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Articles by T Kojima
Total Records ( 5 ) for T Kojima
  S Mochizuki , T Yoshino , T Kojima , N Fuse , H Ikematsu , K Minashi , T Yano , M Tahara , K Kaneko , T Doi , K Koike and A. Ohtsu
  Objective

The risk of venous thromboembolism has been reported to increase when receiving bevacizumab. Many cancer patients are reported to have elevated D-dimer levels. It is not clear what D-dimer level might indicate an increased risk of venous thromboembolism in the colorectal cancer patients treated with bevacizumab-containing chemotherapy.

Methods

The D-dimer levels and any event concurrent with an elevated D-dimer level were evaluated in patients receiving bevacizumab. The D-dimer cut-off level was determined using the receiver-operating characteristic analysis. The selection criteria were as follows: histologically proven metastatic and unresectable colorectal adenocarcinoma; no prior chemotherapy containing bevacizumab; D-dimer test performed repetitively on the baseline and during bevacizumab administration; no venous thromboembolism identified at the baseline; and enhanced computed tomographic scan performed every 2 months.

Results

Sixty-nine patients were included. The chemotherapy regimens with bevacizumab included the regimen of 5-fluorouracil, leucovorin and oxaliplatin (FOLFOX), the regimen of 5-fluorouracil, leucovorin and irinotecan (FOLFIRI), and leucovorin-modulated 5-fluorouracil. The median baseline D-dimer level was 1.2 µg/ml. The appropriate D-dimer cut-off level was 3 µg/ml with the negative predictive value of 98% and relative risk of 6.9. Twenty-one of 69 patients showed elevated D-dimer levels of >3 µg/ml, with 11 patients for unknown reasons, 6 with tumor progression, 3 with venous thromboembolism and 1 with sepsis. In the remaining 48 patients whose D-dimer levels were ≤3 µg/ml, only one patient developed a venous thromboembolism.

Conclusions

A D-dimer cut-off level of 3 µg/ml might be a useful indicator level to exclude venous thromboembolism or show an increased risk for venous thromboembolism in colorectal cancer patients treated with bevacizumab-containing chemotherapy.

  S Hironaka , K Yamazaki , K Taku , T Yokota , K Shitara , T Kojima , S Ueda , N Machida , K Muro and N. Boku
  Objective

S-1 plus cisplatin is standard treatment for advanced gastric cancer in Japan. Triplet therapy with docetaxel, cisplatin and fluoropyrimidine showed a survival benefit over doublet therapy, but was associated with substantial toxicities. We investigated the maximum tolerated dose of combination chemotherapy with divided-dose docetaxel added to standard-dose S-1 plus cisplatin in advanced gastric cancer patients.

Methods

Patients with advanced gastric cancer, naive to chemotherapy or not refractory to fluoropyrimidine, were enrolled. Fixed doses of S-1 (40 mg/m2 twice daily for 3 weeks) and cisplatin (60 mg/m2 on day 1) were administered with increasing docetaxel dose levels of 20 mg/m2 (dose level 1), 25 mg/m2 (dose level 2) and 30 mg/m2 (dose level 3) on days 1, 8 and 15, or 40 mg/m2 (dose level 4) on days 1 and 15 of a 5-week cycle. Treatment cycles were repeated until disease progression, patient's refusal or unacceptable toxicity occurred.

Results

Fifteen patients were enrolled. During the first cycle, no dose-limiting toxicity was observed at dose levels 1 and 2. At dose level 3, grade 3 febrile neutropenia was seen in one patient. At dose level 4, grade 3 infection and grade 3 abdominal pain were observed. Thus, dose level 4 was determined to be the maximum tolerated dose. The response rate was 54% (7/13), and median progression-free survival and overall survival were 243 and 383 days, respectively.

Conclusions

The recommended dose of docetaxel added to standard-dose S-1 (80 mg/m2 days 1–21) plus cisplatin (60 mg/m2 day 1) was 40 mg/m2 on days 1 and 15 of a 5-week cycle.

  T Shukuya , H Yasui , N Boku , Y Onozawa , A Fukutomi , K Yamazaki , K Taku , T Kojima and N. Machida
  Objectives

Peritoneal metastasis is one of the major sites of disease progression of pancreatic cancer. There have been few trials in the second-line setting after gemcitabine failure because patients can hardly be candidates for chemotherapy after failure in the first-line chemotherapy, especially those with malignant ascites. The safety and efficacy of weekly paclitaxel therapy was evaluated for pancreatic cancer patients with malignant ascites in this retrospective study.

Methods

The subjects of this retrospective study were 23 advanced pancreatic cancer patients with malignant ascites who received weekly paclitaxel therapy after gemcitabine failure. Paclitaxel (80 mg/m2, div. for 1 h) was administered on Days 1, 8 and 15, every 4 weeks.

Results

While the disease control rate was 35%, decrease of ascites was obtained in 30% of the patients and ascites control rate was 61%. The median survival time was 101 days. Toxicities were mild, although one treatment-related death occurred.

Conclusions

Weekly paclitaxel therapy may be useful treatment option for pancreatic cancer patients with malignant ascites after gemcitabine failure.

  M Li , Y Seki , P. H. L Freitas , M Nagata , T Kojima , S Sultana , S Ubaidus , T Maeda , J Shimomura , J. E Henderson , M Tamura , K Oda , Z Liu , Y Guo , R Suzuki , T Yamamoto , R Takagi and N. Amizuka
 

The signaling axis comprising the parathyroid hormone (PTH)-related peptide (PTHrP), the PTH/PTHrP receptor and the fibroblast growth factor receptor 3 (FGFR3) plays a central role in chondrocyte proliferation. The Indian hedgehog (IHH) gene is normally expressed in early hypertrophic chondrocytes, and its negative feedback loop was shown to regulate PTH/PTHrP receptor signaling. In this study, we examined the regulation of PTH/PTHrP receptor gene expression in a FGFR3-transfected chondrocytic cell line, CFK2. Expression of IHH could not be verified on these cells, with consequent absence of hypertrophic differentiation. Also, expression of the PTH/PTHrP receptor (75% reduction of total mRNA) and the PTHrP (50% reduction) genes was reduced in CFK2 cells transfected with FGFR3 cDNA. Interestingly, we verified significant reduction in cell growth and increased apoptosis in the transfected cells. STAT1 was detected in the nuclei of the CFK2 cells transfected with FGFR3 cDNA, indicating predominance of the JAK/STAT signaling pathway. The reduction in PTH/PTHrP receptor gene in CFK2 cells overexpressing FGFR3 was partially blocked by treatment with an inhibitor of JAK3 (WHI-P131), but not with an inhibitor of MAPK (SB203580) or JAK2 (AG490). Altogether, these findings suggest that FGFR3 down-regulates PTH/PTHrP receptor gene expression via the JAK/STAT signaling in chondrocytic cells.

  K Narimatsu , M Li , P. H. L de Freitas , S Sultana , S Ubaidus , T Kojima , L Zhucheng , G Ying , R Suzuki , T Yamamoto , K Oda and N. Amizuka
 

Preosteoblasts are currently defined as the precursors of mature osteoblasts. These cells are morphologically diverse and may represent a continuum during osteoblast differentiation. We have attempted to categorize the different preosteoblastic phenotypes in vivo by examining bone cells expressing the runt-related transcription factor 2, alkaline phosphatase and BrdU incorporation – histological traits of a preosteoblast – under transmission electron microscopy (TEM). TEM observations demonstrated, at least, in part two preosteoblastic subtypes: (i) a cell rich in cisterns of rough endoplasmic reticulum (rER) with vesicles and vacuoles and (ii) a subtype featuring extended cytoplasmic processes that connect with distant cells, with a small amount of scattered cisterns of rER and with many vesicles and vacuoles. ER-rich cells, whose cellular machinery is similar to that of an osteoblast, were often seen adjacent to mature osteoblasts, and therefore, may be ready for terminal differentiation. In contrast, ER-poor and vesicle-rich cells extended their cytoplasmic processes to mature osteoblasts and, frequently, to bone-resorbing osteoclasts. The abundant vesicles and vacuoles identified in this cell type indicate that this cell is involved in vesicular transport rather than matrix synthesis activity. In summary, our study verified the morphological diversity and the ultrastructural properties of osteoblastic cells in vivo.

 
 
 
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