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Articles by K Tanaka
Total Records ( 8 ) for K Tanaka
  K Tanaka , F Akiyama , N Nishikawa , K Kimura , N Gomi , K Oda and T. Iwase

OBJECTIVE. We describe the case of a woman with a left breast mass. At mammography, the mass was shown to be irregular and accompanied by coarse calcification. Core needle biopsy revealed invasive carcinoma and a mastectomy was performed. Histopathology showed fibrosis with partial hyalinization eccentrically placed within the tumor with a large area of calcification at the core.

CONCLUSION. Benign calcifications within a breast mass are not diagnostic of a benign process if the imaging characteristics of the mass are suspicious.

  A Miyaki , S Maeda , M Yoshizawa , M Misono , Y Saito , H Sasai , T Endo , Y Nakata , K Tanaka and R. Ajisaka

Obesity and reduction in central arterial distensibility, respectively, have been identified as powerful and independent risk factors for cardiovascular disease. However, the effect of weight reduction on central arterial function in obese subjects has not yet been clarified. We investigated whether low-calorie diet-induced weight reduction affects central arterial distensibility and endothelial function in middle-aged obese men. Twelve obese men (age: 45+2 yrs, BMI: 30+1 kg/m 2) completed a 12-week dietary intervention. Caloric restriction induced significantly weight loss and decrease in BMI. After the program, carotid arterial compliance significantly increased and b-stiffness index and aortic pulse-wave velocity remarkably decreased. Concentrations of plasma endothelin-1 (ET-1) significantly decreased and plasma nitric oxide (NO) markedly increased after the program. Weight reduction by low-calorie diet in obese men increases central arterial distensibility, which may contribute to the improvement in endothelial function, as noted by a decrease in ET-1 and an increase in NO.

  F. J Swartling , M. R Grimmer , C. S Hackett , P. A Northcott , Q. W Fan , D. D Goldenberg , J Lau , S Masic , K Nguyen , S Yakovenko , X. N Zhe , H. C Flynn Gilmer , R Collins , M Nagaoka , J. J Phillips , R. B Jenkins , T Tihan , S. R Vandenberg , C. D James , K Tanaka , M. D Taylor , W. A Weiss and L. Chesler

Medulloblastoma (MB) is the most common malignant brain tumor of childhood. Sonic Hedgehog (SHH) signaling drives a minority of MB, correlating with desmoplastic pathology and favorable outcome. The majority, however, arises independently of SHH and displays classic or large cell anaplastic (LCA) pathology and poor prognosis. To identify common signaling abnormalities, we profiled mRNA, demonstrating misexpression of MYCN in the majority of human MB and negligible expression in normal cerebella. We clarified a role in pathogenesis by targeting MYCN (and luciferase) to cerebella of transgenic mice. MYCN-driven MB showed either classic or LCA pathologies, with Shh signaling activated in ~5% of tumors, demonstrating that MYCN can drive MB independently of Shh. MB arose at high penetrance, consistent with a role for MYCN in initiation. Tumor burden correlated with bioluminescence, with rare metastatic spread to the leptomeninges, suggesting roles for MYCN in both progression and metastasis. Transient pharmacological down-regulation of MYCN led to both clearance and senescence of tumor cells, and improved survival. Targeted expression of MYCN thus contributes to initiation, progression, and maintenance of MB, suggesting a central role for MYCN in pathogenesis.

  Y Inoue , Y Toiyama , K Tanaka , C Miki and M. Kusunoki

Analyses were performed to assess whether the use of chemotherapeutic agents or regimens against colorectal cancer (CRC) differed among countries, especially the United States (USA), the European Union (EU) and Japan.


The data source for this study was the IMS Health, Oncology AnalyzerTM. We utilized data on the use of anticancer drugs and follow-up information for patients with CRC from April 2006 to March 2007, collected from the USA, the EU (G5: France, Germany, Italy, Spain and the UK) and Japan. A total of 102 502 patients were enrolled.


Wide differences were found in the actual regimens adopted by each region and nation. In other words, the concept of oncologist-related variability in chemotherapy for CRC was clearly seen. Factors such as a nation's historical characteristics and the healthcare policies of respective governments, including drug approval and cost-effectiveness, also appeared to have roles. However, comparisons of 5-year relative survival rates from population-based cancer registries in the USA, the EU and Japan showed that survival rates for CRC in the three regions did not differ widely, despite differences in the actual use of medical therapy. This may suggest that regional usage trends for anticancer regimens were optimal, although the application of chemotherapy was not the intentional standardization.


Global information exchanges regarding oncologist-related factors along with global evidence could result in patient survival being prolonged by the establishment of intentional standardized treatments suited for regional characteristics.

  T Hara , K Tanaka , K Maehata , K Mitsuda , N. Y Yamasaki , M Ohsaki , K Watanabe , X Yu , T Ito and Y. Yamanaka

A new energy dispersive X-ray spectrometer (EDS) with a mi- crocalorimeter detector equipped with a transmission electron microscope (TEM) has been developed for high- accuracy compositional analysis in the nanoscale. A superconducting transition-edge-sensor-type microcalorimeter is applied as the detector. A cryogen-free cooling system, which consists of a mechanical and a dilution refrigerator, is selected to achieve long-term temperature stability. In order to mount these detector and refrigerators on a TEM, the cooling system is specially designed such that these two refrigerators are separated. Also, the detector position and arrangement are carefully designed to avoid adverse affects between the superconductor detector and the TEM lens system. Using the developed EDS system, at present, an energy resolution of 21.92 eV full-width-at-half maximum has been achieved at the Cr K line. This value is about seven times better than that of the current typical commercial Si(Li) detector, which is usually around 140 eV. The developed microcalorimeter EDS system can measure a wide energy range, 1–20 keV, at one time with this high energy resolution that can resolve peaks from most of the elements. Although several further developments will be needed to enable practical use, highly accurate compositional analysis with high energy resolution will be realized by this microcalorimeter EDS system.

  H Ikehata , R Okuyama , E Ogawa , S Nakamura , A Usami , T Mori , K Tanaka , S Aiba and T. Ono

p53 suppresses the genomic instability provoked by genotoxic agents. Ultraviolet (UV) B induces skin cancers by producing DNA damage and mutations in the skin genome, whereas the skin tissue responds to the UVB insult with cell cycle arrest and apoptosis as well as damage exclusion by DNA repair. To address the p53 contribution to these skin responses in vivo, we analyzed the time course of DNA damage removal, apoptosis induction and hyperplasia in the skin after UVB irradiation in p53-knockout mice. We also examined UVB-induced mutations in the skin. We found that p53 deficiency does not abolish the UVB-induced apoptotic response in the epidermis but delays the process and the following hyperplasia 12–24 h. Regardless of the p53 genotype, 1 kJ/m2 UVB induced a total replacement of the epidermal layer by destroying the damaged epidermis by apoptosis and rebuilding a new one through hyperplasia. We failed to detect a clear defect in removal of UVB-induced DNA photolesions from the genome of the p53-deficient skin except for a delay in the epidermis, which seemed to result from the delay in the apoptotic response. However, we found that p53 deficiency enhanced UVB-induced mutagenesis. Furthermore, in a genetic study using Xpa-knockout mice, we showed that the enhanced mutagenic response depends on the activity of nucleotide excision repair (NER), which was also supported by the mutation spectrum observed in the UVB-exposed p53-knockout mice. These results indicate that p53 protects the skin genome from the UVB genotoxicity by facilitating NER, whereas its contribution to the UVB-induced apoptosis is limited.

  M Morita , K Hamao , S Izumi , E Okumura , K Tanaka , T Kishimoto and H. Hosoya

The large GTPase dynamin is strongly accumulated in the constricted area including midzonal microtubules of dividing cells. The proline-rich domain (PRD) of dynamin has been considered as a microtubule-binding domain. However, it remains unclear how PRD controls dynamin–microtubule interaction in mitotic cells. Here, we found that the microtubule-binding activity of PRD is low in dynamin-2. One of the mitosis-specific kinase activities to PRD in HeLa cells was identified as cyclin B-Cdc2 kinase. The kinase phosphorylated PRD at Ser764 and/or Thr766 and reduced the microtubule-binding activity of PRD. These results suggest that phosphorylation of PRD by cyclin B-Cdc2 kinase plays an important role to control dynamin-2–microtubule interaction in mitotic HeLa cells.

  V. A Tallada , K Tanaka , M Yanagida and I. M. Hagan

The fission yeast spindle pole body (SPB) comprises a cytoplasmic structure that is separated from an ill-defined nuclear component by the nuclear envelope. Upon mitotic commitment, the nuclear envelope separating these domains disperses as the two SPBs integrate into a hole that forms in the nuclear envelope. The SPB component Cut12 is linked to cell cycle control, as dominant cut12.s11 mutations suppress the mitotic commitment defect of cdc25.22 cells and elevated Cdc25 levels suppress the monopolar spindle phenotype of cut12.1 loss of function mutations. We show that the cut12.1 monopolar phenotype arises from a failure to activate and integrate the new SPB into the nuclear envelope. The activation of the old SPB was frequently delayed, and its integration into the nuclear envelope was defective, resulting in leakage of the nucleoplasm into the cytoplasm through large gaps in the nuclear envelope. We propose that these activation/integration defects arise from a local deficiency in mitosis-promoting factor activation at the new SPB.

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