Faculty Profiles - Tanioka Maki

Papers - Tanioka Maki

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HER2陽性乳癌に対するPaclitaxel+trastuzumabとFEC療法併用術前化学療法(KBCOG05)

高尾信太郎, 広利浩一, 前川陽子, 田根香織, 谷岡真樹, 松本光史, 宮下勝, 奥野敏隆, 小西宗治, 重岡靖, 三好康雄

日本癌治療学会誌 48 ( 3 ) 1579 - 1579 2013.9

A randomised, placebo-controlled, double-blind study of aprepitant in nondrinking women younger than 70 years receiving moderately emetogenic chemotherapy.

Tanioka M, Kitao A, Matsumoto K, Shibata N, Yamaguchi S, Fujiwara K, Minami H, Katakami N, Morita S, Negoro S

2013.8

A microarray-based gene expression analysis to identify diagnostic biomarkers for unknown primary cancer. International journal

Kurahashi I, Fujita Y, Arao T, Kurata T, Koh Y, Sakai K, Matsumoto K, Tanioka M, Takeda K, Takiguchi Y, Yamamoto N, Tsuya A, Matsubara N, Mukai H, Minami H, Chayahara N, Yamanaka Y, Miwa K, Takahashi S, Takahashi S, Nakagawa K, Nishio K

PloS one 8 ( 5 ) e63249 2013

Language：English Publishing type：Research paper (scientific journal)

BACKGROUND: The biological basis for cancer of unknown primary (CUP) at the molecular level remains largely unknown, with no evidence of whether a common biological entity exists. Here, we assessed the possibility of identifying a common diagnostic biomarker for CUP using a microarray gene expression analysis. METHODS: Tumor mRNA samples from 60 patients with CUP were analyzed using the Affymetrix U133A Plus 2.0 GeneChip and were normalized by asinh (hyperbolic arc sine) transformation to construct a mean gene-expression profile specific to CUP. A gene-expression profile specific to non-CUP group was constructed using publicly available raw microarray datasets. The t-tests were performed to compare the CUP with non-CUP groups and the top 59 CUP specific genes with the highest fold change were selected (p-value<0.001). RESULTS: Among the 44 genes that were up-regulated in the CUP group, 6 genes for ribosomal proteins were identified. Two of these genes (RPS7 and RPL11) are known to be involved in the Mdm2-p53 pathway. We also identified several genes related to metastasis and apoptosis, suggesting a biological attribute of CUP. CONCLUSIONS: The protein products of the up-regulated and down-regulated genes identified in this study may be clinically useful as unique biomarkers for CUP.

DOI： 10.1371/journal.pone.0063249

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A phase I study of BMS-690514 in Japanese patients with advanced or metastatic solid tumors. International journal

Nokihara H, Yamamoto N, Yamada Y, Yamada K, Hirata T, Goto Y, Tanioka M, Ikeda Y, Tamura T

Cancer chemotherapy and pharmacology 70 ( 4 ) 559 - 65 2012.10

Language：English Publishing type：Research paper (scientific journal)

PURPOSE: BMS-690514 is a novel oral tyrosine kinase inhibitor of ErbB and vascular endothelial growth factor receptor. This open-label phase I dose-escalation study (ClinicalTrials.gov Identifier: NCT00516451) aimed to assess the safety, preliminary efficacy, pharmacokinetics, and pharmacodynamics of BMS-690514 in Japanese patients with advanced or metastatic solid tumors. METHODS: Patients with advanced or metastatic solid tumors received oral BMS-690514 once daily continuously until disease progression or intolerable toxicity occurred. Dose-limiting toxicity (DLT) was evaluated from the first dose to Day 29. Dose levels at 100 and 200 mg were investigated. Assessments included adverse events, tumor response, pharmacokinetics, pharmacodynamics, 2 [18F] fluoro-2-deoxyglucose positron-emitting tomography, and epidermal growth factor receptor and K-ras mutations. RESULTS: BMS-690514 at the dose of 100 mg (n = 3) or 200 mg (n = 3) was administered once daily to totally nine patients and was well tolerated up to 200 mg. No treatment-related serious adverse events or DLTs were reported. Frequently observed treatment-related AEs were acne, diarrhea, dry skin, hypertension, stomatitis, blood fibrinogen increased, hemoglobin decreased, pruritus, and hypoalbuminemia. These were generally reported as Grade 1 and 2. Five of 9 patients (56 %) had stable disease. Plasma concentrations of BMS-690514 reached Cmax within 3 h and declined with an effective half-life of approximately 10 and 12 h at 100 and 200 mg, respectively. CONCLUSIONS: Oral BMS-690514 was well tolerated in Japanese patients with advanced or metastatic solid tumors up to 200 mg.

DOI： 10.1007/s00280-012-1932-9

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Figitumumab combined with carboplatin and paclitaxel in treatment-naive Japanese patients with advanced non-small cell lung cancer. International journal

Goto Y, Sekine I, Tanioka M, Shibata T, Tanai C, Asahina H, Nokihara H, Yamamoto N, Kunitoh H, Ohe Y, Kikkawa H, Ohki E, Tamura T

Investigational new drugs 30 ( 4 ) 1548 - 56 2012.8

Language：English Publishing type：Research paper (scientific journal)

OBJECTIVES: The insulin-like growth factor (IGF) signaling pathway has been implicated in the pathogenesis of numerous tumor types, including non-small cell lung cancer (NSCLC). Figitumumab is a fully human IgG2 monoclonal antibody against IGF-1 receptor (IGF-1R). METHODS: This phase I, open-label, dose-escalation study (ClinicalTrials.gov: NCT00603538) assessed the safety and tolerability of figitumumab (6, 10 and 20 mg/kg) in combination with carboplatin (area under the curve: 6 mg·min/mL) and paclitaxel (200 mg/m(2)) in Japanese patients (N = 19) with chemotherapy-naïve, advanced NSCLC. Treatments were administered intravenously on day 1 of a 21-day cycle for four to six cycles. Pharmacokinetics, biomarkers, and antitumor activity were also evaluated. RESULTS: Figitumumab in combination with carboplatin and paclitaxel was well tolerated at doses up to 20 mg/kg; no dose-limiting toxicities were observed at this dose level. When given in combination, figitumumab plasma exposure increased in an approximately dose-proportional manner. The approximate 2-fold accumulation following repeated administration supported the 21-day regimen as appropriate for figitumumab administration. Serum total IGF-1 and IGF binding protein-3 concentrations increased following figitumumab dosing, but a clear dose-dependent relationship was not demonstrated. Seven of 18 evaluable patients experienced a partial response. CONCLUSIONS: Figitumumab 20 mg/kg in combination with carboplatin and paclitaxel was well tolerated in chemotherapy-naïve Japanese patients with NSCLC. Further analysis of biomarker data is necessary for the development of figitumumab therapy.

DOI： 10.1007/s10637-011-9715-4

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An open-label, phase 1 study evaluating safety, tolerability, and pharmacokinetics of linifanib (ABT-869) in Japanese patients with solid tumors. International journal

Asahina H, Tamura Y, Nokihara H, Yamamoto N, Seki Y, Shibata T, Goto Y, Tanioka M, Yamada Y, Coates A, Chiu YL, Li X, Pradhan R, Ansell PJ, McKeegan EM, McKee MD, Carlson DM, Tamura T

Cancer chemotherapy and pharmacology 69 ( 6 ) 1477 - 86 2012.6

Language：English Publishing type：Research paper (scientific journal)

PURPOSE: This phase 1 study assessed the safety, tolerability, pharmacokinetics, and preliminary antitumor activity of linifanib in Japanese patients with advanced solid tumors. METHODS: Patients were assigned to one of four sequential cohorts (0.05, 0.10, 0.20, or 0.25 mg/kg) of oral, once-daily linifanib on a 21-day cycle. Adverse events (AEs) were assessed per common terminology criteria for adverse events v3.0; tumor responses were assessed by response evaluation criteria in solid tumors. RESULTS: Eighteen patients were enrolled. Eleven (61%) received ≥3 prior therapies. Dose-limiting toxicities were Grade 3 ALT increase (0.10 mg/kg linifanib) and Grade 1 T-wave inversion (0.25 mg/kg linifanib) requiring dose interruption for >7 days and discontinuation on day 29. The most common linifanib-related AE was hypertension. Other significant treatment-related AEs included proteinuria, fatigue, and palmar-plantar erythrodysaesthesia. Linifanib pharmacokinetics were dose-proportional across 0.10-0.25 mg/kg. Two patients (11.1%) had confirmed partial responses, 12 had a best response of stable disease (11 had stable disease for ≥12 weeks), and four patients were not evaluable due to incomplete data. Four patients (lung cancer, breast cancer, thymic cancer, sarcoma) have continued linifanib for ≥48 weeks (range, 48-96+ weeks). CONCLUSION: Linifanib was well tolerated with promising preliminary clinical activity in Japanese patients. Later-phase global studies examining linifanib efficacy will include Japanese patients.

DOI： 10.1007/s00280-012-1846-6

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Phase I study for ridaforolimus, an oral mTOR inhibitor, in Japanese patients with advanced solid tumors. International journal

Seki Y, Yamamoto N, Tamura Y, Goto Y, Shibata T, Tanioka M, Asahina H, Nokihara H, Yamada Y, Shimamoto T, Noguchi K, Tamura T

Cancer chemotherapy and pharmacology 69 ( 4 ) 1099 - 105 2012.4

Language：English Publishing type：Research paper (scientific journal)

PURPOSE: Ridaforolimus is a non-prodrug mTOR inhibitor. The safety, pharmacokinetics (PK), and antitumor activity of oral ridaforolimus were assessed in Japanese patients with refractory solid tumors. METHODS: Ridaforolimus (20 or 40 mg) was administered as a single dose on Day 1, followed by once daily dosing five times a week for a 3-week cycle beginning on Day 8. Full PK sampling was performed on Days 1 and 26. RESULTS: Thirteen patients (7 at 20 mg and 6 at 40 mg) were enrolled. The median treatment duration was 82 days. The most common drug-related adverse events were stomatitis, hypertriglyceridemia, and proteinuria. Two patients had dose-limiting toxicities (grade 3 stomatitis at 20 mg, and grade 3 anorexia and vomiting at 40 mg). Four patients had grade 1 interstitial pneumonitis. Ridaforolimus in the whole blood was rapidly absorbed and slowly eliminated with a half-life of approximately 56-58 h after a single dose. Two patients (with non-small cell lung cancer and angiosarcoma, respectively) achieved a partial response, and five patients (one with thymic cancer and four with soft tissue sarcomas) had a stable disease for ≥ 16 weeks. CONCLUSIONS: Ridaforolimus was well tolerated up to a dose of 40 mg in Japanese patients. Preliminary evidence of antitumor activity was observed for patients with solid tumors. Further investigation at this dose is warranted.

DOI： 10.1007/s00280-011-1788-4

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A Phase I, dose-finding and pharmacokinetic study of olaparib (AZD2281) in Japanese patients with advanced solid tumors. International journal

Yamamoto N, Nokihara H, Yamada Y, Goto Y, Tanioka M, Shibata T, Yamada K, Asahina H, Kawata T, Shi X, Tamura T

Cancer science 103 ( 3 ) 504 - 9 2012.3

Language：English Publishing type：Research paper (scientific journal)

Olaparib (AZD2281) is an orally active Poly(ADP-ribose) polymerase (PARP) inhibitor with favorable antitumor activity in advanced ovarian and breast cancers with BRCA1/2 mutations in Western (USA and European) studies. This Phase I dose-finding study evaluated the tolerability, pharmacokinetics, PARP inhibitory activity, and antitumor activity of olaparib in Japanese patients with solid tumors. Olaparib was administered as a single-dose on day 1, followed by twice-daily dosing for 28 days from 48 h after a single dose. Doses were escalated from 100 mg b.i.d. in successive cohorts, up to a maximum of 400 mg b.i.d. The present study enrolled 12 patients (n = 3, 3, and 6 in 100, 200 and 400-mg b.i.d. levels, respectively). The most common adverse events were nausea, increased blood creatinine, decreased hematocrit, leukopenia and lymphopenia; dose-limiting toxicities were not observed up to and including the 400-mg b.i.d. dose level. Following twice-daily dosing, olaparib showed no marked increase in exposure at steady state over that expected from the single-dose pharmacokinetics. PARP-1 inhibition was observed from the 100-mg b.i.d. dose level in peripheral blood mononuclear cells from 6 h post-dose on day 1 during the multiple-dosing period. A patient with metastatic breast cancer (100 mg b.i.d.) had a partial response for 13 months and four patients (two each in the 200 and 400-mg b.i.d. levels) had stable disease >8 weeks. Olaparib was well tolerated up to the 400-mg b.i.d. dose in Japanese patients with solid tumors. Preliminary evidence of antitumor activity was observed.

DOI： 10.1111/j.1349-7006.2011.02179.x

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Second platinum therapy in patients with uterine cervical cancer previously treated with platinum chemotherapy. International journal

Tanioka M, Katsumata N, Yonemori K, Kouno T, Shimizu C, Tamura K, Ando M, Fujiwara Y

Cancer chemotherapy and pharmacology 68 ( 2 ) 337 - 42 2011.8

Language：English Publishing type：Research paper (scientific journal)

BACKGROUND: After the front-line platinum-based regimens including concurrent chemoradiotherapy (CCRT) in patients with advanced or recurrent cervical cancer, platinum-based regimens are often used again. PATIENTS AND METHODS: We retrospectively studied the predictors of response to second platinum therapy and prognostic factors of survival of 65 women who had received ≥ 2 platinum-based regimens in order to evaluate the effects of platinum-free interval (PFI), i.e., the interval between the platinum therapies. RESULTS: The median survival and PFI were 11.0 and 11.1 months, respectively. The response rate was 42% overall and 36% in the 36 patients who had received CCRT. The response rate increased in parallel with the length of the PFI. Multivariate analyses showed a PFI for ≥ 12 months (odds ratio [OR] = 0.20), a PS of 0 (OR = 0.16) and a maximum tumor diameter ≤ 30 mm (OR = 0.18) were predictive of response. Multivariate analyses also revealed a PFI for ≥ 6 months (hazard ratio [HR] = 0.44) and a PS of 0 (HR = 0.30) were prognostic of survival. CONCLUSION: Our exploratory study demonstrated that PFI has both predictive and prognostic value for second platinum therapy in patients with advanced or recurrent cervical cancer.

DOI： 10.1007/s00280-010-1494-7

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Phase I study of LY2181308, an antisense oligonucleotide against survivin, in patients with advanced solid tumors.

Tanioka M, Nokihara H, Yamamoto N, Yamada Y, Yamada K, Goto Y, Fujimoto T, Sekiguchi R, Uenaka K, Callies S, Tamura T

2011.8

Clinical characteristics and outcomes of women with stage IV endometrial cancer.

Tanioka M, Katsumata N, Sasajima Y, Ikeda S, Kato T, Onda T, Kasamatsu T, Fujiwara Y

2010.12

Predictors of recurrence in breast cancer patients with a pathologic complete response after neoadjuvant chemotherapy.

Tanioka M, Shimizu C, Yonemori K, Yoshimura K, Tamura K, Kouno T, Ando M, Katsumata N, Tsuda H, Kinoshita T, Fujiwara Y

2010.7

Phase 1 open-label study evaluating pharmacokinetics, safety, and tolerability of linifanib in Japanese patients with solid tumors Reviewed

Tomohide Tamura, Noboru Yamamoto, Hiroshi Nokihara, Yasuhide Yamada, Hajime Asahina, Takashi Shibata, Yasushi Goto, Maki Tanioka, Yosuke Tamura, Yoshitaka Seki, Yi-Lin Chiu, Neeraj Gupta, Dawn Carlson

MOLECULAR CANCER THERAPEUTICS 8 ( 12 ) 2009.12

Establishment of the acute myeloid leukemia cell line Kasumi-6 from a patient with a dominant-negative mutation in the DNA-binding region of the C/EBPalpha gene. International journal

Asou H, Gombart AF, Takeuchi S, Tanaka H, Tanioka M, Matsui H, Kimura A, Inaba T, Koeffler HP

Genes, chromosomes & cancer 36 ( 2 ) 167 - 74 2003.2

Language：English Publishing type：Research paper (scientific journal)

A myeloid leukemia cell line designated Kasumi-6 was established from the bone marrow cells of an individual with acute myeloid leukemia, subtype M2. Both the original leukemic cells and the Kasumi-6 cell line harbor a hemizygous point mutation in the gene encoding the CCAAT/enhancer binding protein alpha (C/EBPalpha), a critical myeloid transcriptional factor. The C to G transition at nucleotide 1063 of the C/EBPalpha gene results in amino acid transition R305P in the fork or hinge region between the DNA-binding basic region and the leucine zipper dimerization domain of the C/EBPalpha protein. The Kasumi-6 cells expressed both the p42 and p30 isoforms of the C/EBPalpha protein endogenously, but electrophoretic mobility shift assays demonstrated an absence of C/EBPalpha binding to its respective site. Exogenous expression of the mutant form of C/EBPalpha demonstrated that it was unable to bind DNA and activate transcription from a G-CSF receptor-luciferase reporter construct. Furthermore, coexpression of the wild-type and mutant forms revealed that the mutant form repressed reporter gene activation by the wild type in a dose-responsive manner. This was concomitant with a dose-responsive decrease in wild-type protein binding to the G-CSF receptor C/EBP site. The data suggest that the R305P alteration confers a dominant-negative property on the mutant C/EBPalpha protein whereby the mutant polypeptide heterodimerizes with the wild-type polypeptide and prevents it from binding to DNA, thus blocking transcriptional activation. The Kasumi-6 cell line can serve as a model to study the cellular and molecular biology of the non-t(8;21) M2 type of myeloid leukemia and can elucidate the role of mutated C/EBPalpha in leukemogenesis.

DOI： 10.1002/gcc.10161

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