Japan. miyasakak@tokyo-kasei.ac.jp ·Geriatr Gerontol Int · Pubmed #20590827.

ABSTRACT: AIMS: Most of the acetaldehyde, a recognized animal carcinogen, generated during alcohol metabolism is eliminated by liver mitochondrial aldehyde dehydrogenase 2 (ALDH2). More than 40% of Japanese people have the inactive form of ALDH2, and inactive ALDH2 is a risk factor for multiple cancer of the esophagus, as well as head and neck cancer. Possible associations between pancreatic cancer and ALDH2 gene polymorphism, as well as between colon cancer and ALDH2 gene polymorphism, in conjunction with smoking and/or drinking habits, were examined in a Japanese population. METHODS: Patients with pancreatic cancer (n = 187) and with colon cancer (n = 49) were examined. The drinking (5 g ethanol consumption/day) and/or smoking habits as well as ALDH2 gene polymorphism were examined. The age-matched control subjects were recruited in the NILS Longitudinal Study of Aging (LSA). RESULTS: Aging, smoking and inactive ALDH2, but not alcohol, are independent risk factors for pancreatic cancer. The frequency of smoking habits tended to be higher in patients with colon cancer compared with the patients without cancer. However, age, body mass index or the distribution of ALDH2 genotypes did not differ significantly among the patients with colon cancer, colon polyps and others. CONCLUSIONS: Inactive ALDH2 is an independent risk factor for pancreatic cancer, but inactive ALDH2 might not be a risk for colon cancer.

12 Minor Giardiasis in the pancreas accompanied by pancreatic cancer. 2011

Furukawa, Masayuki / Lee, Lingaku / Ikegami, Toru / Maeda, Takashi / Nishiyama, Kenichi / Itaba, Souichi / Funakoshi, Akihiro. · ·Pancreas · Pubmed #21160381.

ABSTRACT: -- No abstract --