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1. Infliximab dose adjustment can improve the clinical and radiographic outcomes of rheumatoid arthritis patients: REVIVE study results

Author

Nozaki Y, Nagare Y, Ashida C, Tomita D, Okada A, Inoue A, Kinoshita K, Funauchi M, and Matsumura I

Subjects
rheumatoid arthritis, DAS28, infliximab, mTSS, dose adjustment, REVIVE, Medicine (General), R5-920
Abstract

Yuji Nozaki, Yasuaki Nagare, Chisato Ashida, Daisuke Tomita, Akinori Okada, Asuka Inoue, Koji Kinoshita, Masanori Funauchi, Itaru Matsumura Department of Hematology and Rheumatology, Kindai University School of Medicine, Osaka, Japan Purpose: We evaluated the clinical responses and radiographic outcomes of 90 patients with rheumatoid arthritis (RA) undergoing continuous or dose-adjusted infliximab treatment over 104 weeks.Patients and methods: Patients received 3 mg/kg infliximab continuously (the contin group; n=50), or the dose escalation and de-escalation of infliximab (3, 6, and 10 mg/kg) from week 14 (the adjusted group; n=40) based on the patient’s Disease Activity Score in 28 joints (DAS28). The retention rate, clinical response, and radiographic assessment were determined at week 104.Results: The contin and adjusted groups’ retention rates at week 104 were 56.8 and 66.7%, and the groups’ low disease activity in the DAS28 was 39.1 and 66.7%, respectively. Remission based on the DAS28 and the American College of Rheumatology (ACR)/European League against Rheumatism (EULAR) Boolean-based criteria was significantly increased in the adjusted group. In the radiographic assessment, there was also a significant reduction in the mean changes in total Sharp score. The cumulative rates of any adverse effects showed no significant difference between the groups.Conclusion: In an assessment of adequate DAS28 results, the RA patients who did not respond to the initial dose of infliximab showed improved clinical responses and radiographic assessment after a dose adjustment of infliximab, without an increased risk of serious adverse events. Keywords: rheumatoid arthritis, DAS28, infliximab, mTSS, dose adjustment, REVIVE

Published
2018

3. Venetoclax plus low-dose cytarabine in Japanese patients with untreated acute myeloid leukaemia ineligible for intensive chemotherapy

Author

Yamauchi, T, Yoshida, C, Usuki, K, Takada, S, Matsumura, I, Dobashi, N, Miyazaki, Y, Miyamoto, T, Iida, H, Asou, N, Kuroda, J, Ichikawa, S, Komatsu, N, Mendes, W, Honda, H, Okubo, S, Kurokawa, M, Jiang, Q, Wei, A, Ishizawa, K, Yamauchi, T, Yoshida, C, Usuki, K, Takada, S, Matsumura, I, Dobashi, N, Miyazaki, Y, Miyamoto, T, Iida, H, Asou, N, Kuroda, J, Ichikawa, S, Komatsu, N, Mendes, W, Honda, H, Okubo, S, Kurokawa, M, Jiang, Q, Wei, A, and Ishizawa, K

Abstract

BACKGROUND: In a multinational phase 3 trial (VIALE-C), venetoclax plus low-dose cytarabine prolonged overall survival vs placebo plus low-dose cytarabine in patients with newly diagnosed acute myeloid leukaemia ineligible for intensive chemotherapy, although it was not statistically significant. Herein, we assess the benefit of venetoclax plus low-dose cytarabine in the Japanese subgroup of VIALE-C patients (n = 27). METHODS: VIALE-C, a randomized (2:1), double-blind study (NCT03069352), enrolled untreated patients (≥18 years) with acute myeloid leukaemia. Patients received venetoclax (600 mg days 1-28, 4-day ramp-up in cycle 1) or placebo in 28-day cycles with low-dose cytarabine (20 mg/m2 days 1-10). The primary endpoint was median overall survival. RESULTS: In the Japanese subgroup, at a 6-month follow-up from the primary analysis, median overall survival for venetoclax (n = 18) and placebo (n = 9), plus low-dose cytarabine, was 4.7 and 8.1 months, respectively (hazard ratio, 0.928, 95% confidence intervals : 0.399, 2.156). The rate of complete remission plus complete remission with incomplete blood count recovery was higher with venetoclax plus low-dose cytarabine (44.4%) vs placebo plus low-dose cytarabine (11.1%). All patients experienced at least 1 adverse event. The most common grade ≥3 adverse events with venetoclax or placebo, plus low-dose cytarabine, were febrile neutropenia (50.0% vs 44.4%, respectively) and thrombocytopenia (27.8% vs 44.4%, respectively). Serious adverse events were reported in 50.0 and 33.3% of patients in the venetoclax and placebo, plus low-dose cytarabine arms, respectively; pneumonia was the most common (22.2% each). CONCLUSIONS: Limited survival benefit in the Japanese subgroup can be attributed to small patient numbers and to baseline imbalances observed between treatment arms, with more patients in the venetoclax plus low-dose cytarabine arm presenting poor prognostic factors. Venetoclax plus low-dose cytarabine was well toler

Published
2021

8. A large flux of particulate matter in the deep Japan Trench observed just after the 1994 Sanriku-Oki earthquake

Author

Itou, M., Matsumura, I., and Noriki, S.

Subjects
Japan -- Environmental aspects, Earthquakes -- Japan, Sedimentation and deposition -- Environmental aspects, Earth sciences
Abstract

A comparison is presented between three time-series traps deployed between Oct 1994 to May 1995 in the Japan Trench, at depths of 1km, 4.2 km and 6.8 km. The Sanriku-Oki earthquake, which occurred on Dec 28, 1994, produced a marked increase in non-biogenic material at 4.2 km and 6.8 km, but disparate ratios of manganese and aluminum at these two depths suggest differences in their particulate material source areas; it is posited that the 6.8 km fluxes originate from the eastern slop of the Trench.

Published
2000

9. Pembrolizumab plus lenalidomide and dexamethasone for patients with treatment-naive multiple myeloma (KEYNOTE-185): a randomised, open-label, phase 3 trial.

Author

Usmani S.Z., Oriol A., Karlin L., Cavo M., Rifkin R.M., Hayek F., Kirschner E., Bharany N., Overton L., Mannem S., Harroff A., Jain S., Roque T., McIntyre K., Yasencha C.K., Houck W., Schjesvold F., Yimer H.A., LeBlanc R., Takezako N., McCroskey R.D., Lim A.B.M., Suzuki K., Kosugi H., Grigoriadis G., Avivi I., Facon T., Jagannath S., Lonial S., Ghori R.U., Farooqui M.Z.H., Marinello P., San-Miguel J., Lim A., Walker T., Nicol A., Reece D., Elemary M., Boudreault Pedneault J.S., Attal M., Weisel K., Engelhardt M., Mackensen A., Quinn J., Cohen A., Magen-Nativ H., Benyamini N., Larocca A., Matsumoto M., Iida S., Ishikawa T., Kondo Y., Sunami K., Ando K., Teshima T., Chou T., Iwasaki H., Miki H., Matsumura I., Onishi Y., Izutsu K., Kizaki M., George A., Blacklock H., Simpson D., Waage A., Samoilova O., Nikitin E., Chagorova T., McDonald A., Patel M., Oriol Rocafiguera A., San Miguel Izquierdo J., Mateos M., Streetly M., Forsyth P., Jackson G., Jenkins S., Rifkin R., Yimer H., McCroskey R., Martincic D., Tarantolo S., Larson S., Faroun Y., Vaughn J., Baz R., Saylors G., Neppalli A., Raptis A., Fung H., Janosky M., Stevens D., Coleman M., Costa D., Cross S., Fanning S., Berges D.F., Harris T., Zackon I., Atanackovic D., Lee K., Oliff I., Lee W., Bensinger W., Lutzky J., Baron A., Usmani S.Z., Oriol A., Karlin L., Cavo M., Rifkin R.M., Hayek F., Kirschner E., Bharany N., Overton L., Mannem S., Harroff A., Jain S., Roque T., McIntyre K., Yasencha C.K., Houck W., Schjesvold F., Yimer H.A., LeBlanc R., Takezako N., McCroskey R.D., Lim A.B.M., Suzuki K., Kosugi H., Grigoriadis G., Avivi I., Facon T., Jagannath S., Lonial S., Ghori R.U., Farooqui M.Z.H., Marinello P., San-Miguel J., Lim A., Walker T., Nicol A., Reece D., Elemary M., Boudreault Pedneault J.S., Attal M., Weisel K., Engelhardt M., Mackensen A., Quinn J., Cohen A., Magen-Nativ H., Benyamini N., Larocca A., Matsumoto M., Iida S., Ishikawa T., Kondo Y., Sunami K., Ando K., Teshima T., Chou T., Iwasaki H., Miki H., Matsumura I., Onishi Y., Izutsu K., Kizaki M., George A., Blacklock H., Simpson D., Waage A., Samoilova O., Nikitin E., Chagorova T., McDonald A., Patel M., Oriol Rocafiguera A., San Miguel Izquierdo J., Mateos M., Streetly M., Forsyth P., Jackson G., Jenkins S., Rifkin R., Yimer H., McCroskey R., Martincic D., Tarantolo S., Larson S., Faroun Y., Vaughn J., Baz R., Saylors G., Neppalli A., Raptis A., Fung H., Janosky M., Stevens D., Coleman M., Costa D., Cross S., Fanning S., Berges D.F., Harris T., Zackon I., Atanackovic D., Lee K., Oliff I., Lee W., Bensinger W., Lutzky J., and Baron A.

Abstract

Background: Lenalidomide and dexamethasone has been a standard of care in transplant-ineligible patients with newly diagnosed multiple myeloma. The addition of a third drug to the combination is likely to improve treatment efficacy. KEYNOTE-185 assessed the efficacy and safety of lenalidomide and dexamethasone with and without pembrolizumab in patients with previously untreated multiple myeloma. Here, we present the results of an unplanned interim analysis done to assess the benefit-risk of the combination at the request of the US Food and Drug Administration (FDA). Method(s): KEYNOTE-185 was a randomised, open-label, phase 3 trial done at 95 medical centres across 15 countries (Australia, Canada, France, Germany, Ireland, Israel, Italy, Japan, New Zealand, Norway, Russia, South Africa, Spain, UK, and USA). Transplantation-ineligible patients aged 18 years and older with newly diagnosed multiple myeloma, Eastern Cooperative Oncology Group performance status of 0 or 1, and who were treatment naive were enrolled, and randomly assigned 1:1 to receive either pembrolizumab plus lenalidomide and dexamethasone or lenalidomide and dexamethasone alone using an interactive voice or integrated web response system. Patients received oral lenalidomide 25 mg on days 1-21 and oral dexamethasone 40 mg on days 1, 8, 15, and 22 of repeated 28-day cycles, with or without intravenous pembrolizumab 200 mg every 3 weeks. The primary endpoint was progression-free survival, which was investigator-assessed because of early trial termination. Efficacy was analysed in all randomly assigned patients and safety was analysed in all patients who received at least one dose of study drug. This trial is registered at ClinicalTrials.gov, number NCT02579863, and it is closed for accrual. Finding(s): Between Jan 7, 2016, and June 9, 2017, 301 patients were randomly assigned to the pembrolizumab plus lenalidomide and dexamethasone group (n=151) or the lenalidomide and dexamethasone group (n=150). On Jul

Published
2019

10. PS1344 PHASE 1/2 STUDY OF DSP-7888 IN PATIENTS WITH HIGHER-RISK (HR) MYELODYSPLASTIC SYNDROMES (MDS) AFTER FAILURE OF AZACITIDINE (AZA) THERAPY

Author

Usuki, K., primary, Ueda, Y., additional, Fujita, J., additional, Matsumura, I., additional, Aotsuka, N., additional, Sekiguchi, N., additional, Nakazato, T., additional, Iwasaki, H., additional, Watanabe, A., additional, Sugimoto, S., additional, Koga-Yamakawa, E., additional, Naoe, T., additional, Kizaki, M., additional, Heike, Y., additional, Miyazaki, Y., additional, and Akashi, K., additional

Published
2019
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13. Nilotinib versus imatinib for newly diagnosed chronic myeloid leukemia

Author

Saglio G, Kim DW, Issaragrisil S, le Coutre P, Etienne G, Lobo C, Pasquini R, Clark RE, Hochhaus A, Hughes TP, Gallagher N, Hoenekopp A, Dong M, Haque A, Larson RA, Kantarjian HM, Moiraghi B, Perez M, Greil R, Valent P, Bosly A, Martiat P, Noens L, André M, Verhoef G, Conchon M, Souza C, Nonino A, Hungria V, Zanichelli MA, Colturato V, Forrest D, Lipton JH, Savoie ML, Delage R, Lalancette M, Quintero G, Gomez M, Klamova H, Faber E, Bjerrum OW, Fredriksen H, Vestergaard H, Marcher C, Kamel H, Elzawam H, Porkka K, Remes K, Reiffers J, Guilhot F, Facon T, Tulliez M, Guerci Bresler AP, Nicolini FE, Charbonnier A, Rea D, Johnson Ansah A, Legros L, Harousseau JL, Rigal Huguet F, Escoffre M, Gardembas M, Guyotat D, Cahn JY, Gattermann N, Ottmann O, Niederwieser D, Stegelmann F, Schafhausen P, Brümmendorf T, Duyster J, Blumenstengel K, Scheid C, Kneba M, Kwong YL, Masszi T, Petrini M, Alimena G, Di Raimondo F, Rosti G, Rotoli B, Pungolino E, Amadori S, Abruzzese E, Fioritoni G, Lauria F, Bosi A, Martelli M, Rambaldi A, Ferrara F, Nobile F, Gobbi M, Carella AM, Orlandi EM, Leoni P, Tiribelli M, Levis A, Imamura M, Takahashi N, Tsukamoto N, Chiba S, Nagai T, Okamoto S, Miura O, Kurokawa M, Ohnishi K, Toba K, Nakao S, Tomita A, Miyamura K, Hino M, Maeda Y, Kimura A, Kawaguchi T, Miyazaki Y, Nakaseko C, Jinnai I, Matsuda A, Matsumura I, Ishikawa J, Ohyashiki K, Okada M, Usuki K, Kobayashi Y, Ohishi K, Imai K, Miyawaki S, Kanda Y, Park SY, Kim HJ, Sohn SK, Lee KH, Jung CW, Ong TC, Gómez Almaguer D, Kassack J, Ossenkoppele GJ, Gedde Dahl T, Hjorth Hansen H, Jedrzejczak W, Dmoszynska A, Starzak Dwozdz J, Holowiecki J, Kyrcz Krzemieñ S, Kuliczkowski K, Zaritsky A, Turkina A, Pospelova T, Goh YT, Koh LP, Demitrovicova L, Mistrik M, Ruff P, Louw V, Dreosti LM, Novitzky N, Cohen G, Cervantes F, Cañizo C, de Paz R, del Castillo S, Perez Encinas M, Sanz Alonso M, Marin F, Pérez López R, Hernandez Boluda J, Echeveste Gutierrez MA, Odriozola J, Herrera P, Steegman JL, Conde E, Lopez P, Giraldo P, Boque C, Heredia B, Font AJ, Rodriguez RF, Rodriguez MJ, Batlle J, Stenke L, Lehmann S, Wadenvik H, Simonsson B, Markevärn B, Själander A, Richter J, Bjoreman M, Eriksson KM, Chalandon Y, Shih LY, Yao M, Wang MC, Jootar S, Bunworasate U, Ulkü B, Haznedar R, Undar B, Sahin B, Marin D, Smith G, Byrne J, Holyoake T, Kalaycio M, Akard L, Heaney M, Al Janadi A, Goldberg S, Powell B, Harker WG, Shea T, Gingrich R, Glass J, Paquette R, Siegrist C, Woodson M, Fehrenbacher L, Koh H, Flinn I, Arrowsmith E, Ervin T, Guerra M, Wallach H, Berry W, Burke J, Edenfield W, Guzley G, Davis J, Richards D, Schlossman D, Kolibaba K, Alemany C, Savin M, Robbins G, Lopez J, Goldman JM, Camm J, Schiffer CA, Sargent D.J., PANE, FABRIZIO, Saglio, G, Kim, Dw, Issaragrisil, S, le Coutre, P, Etienne, G, Lobo, C, Pasquini, R, Clark, Re, Hochhaus, A, Hughes, Tp, Gallagher, N, Hoenekopp, A, Dong, M, Haque, A, Larson, Ra, Kantarjian, Hm, Moiraghi, B, Perez, M, Greil, R, Valent, P, Bosly, A, Martiat, P, Noens, L, André, M, Verhoef, G, Conchon, M, Souza, C, Nonino, A, Hungria, V, Zanichelli, Ma, Colturato, V, Forrest, D, Lipton, Jh, Savoie, Ml, Delage, R, Lalancette, M, Quintero, G, Gomez, M, Klamova, H, Faber, E, Bjerrum, Ow, Fredriksen, H, Vestergaard, H, Marcher, C, Kamel, H, Elzawam, H, Porkka, K, Remes, K, Reiffers, J, Guilhot, F, Facon, T, Tulliez, M, Guerci Bresler, Ap, Nicolini, Fe, Charbonnier, A, Rea, D, Johnson Ansah, A, Legros, L, Harousseau, Jl, Rigal Huguet, F, Escoffre, M, Gardembas, M, Guyotat, D, Cahn, Jy, Gattermann, N, Ottmann, O, Niederwieser, D, Stegelmann, F, Schafhausen, P, Brümmendorf, T, Duyster, J, Blumenstengel, K, Scheid, C, Kneba, M, Kwong, Yl, Masszi, T, Petrini, M, Alimena, G, Di Raimondo, F, Rosti, G, Rotoli, B, Pane, Fabrizio, Pungolino, E, Amadori, S, Abruzzese, E, Fioritoni, G, Lauria, F, Bosi, A, Martelli, M, Rambaldi, A, Ferrara, F, Nobile, F, Gobbi, M, Carella, Am, Orlandi, Em, Leoni, P, Tiribelli, M, Levis, A, Imamura, M, Takahashi, N, Tsukamoto, N, Chiba, S, Nagai, T, Okamoto, S, Miura, O, Kurokawa, M, Ohnishi, K, Toba, K, Nakao, S, Tomita, A, Miyamura, K, Hino, M, Maeda, Y, Kimura, A, Kawaguchi, T, Miyazaki, Y, Nakaseko, C, Jinnai, I, Matsuda, A, Matsumura, I, Ishikawa, J, Ohyashiki, K, Okada, M, Usuki, K, Kobayashi, Y, Ohishi, K, Imai, K, Miyawaki, S, Kanda, Y, Park, Sy, Kim, Hj, Sohn, Sk, Lee, Kh, Jung, Cw, Ong, Tc, Gómez Almaguer, D, Kassack, J, Ossenkoppele, Gj, Gedde Dahl, T, Hjorth Hansen, H, Jedrzejczak, W, Dmoszynska, A, Starzak Dwozdz, J, Holowiecki, J, Kyrcz Krzemieñ, S, Kuliczkowski, K, Zaritsky, A, Turkina, A, Pospelova, T, Goh, Yt, Koh, Lp, Demitrovicova, L, Mistrik, M, Ruff, P, Louw, V, Dreosti, Lm, Novitzky, N, Cohen, G, Cervantes, F, Cañizo, C, de Paz, R, del Castillo, S, Perez Encinas, M, Sanz Alonso, M, Marin, F, Pérez López, R, Hernandez Boluda, J, Echeveste Gutierrez, Ma, Odriozola, J, Herrera, P, Steegman, Jl, Conde, E, Lopez, P, Giraldo, P, Boque, C, Heredia, B, Font, Aj, Rodriguez, Rf, Rodriguez, Mj, Batlle, J, Stenke, L, Lehmann, S, Wadenvik, H, Simonsson, B, Markevärn, B, Själander, A, Richter, J, Bjoreman, M, Eriksson, Km, Chalandon, Y, Shih, Ly, Yao, M, Wang, Mc, Jootar, S, Bunworasate, U, Ulkü, B, Haznedar, R, Undar, B, Sahin, B, Marin, D, Smith, G, Byrne, J, Holyoake, T, Kalaycio, M, Akard, L, Heaney, M, Al Janadi, A, Goldberg, S, Powell, B, Harker, Wg, Shea, T, Gingrich, R, Glass, J, Paquette, R, Siegrist, C, Woodson, M, Fehrenbacher, L, Koh, H, Flinn, I, Arrowsmith, E, Ervin, T, Guerra, M, Wallach, H, Berry, W, Burke, J, Edenfield, W, Guzley, G, Davis, J, Richards, D, Schlossman, D, Kolibaba, K, Alemany, C, Savin, M, Robbins, G, Lopez, J, Goldman, Jm, Camm, J, Schiffer, Ca, and Sargent, D. J.

Published
2010

18. Endogenous Tim-1 promotes severe systemic autoimmunity and renal disease MRL-Faslpr mice.

Author

Nozaki Y., Richard Kitching A., Akiba H., Yagita H., Kinoshita K., Funauchi M., Matsumura I., Nozaki Y., Richard Kitching A., Akiba H., Yagita H., Kinoshita K., Funauchi M., and Matsumura I.

Abstract

The T-cell immunoglobulin mucin 1, also known as kidney injury molecule-1, modulates CD4+ T-cell responses and is also expressed by damaged proximal tubules within the kidney. Both Th subset imbalance (Th1/Th2/Th17) and regulatory T-cell and B-cell alterations contribute to the pathogenesis of autoimmune disease. This study investigated the effects of an inhibitory anti-T-cell immunoglobulin mucin 1 antibody (RMT1-10) in lupus-prone MRL-Faslpr mice. MRL-Faslpr mice were treated with RMT1-10 or a control antibody intraperitoneally twice weekly from 3 mo of age for 16 wk. RMT1-10 treatment significantly improved survival, limited the development of lymphadenopathy and skin lesions, preserved renal function and decreased proteinuria, reduced serum anti-DNA antibody levels, and attenuated renal leukocyte accumulation. Th1 and Th17 cellular responses systemically and intrarenally were reduced, but regulatory T and B cells were increased. RMT1-10 treatment also reduced glomerular immunoglobulin and C3 deposition and suppressed cellular proliferation and apoptosis. Urinary excretion and renal expression of kidney injury molecule-1 was reduced, reflecting diminished interstitial injury. As RMT1-10 attenuated established lupus nephritis, manipulating immune system T-cell immunoglobulin mucin 1 may represent a therapeutic strategy in autoimmune diseases affecting the kidney. © 2014 the American Physiological Society.

Published
2014

20. Reciprocal inhibition between MyoD and STAT3 in the regulation of growth and differentiation of myoblasts

Author

Kataoka Y. 1, Matsumura I. 2, Ezoe S. 3, Nakata S. 4, Takigawa E. 5, Sato Y. 6, Kawasaki A.7, Yokota T. 8, Nakajima K. 9, Felsani A. 10, and Kanakura Y. 11

Subjects
STAT3, Espressione genica, Miogenesi, Differenziamento, musculoskeletal system, MyoD, tissues
Abstract

The development of myoblasts is regulated by various growth factors as well as by intrinsic muscle-specific transcriptional factors. In this study, we analyzed the roles for STAT3 in the growth and differentiation of myoblasts in terms of cell cycle regulation and interaction with MyoD using C2C12 cells. Here we found that STAT3 inhibited myogenic differentiation induced by low serum or MyoD as efficiently as the Ras/mitogen-activated protein kinase cascade. As for this mechanism, we found that STAT3 not only promoted cell cycle progression through the induction of c-myc but also inhibited MyoD activities through direct interaction. STAT3 inhibited not only DNA binding activities of MyoD but also its transcriptional activities. However, the inhibited transcriptional activities were restored by the supplement of p300/CBP and PCAF, suggesting that STAT3 might deprive MyoD of these transcriptional cofactors. In addition, we found that MyoD inhibited DNA binding activities of STAT3, thereby inhibiting STAT3-dependent cell growth and survival of Ba/F3 cells. These results suggest that the development of muscle cells is regulated by the coordination of cytokine signals and intrinsic transcription factors.

Published
2003

21. The price of drugs for chronic myeloid leukemia (CML) is a reflection of the unsustainable prices of cancer drugs: From the perspective of a large group of CML experts

Author

Abboud, C, Berman, E, Cohen, A, Cortes, J, Deangelo, D, Deininger, M, Devine, S, Druker, B, Fathi, A, Jabbour, E, Jagasia, M, Kantarjian, H, Khoury, J, Laneuville, P, Larson, R, Lipton, J, Moore, J, Mughal, T, O'Brien, S, Pinilla-Ibarz, J, Quintas-Cardama, A, Radich, J, Reddy, V, Schiffer, C, Shah, N, Shami, P, Silver, R, Snyder, D, Stone, R, Talpaz, M, Tefferi, A, Van Etten, R, Wetzler, M, Abruzzese, E, Apperley, J, Breccia, M, Byrne, J, Cervantes, F, Chelysheva, E, Clark, R, De Lavallade, H, Dyagil, I, Gambacorti-Passerini, C, Goldman, J, Haznedaroglu, I, Hjorth-Hansen, H, Holyoake, T, Huntly, B, Le Coutre, P, Lomaia, E, Mahon, F, Marin-Costa, D, Martinelli, G, Mayer, J, Milojkovic, D, Olavarria, E, Porkka, K, Richter, J, Rousselot, P, Saglio, G, Saydam, G, Stentoft, J, Turkina, A, Vigneri, P, Zaritskey, A, Aguayo, A, Ayala, M, Bendit, I, Bengio, R, Best, C, Bullorsky, E, Cervera, E, Desouza, C, Fanilla, E, Gomez-Almaguer, D, Hamerschlak, N, Lopez, J, Magarinos, A, Meillon, L, Milone, J, Moiraghi, B, Pasquini, R, Pavlovsky, C, Ruiz-Arguelles, G, Spector, N, Arthur, C, Browett, P, Grigg, A, Jianda, H, Huang, X, Hughes, T, Jiang, Q, Jootar, S, Kim, D, Malhotra, H, Malhotra, P, Matsumura, I, Melo, J, Ohnishi, K, Ohno, R, Saikia, T, Schwarer, A, Takahashi, N, Tam, C, Tauchi, T, Usuki, K, Wang, J, Abdel-Rahman, F, Aljurf, M, Bazarba-Chi, A, Yehuda, D, Chaudhri, N, Durosinmi, M, Kamel, H, Louw, V, Matti, B, Nagler, A, Raanani, P, Salem, Z, Abboud, Camille, Berman, Ellin, Cohen, Adam, Cortes, Jorge, DeAngelo, Daniel, Deininger, Michael, Devine, Steven, Druker, Brian, Fathi, Amir, Jabbour, Elias, Jagasia, Madan, Kantarjian, Hagop, Khoury, Jean, Laneuville, Pierre, Larson, Richard, Lipton, Jeffrey, Moore, Joseph O., Mughal, Tariq, O'Brien, Susan, Pinilla-Ibarz, Javier, Quintas-Cardama, Alfonso, Radich, Jerald, Reddy, Vishnu, Schiffer, Charles, Shah, Neil, Shami, Paul, Silver, Richard T., Snyder, David, Stone, Richard, Talpaz, Moshe, Tefferi, Ayalew, Van Etten, Richard A., Wetzler, Meir, Abruzzese, Elisabetta, Apperley, Jane, Breccia, Massimo, Byrne, Jenny, Cervantes, Francisco, Chelysheva, Ekaterina, Clark, R. E., De Lavallade, Hugues, Dyagil, Iryna, Gambacorti-Passerini, Carlo, Goldman, John, Haznedaroglu, Ibrahim, Hjorth-Hansen, Henrik, Holyoake, Tessa, Huntly, Brian, Le Coutre, Philipp, Lomaia, Elza, Mahon, Francois-Xavier, Marin-Costa, David, Martinelli, Giovanni, Mayer, Jiri, Milojkovic, Dragana, Olavarria, Eduardo, Porkka, Kimmo, Richter, Johan, Rousselot, Philippe, Saglio, Giuseppe, Saydam, Guray, Stentoft, Jesper, Turkina, Anna, Vigneri, Paolo, Zaritskey, Andrey, Aguayo, Alvaro, Ayala, Manuel, Bendit, Israel, Bengio, Raquel Maria, Best, Carlos, Bullorsky, Eduardo, Cervera, Eduardo, Desouza, Carmino, Fanilla, Ernesto, Gomez-Almaguer, David, Hamerschlak, Nelson, Lopez, Jose, Magarinos, Alicia, Meillon, Luis, Milone, Jorge, Moiraghi, Beatriz, Pasquini, Ricardo, Pavlovsky, Carolina, Ruiz-Arguelles, Guillermo J., Spector, Nelson, Arthur, Christopher, Browett, Peter, Grigg, Andrew, Hu, Jianda, Huang, Xiao-jun, Hughes, Tim, Jiang, Qian, Jootar, Saengsuree, Kim, Dong-Wook, Malhotra, Hemant, Malhotra, Pankaj, Matsumura, Itaru, Melo, Junia, Ohnishi, Kazunori, Ohno, Ryuzo, Saikia, Tapan, Schwarer, Anthony P., Takahashi, Naoto, Tam, Constantine, Tauchi, Tetsuzo, Usuki, Kensuke, Wang, Jianxiang, Abdel-Rahman, Fawzi, Aljurf, Mahmoud Deeb Saeed, Bazarba-Chi, Ali, Yehuda, Dina Ben, Chaudhri, Naeem, Durosinmi, Muheez, Kamel, Hossam, Louw, Vernon, Matti, Bassam Francis, Nagler, Arnon, Raanani, Pia, Salem, Ziad, Abboud, C, Berman, E, Cohen, A, Cortes, J, Deangelo, D, Deininger, M, Devine, S, Druker, B, Fathi, A, Jabbour, E, Jagasia, M, Kantarjian, H, Khoury, J, Laneuville, P, Larson, R, Lipton, J, Moore, J, Mughal, T, O'Brien, S, Pinilla-Ibarz, J, Quintas-Cardama, A, Radich, J, Reddy, V, Schiffer, C, Shah, N, Shami, P, Silver, R, Snyder, D, Stone, R, Talpaz, M, Tefferi, A, Van Etten, R, Wetzler, M, Abruzzese, E, Apperley, J, Breccia, M, Byrne, J, Cervantes, F, Chelysheva, E, Clark, R, De Lavallade, H, Dyagil, I, Gambacorti-Passerini, C, Goldman, J, Haznedaroglu, I, Hjorth-Hansen, H, Holyoake, T, Huntly, B, Le Coutre, P, Lomaia, E, Mahon, F, Marin-Costa, D, Martinelli, G, Mayer, J, Milojkovic, D, Olavarria, E, Porkka, K, Richter, J, Rousselot, P, Saglio, G, Saydam, G, Stentoft, J, Turkina, A, Vigneri, P, Zaritskey, A, Aguayo, A, Ayala, M, Bendit, I, Bengio, R, Best, C, Bullorsky, E, Cervera, E, Desouza, C, Fanilla, E, Gomez-Almaguer, D, Hamerschlak, N, Lopez, J, Magarinos, A, Meillon, L, Milone, J, Moiraghi, B, Pasquini, R, Pavlovsky, C, Ruiz-Arguelles, G, Spector, N, Arthur, C, Browett, P, Grigg, A, Jianda, H, Huang, X, Hughes, T, Jiang, Q, Jootar, S, Kim, D, Malhotra, H, Malhotra, P, Matsumura, I, Melo, J, Ohnishi, K, Ohno, R, Saikia, T, Schwarer, A, Takahashi, N, Tam, C, Tauchi, T, Usuki, K, Wang, J, Abdel-Rahman, F, Aljurf, M, Bazarba-Chi, A, Yehuda, D, Chaudhri, N, Durosinmi, M, Kamel, H, Louw, V, Matti, B, Nagler, A, Raanani, P, Salem, Z, Abboud, Camille, Berman, Ellin, Cohen, Adam, Cortes, Jorge, DeAngelo, Daniel, Deininger, Michael, Devine, Steven, Druker, Brian, Fathi, Amir, Jabbour, Elias, Jagasia, Madan, Kantarjian, Hagop, Khoury, Jean, Laneuville, Pierre, Larson, Richard, Lipton, Jeffrey, Moore, Joseph O., Mughal, Tariq, O'Brien, Susan, Pinilla-Ibarz, Javier, Quintas-Cardama, Alfonso, Radich, Jerald, Reddy, Vishnu, Schiffer, Charles, Shah, Neil, Shami, Paul, Silver, Richard T., Snyder, David, Stone, Richard, Talpaz, Moshe, Tefferi, Ayalew, Van Etten, Richard A., Wetzler, Meir, Abruzzese, Elisabetta, Apperley, Jane, Breccia, Massimo, Byrne, Jenny, Cervantes, Francisco, Chelysheva, Ekaterina, Clark, R. E., De Lavallade, Hugues, Dyagil, Iryna, Gambacorti-Passerini, Carlo, Goldman, John, Haznedaroglu, Ibrahim, Hjorth-Hansen, Henrik, Holyoake, Tessa, Huntly, Brian, Le Coutre, Philipp, Lomaia, Elza, Mahon, Francois-Xavier, Marin-Costa, David, Martinelli, Giovanni, Mayer, Jiri, Milojkovic, Dragana, Olavarria, Eduardo, Porkka, Kimmo, Richter, Johan, Rousselot, Philippe, Saglio, Giuseppe, Saydam, Guray, Stentoft, Jesper, Turkina, Anna, Vigneri, Paolo, Zaritskey, Andrey, Aguayo, Alvaro, Ayala, Manuel, Bendit, Israel, Bengio, Raquel Maria, Best, Carlos, Bullorsky, Eduardo, Cervera, Eduardo, Desouza, Carmino, Fanilla, Ernesto, Gomez-Almaguer, David, Hamerschlak, Nelson, Lopez, Jose, Magarinos, Alicia, Meillon, Luis, Milone, Jorge, Moiraghi, Beatriz, Pasquini, Ricardo, Pavlovsky, Carolina, Ruiz-Arguelles, Guillermo J., Spector, Nelson, Arthur, Christopher, Browett, Peter, Grigg, Andrew, Hu, Jianda, Huang, Xiao-jun, Hughes, Tim, Jiang, Qian, Jootar, Saengsuree, Kim, Dong-Wook, Malhotra, Hemant, Malhotra, Pankaj, Matsumura, Itaru, Melo, Junia, Ohnishi, Kazunori, Ohno, Ryuzo, Saikia, Tapan, Schwarer, Anthony P., Takahashi, Naoto, Tam, Constantine, Tauchi, Tetsuzo, Usuki, Kensuke, Wang, Jianxiang, Abdel-Rahman, Fawzi, Aljurf, Mahmoud Deeb Saeed, Bazarba-Chi, Ali, Yehuda, Dina Ben, Chaudhri, Naeem, Durosinmi, Muheez, Kamel, Hossam, Louw, Vernon, Matti, Bassam Francis, Nagler, Arnon, Raanani, Pia, and Salem, Ziad

Abstract

As a group of more than 100 experts in chronic myeloid leukemia (CML), we draw attention to the high prices of cancer drugs, with the particular focus on the prices of approved tyrosine kinase inhibitors for the treatment of CML. This editorial addresses the multiple factors involved in cancer drug pricing and their impact on individual patients and health care policies, and argues for the need to (1) lower the prices of cancer drugs to allow more patients to afford them and (2) maintain sound long-term health care policies.

Published
2013

22. Plug And Play Photosynthesis

Author

Jones, A, Bayer, T, Bibby, T, Cronin, L, Golbeck, J, Kramer, D, Matsumura, I, Jones, A, Bayer, T, Bibby, T, Cronin, L, Golbeck, J, Kramer, D, and Matsumura, I

Abstract

NA

Published
2012

23. Cytokines prevent dexamethasone-induced apoptosis via the activation of mitogen-activated protein kinase and phosphatidylinositol 3-kinase pathways in a new multiple myeloma cell line

Author

Ogawa M, Nishiura T, Oritani K, Yoshida H, Yoshimura M, Okajima Y, Ishikawa J, Hashimoto K, Matsumura I, Yoshiaki Tomiyama, and Matsuzawa Y

Subjects
Mitogen-Activated Protein Kinase 1, Caspase 3, Interleukin-6, MAP Kinase Signaling System, Apoptosis, Receptor, Interferon alpha-beta, Receptors, Interleukin-6, Dexamethasone, Recombinant Proteins, Receptor, IGF Type 1, Gene Expression Regulation, Neoplastic, Phosphatidylinositol 3-Kinases, Caspases, Interferon Type I, Tumor Cells, Cultured, Humans, Female, Insulin-Like Growth Factor I, Multiple Myeloma, Aged, Receptors, Interferon, Signal Transduction
Abstract

A new human myeloma cell line, OPM-6, was established from the peripheral blood of a patient with advanced IgG-kappa plasma cell leukemia. Cytogenetic and phenotypic analysis confirmed that the cells were derived from the patient's leukemic cells. Insulin-like growth factor-1 (IGF-1) acts as an autocrine growth factor in these cells. In addition, OPM-6 cells were particularly sensitive to dexamethasone (DEX), when endogenous IGF-1 was blocked. Under these conditions,95% of the DEX-treated cells died within 36 h. Therefore, OPM-6 represents a potentially powerful tool for the analysis of the molecular mechanisms of DEX-induced apoptosis, because it is possible to easily analyze the direct effects of DEX using this system. Using this culture system of OPM-6, we demonstrated that the treatment with DEX plus a monoclonal antibody to the human IGF-1 receptor (alphaIGF-1R) leads to the down-regulation of the gene expression of Bcl-xL, an antiapoptotic gene, and the activation of CPP32 during this apoptotic process. IFN-alpha as well as IL-6 prevented DEX plus alphaIGF-1R-induced apoptosis, and this prevention was blocked by the mitogen-activated protein kinase kinase inhibitor, PD098059, or the phosphatidylinositol 3-kinase inhibitor, wortmannin. Therefore, both IL-6 and IFN-alpha blocked DEX plus alphaIGF-1R-induced apoptosis through activation of the mitogen-activated protein kinase and phosphatidylinositol 3-kinase pathways.

Published
2000

24. Full oncogenic activities of v-Src are mediated by multiple signaling pathways. Ras as an essential mediator for cell survival

Author

Odajima J, Matsumura I, Sonoyama J, Daino H, Kawasaki A, Tanaka H, Inohara N, Kitamura T, Julian Downward, Nakajima K, Hirano T, and Kanakura Y

Subjects
STAT3 Transcription Factor, B-Lymphocytes, Cell Survival, Stem Cells, Down-Regulation, Apoptosis, Oncogene Protein pp60(v-src), DNA-Binding Proteins, Mice, Phosphatidylinositol 3-Kinases, Cell Transformation, Neoplastic, Proto-Oncogene Proteins c-bcl-2, Trans-Activators, ras Proteins, Animals, Interleukin-3, Cell Division, Signal Transduction
Abstract

Tyrosine kinase oncoproteins cause simultaneous activation of multiple intracellular signaling pathways. However, the precise mechanisms by which individual pathways induce oncogenesis are not well understood. We have investigated the roles of individual signaling pathways in v-Src-dependent cell growth and survival by inhibiting one particular pathway. v-Src induced constitutive activation of signal transducers and activators of transcription 3 (STAT3), phosphatidylinositol 3-kinase, and Ras in murine Ba/F3 cells and led to factor-independent proliferation. Dominant-negative mutants of STAT3 (STAT3D) and phosphatidylinositol 3-kinase (Deltap85) inhibited v-Src-dependent growth by approximately 60 and approximately 40%, respectively. Moreover, dominant-negative Ras (N17) induced severe apoptosis, which was accompanied by down-regulation of Bcl-2 and activation of caspase-3. Although cells overexpressing Bcl-2 or caspase-3 inhibitors remained viable even when N17 was expressed, the growth was reduced by approximately 85%. During N17- and STAT3D-induced growth suppression, expression of cyclin D2, cyclin D3, c-myc, and c-fos was suppressed by N17, whereas that of cyclin D2, cyclin E, and c-myc was suppressed by STAT3D. Thus, v-Src-activated Ras and STAT3 are involved in distinct but partly overlapping transcriptional regulation of cell cycle regulatory molecules. These results suggest that the full oncogenic activity of v-Src requires simultaneous activation of multiple signalings, in which Ras is particularly required for survival.

Published
2000

46. Practical Large-Scale Synthesis of Cefmatilen, A New Cephalosporin Antibiotic

Author

Kobayashi, T., Masui, Y., Goto, Y., Kitaura, Y., Mizutani, T., Matsumura, I., Sugata, Y., Ide, Y., Takayama, M., Takahashi, H., and Okuyama, A.

Abstract

A practical large-scale process for the synthesis of cefmatilen hydrochloride hydrate (1), a new oral cephalosporin antibiotic, is described. Several impurities are isolated from a bulk drug and identified. Side reactions are discussed in order to prevent them. The conditions were optimized to control the formation of impurities. The process is amenable to a multikilogram-scale preparation. Several kilograms of compound 1 for clinical trials were successfully prepared by this process from the three starting materials (7-aminocephem hydrochloride 4, triethylammonium acetate 5, and triazole 7) on a pilot scale in overall yields of 61−65% (10−14% higher than those for the previous process).

Published
2004

47. Increased D-type cyclin expression together with decreased cdc2 activity confers megakaryocytic differentiation of a human thrombopoietin-dependent hematopoietic cell line.

Author

Matsumura, I, Tanaka, H, Kawasaki, A, Odajima, J, Daino, H, Hashimoto, K, Wakao, H, Nakajima, K, Kato, T, Miyazaki, H, and Kanakura, Y

Abstract

At the late phase of megakaryocytopoiesis, megakaryocytes undergo endomitosis, which is characterized by DNA replication without cell division. Although a number of cell cycle regulatory molecules have been identified, the precise roles of these molecules in megakaryocytic endomitosis are largely unknown. In a human interleukin-3-dependent cell line transfected with the thrombopoietin (TPO) receptor c-mpl (F-36P-mpl), either treatment with TPO or the overexpression of activated ras (Ha-Ras(G12V)) induced megakaryocytic maturation with polyploid formation. We found that TPO stimulation or Ha-Ras(G12V) expression led to up-regulation of cyclin D1, cyclin D2, and cyclin D3 expression. In addition, expression levels of cyclin A and cyclin B were reduced during the total course of both TPO- and Ha-Ras(G12V)-induced megakaryocytic differentiation, thereby leading to decreased cdc2 kinase activity. Neither the induced expression of cyclin D1, cyclin D2, or cyclin D3 nor the expression of a dominant negative form of cdc2 alone could induce megakaryocytic differentiation of F-36P-mpl cells. In contrast, overexpression of dominant negative cdc2 together with cyclin D1, cyclin D2, or cyclin D3 facilitated megakaryocytic differentiation in the absence of TPO. These results suggest that both D-type cyclin expression and decreased cdc2 kinase activity may participate in megakaryocytic differentiation.

Published
2000

49. Insulin-like growth factor-I augments erythropoietin-induced proliferation through enhanced tyrosine phosphorylation of STAT5.

Author

Okajima, Y, Matsumura, I, Nishiura, T, Hashimoto, K, Yoshida, H, Ishikawa, J, Wakao, H, Yoshimura, A, Kanakura, Y, Tomiyama, Y, and Matsuzawa, Y

Abstract

Insulin-like growth factor (IGF-I) is known to synergistically stimulate the proliferation of hematopoietic cells in combination with other hematopoietic growth factors. However, the precise mechanism underlying the cooperative effects of IGF-I is unknown. In a human interleukin-3 or erythropoietin (EPO)-dependent cell line, F-36P, IGF-I alone failed to stimulate DNA synthesis but did augment the EPO-dependent DNA synthesis of F-36P cells. The treatment of F-36P cells with a combination of EPO and IGF-I (EPO/IGF-I) was found to enhance EPO-induced tyrosine phosphorylation of STAT5, whereas IGF-I alone did not. Furthermore, c-CIS mRNA expression, one of the target molecules of STAT5, was more effectively induced by EPO/IGF-I than by EPO alone. To examine the mechanisms of the EPO- and EPO/IGF-I-induced proliferation of F-36P cells, we expressed dominant negative (dn) mutants of STAT5 and Ras in an inducible system. The EPO-induced DNA synthesis and the cooperative effect of EPO/IGF-I were significantly inhibited by the inducible expression of dn-STAT5 or dn-Ras. In addition, the inducible expression of dn-Ras abolished the IGF-I-enhanced tyrosine phosphorylation of STAT5. These results suggest that IGF-I may augment EPO-induced proliferation by enhancing tyrosine phosphorylation of STAT5 and raise the possibility that Ras may be involved in the augmentation of STAT5 tyrosyl phosphorylation.

Published
1998

50. Oncogenic receptor tyrosine kinase in leukemia

Author

Mizuki M, Ueda S, Matsumura I, JUN ISHIKO, Schwäble J, Serve H, and Kanakura Y

Subjects
Proto-Oncogene Proteins c-kit, Leukemia, Receptor, Platelet-Derived Growth Factor alpha, Oncogene Proteins, Fusion, fms-Like Tyrosine Kinase 3, Proto-Oncogene Proteins, Animals, Humans, Receptor Protein-Tyrosine Kinases
Abstract

Growth, survival and differentiation of hematopoietic cells are regulated by the interaction between hematopoietic growth factors and their receptors. While the defect in this interaction results in an insufficient hematopoiesis, the aberrantly elevated activation leads to the transformation of hematopoietic cells. The constitutive active mutations of receptor tyrosine kinase, such as c-Kit platelet-derived growth factor receptor (PDGFR) or fins-like tyrosine kinase 3 (Flt3), play a major role in the development of hematopoietic neoplasia. The constitutive activation is provoked by several mechanisms, such as making fusion genes by chromosomal translocations, or various mutations involving regulatory regions of the receptor. The chromosomal translocation brings the receptor intracytoplasmic domain juxtaposed to an unrelated molecule which has dimerization or multimerization motif, resulting in the constitutive dimerization of the receptor. The missense, insertion or deletion mutations in the regulatory regions, such as juxtamembrane domain, activation loop and extracellular domain, cause constitutive activation by releasing the respective auto-inhibitory functions of each regulatory region. Constitutive active receptors generate different signals quantitatively and qualitatively from wild type receptor, which mediate the oncogenic phenotype. Given the frequent involvement of constitutive active receptor tyrosine kinase in hematopoietic malignancies, targeted inhibitions of active tyrosine kinase and downstream aberrant signaling are rapidly developing novel therapeutic modality with much promise.

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