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Articles by M Omata
Total Records ( 2 ) for M Omata
  N Yamamichi , R Shimomura , K. i Inada , K Sakurai , T Haraguchi , Y Ozaki , S Fujita , T Mizutani , C Furukawa , M Fujishiro , M Ichinose , K Shiogama , Y Tsutsumi , M Omata and H. Iba

Purpose: To better understand microRNA miR-21 function in carcinogenesis, we analyzed miR-21 expression patterns in different stages of colorectal cancer development using in situ hybridization (ISH).

Experimental Design: Locked nucleic acid (LNA)/DNA probes and a biotin-free tyramide signal amplification system were used in ISH analyses of miRNA expression. Conditions for specific detection of miR-21 were determined using human cell lines and miR-21–expressing lentiviral vectors. Expression was determined in 39 surgically excised colorectal tumors and 34 endoscopically resected colorectal polyps.

Results: In the surgical samples, miR-21 expression was much higher in colorectal cancers than in normal mucosa. Strong miR-21 expression was also observed in cancer-associated stromal fibroblasts, suggesting miR-21 induction by cancer-secreted cytokines. Protein expression of PDCD4, a miR-21 target, was inversely correlated with miR-21 expression, confirming that miR-21 is indeed a negative regulator of PDCD4 in vivo. In the endoscopic samples, miR-21 expression was very high in malignant adenocarcinomas but was not elevated in nontumorigenic polyps. Precancerous adenomas also frequently showed miR-21 up-regulation.

Conclusion: Using the LNA-ISH system for miRNA detection, miR-21 was detectable in precancerous adenomas. The frequency and extent of miR-21 expression increased during the transition from precancerous colorectal adenoma to advanced carcinoma. Expression patterns of miR-21 RNA and its target, tumor suppressor protein PDCD4, were mutually exclusive. This pattern may have clinical application as a biomarker for colorectal cancer development and might be emphasized by self-reinforcing regulatory systems integrated with the miR-21 gene, which has been previously shown in cell culture.

  Y Nakai , H Isayama , T Sasaki , N Sasahira , H Kogure , K Hirano , T Tsujino , H Ijichi , K Tateishi , M Tada , M Omata and K. Koike

We investigated the impact of S-1 on the prognosis of patients with gemcitabine-refractory pancreatic cancer.


A total of 108 patients with gemcitabine-refractory pancreatic cancer were divided by the time of S-1 introduction in our institution: 47 patients who experienced progressive disease before February 2005 (pre-S-1 group) and 61 patients showed progressive disease after February 2005 (post-S-1 group). Introduction rates of second-line chemotherapy and survival were compared. Prognostic factors for residual survival were analyzed using the Cox proportional hazards model.


Introduction rates of second-line chemotherapy were 12.8% in the pre-S-1 group and 45.9% in the post-S-1 group. Second-line chemotherapy was administered to 34 patients: 29 using S-1, 4 using 5-fluorouracil-based chemoradiation and 1 using 5-fluorouracil. The objective response rate, progression-free survival and overall survival for second-line chemotherapy with S-1 were17.2%, 2.5 and 7.7 months, respectively. By the introduction of S-1 in our institution, residual survival was prolonged from 3.1 months in the pre-S-1 group to 6.7 months in the post-S-1 group (P < 0.001). Overall survival from the initiation of gemcitabine was 8.8 months in the pre-S-1 group and 11.3 months in the post-S-1 group (P = 0.013). Multivariate analysis identified the post-S-1 group (hazard ratio, 0.43; P = 0.001), gender, performance status, liver metastasis, and lactate dehydrogenase and C-reactive protein levels at progressive disease for gemcitabine to be prognostic factors for residual survival.


The introduction of S-1 might improve the prognosis of patients with gemcitabine-refractory pancreatic cancer.

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