Biomedical subjects

Tatsuki R Kataoka

Publications and source records attributed to Tatsuki R Kataoka.

11 recordsLinked to original sources

PubMed2006

Function-preserving surgery for breast cancer.

Breast-conserving treatment is well established as a safe method of treatment for the majority of breast cancers. Issues to be addressed concerning breast-conserving treatment include the omission of radiation therapy in low-risk patients, optimal local and systemic treatment for ipsilateral breast tumor recurrence, classification of ipsilateral breast tumor recurrence into true recurrences and new primary cancers, and the selection of patients who are eligible for breast conservation after neoadjuvant chemotherapy. There is much evidence that sentinel node biopsy is an accurate method of screening for axillary nodal status in patients with early breast cancer. Clearly, the avoidance of axillary dissection improves quality of life. The feasibility, accuracy, and timing of sentinel node biopsy in patients undergoing neoadjuvant chemotherapy are not yet clear. Also, the clinical significance of micrometastasis should be evaluated to determine the optimal application of sentinel node biopsy. There is interest in replacing breast-conserving treatment by nonsurgical ablation, although additional findings are needed to show that this technique is a true advance in breast cancer treatment.

Antineoplastic Combined Chemotherapy Protocols↗

PubMed2006

Concomitant hepatocellular carcinoma and non-Hodgkin's lymphoma in a patient with nodular regenerative hyperplasia.

Hepatocellular carcinoma (HCC) is the most common primary cancer in the liver. Liver invasion of non-Hodgkin's lymphoma (NHL) is also often observed. But simultaneous existence of HCC and NHL in a liver is extremely rare. Such patients reported previously had cirrhotic livers. Herein is reported a patient who simultaneously had HCC and NHL in a liver without cirrhosis, but with nodular regenerative hyperplasia (NRH). NHL was of the diffuse large B-cell type. Lymphoma cells invaded the portal vein, and formed thrombi. These thrombi would contribute to the development of NRH by decreasing portal vein blood flow. HCC was of the well-differentiated type and there was a 2 cm-sized nodule at the lateral segment. There is the possibility that NRH was associated with the HCC because NRH is reported as a premalignant lesion. HCC and NHL were colocalized in the liver without hepatic virus infection or cirrhosis, although common cause(s) of development of these malignancies remain unclear in the present case.

Carcinoma, Hepatocellular↗

PubMed2005

Reduced expression of IL-12 receptor beta2 and IL-18 receptor alpha genes in natural killer cells and macrophages derived from B6-mi/mi mice.

The mi transcriptional factor (MITF) is a basic helix-loop-helix leucine zipper-type transcriptional factor. The mi mutant allele encodes an abnormal MITF, in which one out of four consecutive arginines is deleted in the basic domain. The VGA-9-tg (tg) allele is another mutant allele and considered to be a null mutant allele. C57BL/6 (B6)-mi/mi mice showed abnormal phenotypes of natural killer (NK) cells and macrophages, whereas B6-tg/tg mice did not. The expression levels of the genes for the interleukin-12 receptor (IL-12R) beta2 and IL-18Ralpha were reduced in both the NK cells and macrophages of B6-mi/mi mice, while the expression levels of the corresponding genes in B6-tg/tg mice were unaffected. The B6-mi/mi NK cells and B6-mi/mi macrophages showed impaired responses to stimulation with IL-12, IL-18, and IL-12 plus IL-18 stimulation. The abnormal NK cell and macrophage of B6-mi/mi mice appear to be due to decreased expression of the IL-12Rbeta2 and IL-18Ralpha genes.

Animals↗

PubMed2005

A case of phyllodes tumor of the breast with a lesion mimicking fibroadenoma.

We report a case of phyllodes tumor (PT) with multiple lesions partly mimicking fibroadenoma (FA). A 43-year-old woman was referred to our institute because of a left breast mass which was diagnosed as FA clinically. During the follow-up, the mass gradually enlarged and excisional biopsy was performed to rule out malignant lesion. On histological examination, the tumor consisted of three different components; a lesion diagnosed as FA, another lesion as benign PT, and the other lesion as borderline PT. Finally, the tumor was diagnosed as borderline PT. Stromal cellularity may vary from area to area in any given PT. If there are some disagreements among the findings of imagings and cytology for the diagnosis of FA, as was seen in our case, the possibility of coexistence of PT should be considered.

Adult↗

PubMed2004

Involvement of connective tissue-type mast cells in Th1 immune responses via Stat4 expression.

Mast cells are the sentinels of immune systems and, like other immuno-competent cells, they are produced by hematopoietic stem cells. We analyzed the expression of signal transducer and activator of transcription 4 (Stat4), and investigated its role in mast cells. Murine mast cells are usually divided into 2 distinct populations by their distribution and contents of their granules: mucosal mast cells (MMCs) and connective tissue-type mast cells (CTMCs). Stat4 protein was detected in CTMCs but not in MMCs. The absence of Stat4 expression in cultured mast cells was due to the presence of Stat6. In T-helper (Th) cells, Stat4 plays an important role in Th1 shift by inducing a set of genes, such as interferon gamma (IFN-gamma) and interleukin-18 receptor alpha subunit (IL-18Ralpha). As in Th1 shift, we found that Stat4 trans-activated these genes in the Stat4-expressing cultured mast cells, namely, microphthalmia transcription factor (MITF)-deficient cultured MMCs, Stat6-deficient cultured MMCs, and cultured CTMCs. Stat4 also enhanced expression of nitric oxide synthase 2 (NOS2) in CTMCs, which brought about increased levels of NO-dependent cytotoxic activity. These data indicate that expression of Stat4 in CTMCs plays an important role on Th1 immune responses.

Animals↗

PubMed2004

A derivative of oleamide potently inhibits the spontaneous metastasis of mouse melanoma BL6 cells.

We reported previously that the abnormally augmented expression of connexin 26 (Cx26) is responsible for the enhanced spontaneous metastasis of mouse BL6 melanoma cells, and that the exogenous expression of a dominant negative form of Cx26 inhibits the spontaneous metastasis of BL6. Here we show that daily intraperitoneal (i.p.) injections of oleamide, a sleep-inducing lipid hormone, weakly inhibited the spontaneous metastasis of BL6 cells. To obtain a more effective reagent, 19 oleamide derivatives were chemically synthesized and tested for their ability to inhibit the gap junction-mediated intercellular communications (GJIC) that are formed between HeLa cells by the ectopic expression of Cx26 or Cx43. One of these, denoted metastasis inhibitor-18 (MI-18), inhibited the GJIC formed by Cx26 as well as oleamide but unlike oleamide, which is a non-selective inhibitor of connexin, it did not inhibit the GJIC formed by Cx43. Daily i.p. injections of MI-18 potently blocked the spontaneous metastasis of BL6 cells down to 15% of that in the untreated control mice. MI-18 was safe because even after >7 weeks of daily injections, the survival rate of the mice was 93%. We propose that MI-18 may serve as a novel and clinically important prototype of a potent inhibitor of spontaneous metastasis.

Animals↗

PubMed2004

Strain-dependent inhibitory effect of mutant mi-MITF on cytotoxic activities of cultured mast cells and natural killer cells of mice.

MITF is a transcription factor encoded by the mi locus. MITF encoded by mi and Mi(or) mutant alleles (mi-MITF and Mi(or)-MITF, respectively) possessed an inhibitory effect, whereas the tg, mi(ew) and mi(ce) were null mutants. We examined the cytotoxic activities of cultured mast cells (CMCs) and natural killer (NK) cells of various MITF mutants in C57BL/6 (B6) background. Cytotoxic activities of CMCs and NK cells of B6-mi/mi and B6-Mi(or)/Mi(or) mice were remarkably reduced. In B6-tg/tg, B6-mi(ew)/mi(ew) and B6-mi(ce)/mi(ce) mice, however, the cytotoxic activity of CMCs was reduced only slightly and the NK activity was normal. The cytotoxic activity of CMCs paralleled with the expression level of granzyme B (Gr B) mRNA, and the NK activity with that of perforin (Pfn) mRNA. In contrast to the case of B6-mi/mi mice, cytotoxic activities of CMCs and NK cells were not impaired in WB-mi/mi mice. The expression of Gr B mRNA was not reduced in CMCs of WB-mi/mi mice, and that of Pfn mRNA was not reduced in NK cells of WB-mi/mi mice. WB-mi/mi mice appeared to have factor(s) compensating for the inhibitory effect of mi-MITF on the expression of Gr B and Pfn genes.

Animals↗

PubMed2003

Toriello-Carey syndrome associated with respiratory failure and non-mechanical ileus.

Toriello-Carey syndrome comprises agenesis of the corpus callosum, telecanthus, small palpebral fissures, Pierre Robin sequence, abnormal ears, and cardiac defects. We report a boy who has some additional findings, including a severe respiratory failure and intestinal dysmotility. The boy died of these two disorders at age 13 months. Histological examination revealed pulmonary immaturity and a defect of smooth muscle cells in the longitudinal muscle coat of the intestinal musculature, both of which might explain some aspects of the pathophysiology of the patient.

Abnormalities, Multiple↗

PubMed2002

Dual abnormal effects of mutant MITF encoded by Mi(wh) allele on mouse mast cells: decreased but recognizable transactivation and inhibition of transactivation.

MITF is a basic helix-loop-helix leucine zipper-type transcription factor and is important for development of mast cells. MITF encoded by Mi(wh) allele (Mi(wh)-MITF) was mutated at a single amino acid of basic domain, and possessed a deficient but apparent DNA-binding ability. Here, we characterized the unique effects of Mi(wh)-MITF on the expression of mast cell-related genes. The expression level of mouse mast cell protease (mMCP)-4, -5, and -6 genes in Mi(wh)/Mi(wh) cultured mast cells (CMCs) was intermediate between levels of normal (+/+) CMCs and tg/tg CMCs, which did not express any MITFs. Mi(wh)-MITF appeared to show the positive transactivation effect through the remaining DNA-binding ability. On the other hand, the expression level of tryptophan hydroxylase gene was lower in Mi(wh)/Mi(wh) CMCs than in tg/tg CMCs, suggesting the inhibitory effect of Mi(wh)-MITF on the transactivation. Mi(wh)-MITF possessed dual abnormal effects on transactivation of mast cell-related genes.

Alleles↗

PubMed2002

Isoforms of mi transcription factor preferentially expressed in cultured mast cells of mice.

MITF is a basic helix-loop-helix leucine zipper transcription factor, which is important for normal phenotypic expression of mast cells. Three isoforms of MITF have been known in mice, MITF-A, -H, and -M. Since cultured mast cells (CMCs) are useful for studying the function of MITF, we examined isoforms of MITF expressed in CMCs using 5'-RACE, and found a new isoform of MITF, MITF-E. We assessed the relative mRNA amount of various MITF isoforms with reverse transcription-PCR. When the mRNA amount of MITF-E was used as a standard, that of MITF-M was approximately 10%, that of MITF-H was approximately 1%, and that of MITF-A was approximately 0.1%. Although MITF-E was the preferential isoform in CMCs, peritoneal mast cells expressed only MITF-M. The expression profile of MITF isoforms appeared to be influenced by the developing process of mast cells.

3T3 Cells↗

PubMed2001

Interaction and cooperation of mi transcription factor (MITF) and myc-associated zinc-finger protein-related factor (MAZR) for transcription of mouse mast cell protease 6 gene.

The mi transcription factor (MITF) is a basic-helix-loop-helix leucine zipper (bHLH-Zip) transcription factor that is important for the normal phenotypic expression of mast cells. Most transcription factors function in cooperation with other factors by protein-protein interactions. To search proteins interacting with MITF, we carried out a yeast two-hybrid screen and isolated Myc-associated zinc-finger protein related factor (MAZR) as a partner of MITF. When expressed with MITF in NIH/3T3 cells, MAZR was colocalized with MITF. The association of MAZR with MITF was further confirmed by a co-immunoprecipitation study and in vitro binding assay. The zinc-finger domain of MAZR and the Zip domain of MITF were essential for the interaction. MAZR was expressed in cultured mast cells and MST mastocytoma cells containing mouse mast cell protease (mMCP)-6 transcript abundantly. The overexpression of dominant negative MAZR in MST mastocytoma cells reduced the amount of mMCP-6 mRNA. The simultaneous transfection of MAZR and MITF significantly increased the promoter activity of the mMCP-6 gene, indicating that the MAZR and MITF synergistically transactivated the mMCP-6 gene. MAZR appeared to play important roles in the normal phenotypic expression of mast cells in association with MITF.

3T3 Cells↗