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Articles by T Kitamura
Total Records ( 5 ) for T Kitamura
  T Kitamura , M Ogawa and Y. Yamada

We examined the effects of U50,488, a kappa-opioid receptor agonist, and flurbiprofen axetil, a nonsteroidal antiinflammatory drug, in a visceral pain model using conscious rats. U50,488 produced visceral antinociception, but exaggerated the adverse effects on the central nervous system (CNS) at 0.9 mg/kg or more. Naloxone completely antagonized these effects. Flurbiprofen axetil produced visceral antinociception, but exaggerated the adverse effects on the CNS at 80 mg/kg. Coadministration of U50,488 (0.27 mg/kg) and flurbiprofen axetil (50 mg/kg) produced intense visceral antinociception without adverse effects on the CNS, implying therapeutic efficacies of coadministration of kappa-opioid receptor-agonists and nonsteroidal antiinflammatory drugs on visceral pain.

  K Kiguchi , T Kitamura , T Moore , M Rumi , H. C Chang , D Treece , L Ruffino , K Connolly and J. DiGiovanni

The erbB family of receptor tyrosine kinases are known to play important roles in normal epithelial development and epithelial neoplasia. Considerable evidence also suggests that signaling through the epidermal growth factor receptor (EGFR) plays an important role in multistage skin carcinogenesis in mice; however, less is known about the role of erbB2. In this study, to further examine the role of both erbB2 and EGFR in epithelial carcinogenesis, we examined the effect of a dual erbB2/EGFR tyrosine kinase inhibitor, GW2974, given in the diet on skin tumor promotion during two-stage carcinogenesis in wild-type and BK5.erbB2 mice. In BK5.erbB2 mice, erbB2 is overexpressed in the basal layer of epidermis and leads to heightened sensitivity to skin tumor development. GW2974 effectively inhibited skin tumor promotion by 12-O-tetradecanoylphorbol-13-acetate in wild-type and BK5.erbB2 mice, although a more marked effect was seen in BK5.erbB2 mice. In addition, this inhibitory effect was reversible when GW2974 treatment was withdrawn. GW2974 inhibited 12-O-tetradecanoylphorbol-13-acetate–induced epidermal hyperproliferation, which correlated with reduced activation of both the EGFR and erbB2. These results support the hypothesis that both the EGFR and erbB2 play an important role in the development of skin tumors during two-stage skin carcinogenesis, especially during the tumor promotion stage. Furthermore, the marked sensitivity of BK5.erbB2 mice to the inhibitory effects of GW2974 during tumor promotion suggest greater efficacy for this compound when erbB2 is overexpressed or amplified as an early event in the carcinogenic process. Cancer Prev Res; 3(8); 940–52. ©2010 AACR.

  H Akaza , K Kawai , T Tsukamoto , T Fujioka , Y Tomita , T Kitamura , S Ozono , T Miki , S Naito , H Zembutsu and Y. Nakamura

In our previous study, a combination therapy of interleukin-2 and interferon- was found to be more effective than monotherapy, especially for lung metastasis. In order to determine the genetic markers of those who positively responded, a multi-institutional open study was conducted on the patients with lung metastasis. In this paper, the clinical response to our combination therapy is reported.


Untreated patients with lung metastasis were enrolled in this study. Patients received interleukin-2 (0.7 x 106 U/day) and interferon- (6 x 106 IU/day): interleukin-2, 5 days a week and interferon-, 3 days a week for the first 8 weeks, and then both interleukin-2 and interferon-, 2 or 3 days a week for 16 additional weeks.


Forty-two patients were able to be evaluated for response. The overall positive response rate was 35.7% (15 of 42) including 2 patients with complete response. Progression-free patients were observed more frequently in patients with lung metastasis only (80.6%) than those with lung plus other organ metastasis (54.5%). Tumor shrinkage was observed in 81.0% (34 of 42) of patients. Progression-free survival rate at 200 days was 63.6%. Toxicities observed were primarily flu-like symptoms due to the cytokines and were typical of those observed with each single agent.


Combination therapy of interleukin-2 and interferon- was confirmed to be effective for renal cell carcinoma patients with lung metastasis. Identification of genetic markers is now ongoing with the tissue samples from this trial.

  H Kubagawa , S Oka , Y Kubagawa , I Torii , E Takayama , D. W Kang , G. L Gartland , L. F Bertoli , H Mori , H Takatsu , T Kitamura , H Ohno and J. Y. Wang

Although Fc receptors (FcRs) for switched immunoglobulin (Ig) isotypes have been extensively characterized, FcR for IgM (FcµR) has defied identification. By retroviral expression and functional cloning, we have identified a complementary DNA (cDNA) encoding a bona fide FcµR in human B-lineage cDNA libraries. FcµR is defined as a transmembrane sialoglycoprotein of ~60 kD, which contains an extracellular Ig-like domain homologous to two other IgM-binding receptors (polymeric Ig receptor and Fc/µR) but exhibits an exclusive Fcµ-binding specificity. The cytoplasmic tail of FcµR contains conserved Ser and Tyr residues, but none of the Tyr residues match the immunoreceptor tyrosine-based activation, inhibitory, or switch motifs. Unlike other FcRs, the major cell types expressing FcµR are adaptive immune cells, including B and T lymphocytes. After antigen-receptor ligation or phorbol myristate acetate stimulation, FcµR expression was up-regulated on B cells but was down-modulated on T cells, suggesting differential regulation of FcµR expression during B and T cell activation. Although this receptor was initially designated as Fas apoptotic inhibitory molecule 3, or TOSO, our results indicate that FcµR per se has no inhibitory activity in Fas-mediated apoptosis and that such inhibition is only achieved when anti-Fas antibody of an IgM but not IgG isotype is used for inducing apoptosis.

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