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Articles by S Ota
Total Records ( 2 ) for S Ota
  N Yamada , S Ota , Ying Liu , C. M Chang , S Thaker , M Nakamura and M. Ito

Risk factors for pulmonary embolism (PE) have been identified among populations in Western countries but have not been well characterized in Japan. A hospital-based case-control design employed cases with PE, which diagnosed by standard imaging techniques; controls were individuals drawn by systematic random sampling from the hospital admission register. A total of 100 (38 males and 62 females) and 199 controls were identified. Patients with PE were younger (56.5 vs 60.9 years) and more likely to be female. The odds ratio ([OR] adjusted for other factors) and 95% confidence interval (CI) for risk of PE was elevated for the following: female gender, prolonged immobilization, history of prior venous thromboembolism (VTE), lower extremity varicose veins, body mass index (BMI) ≥ 25 kg/m 2, extremity paralysis, and gout/hyperuricemia. Inherited thrombophilia was found in 14 patients with PE (14%). Risk factors for PE in Japan are comparable in magnitude to those in Western countries; only one third of PE cases had received VTE prophylaxis.

  S Ota , Z. Q Zhou , J. M Link and P. J. Hurlin

Mutations in fibroblast growth factor receptors (FGFRs) cause human birth defect syndromes and are associated with a variety of cancers. Although forced expression of mutant activated FGFRs has been shown to oncogenically transform some immortal cell types, their activity in primary cells remains unclear. Here, we show that birth defect and cancer-associated FGFR2 mutants promote DNA-damage signaling and p53-dependent senescence in primary mouse and human cells. Senescence promoted by FGFR mutants was associated with downregulation of c-Myc and forced expression of c-Myc facilitated senescence escape. Whereas c-Myc expression facilitated senescence bypass, mutant FGFR2 signaling suppressed c-Myc-dependent apoptosis and led to oncogenic transformation. Cells transformed by coexpression of a constitutively activated FGFR2 mutant plus c-Myc appeared to be become highly addicted to FGFR-dependent prosurvival activities, as small molecule inhibition of FGFR signaling resulted in robust p53-dependent apoptosis. Our data suggest that senescence-promoting activities of mutant FGFRs may normally limit their oncogenic potential and may be relevant to their ability to disrupt morphogenesis and cause birth defects. Our results also raise the possibility that cancers originating through a combination of constitutive FGFR activation and deregulated Myc expression may be particularly sensitive to small molecule inhibitors of FGF receptors.

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