Search

Your search keyword '"Harazono, Yosuke"' showing total 38 results
Start Over Author "Harazono, Yosuke"
38 results on '"Harazono, Yosuke"'

4. Osteoblastoma in the mandible of an older adult patient without FOS gene rearrangement: A case report and literature review.

Author

Harazono, Yosuke, Yoshitake, Hiroyuki, Fukawa, Yuki, Ikeda, Tohru, and Yoda, Tetsuya

Abstract

Osteoblastoma is a benign bone tumor with predominance in those < 20 years of age and rarely occurs in the maxillofacial region. The identification of FOS gene rearrangements in osteoblastomas has been reported, however, a small subset of osteoblastomas do not show FOS gene rearrangements. There are no reports discussing the relationship between age and FOS gene rearrangement in osteoblastomas. We report the case of a 66-year-old female patient with histological features of osteoblastoma in the mandible without FOS gene rearrangement. According to a review of previously reported cases of osteoblastoma, FOS gene rearrangement is significantly less common in patients > 40 years of age (P = 0.041). Osteoblastomas occurring in older adult patients may exhibit pathogeneses different from those of young patients. Further data, including the relationship between age and FOS gene rearrangement, is necessary to clarify the pathogenesis of osteoblastoma. [ABSTRACT FROM AUTHOR]

Published
2024
Full Text
View/download PDF

19. Radiotherapy Plus Cetuximab for Squamous Cell Carcinoma of the Oral Cavity: A Multicenter Retrospective Study of 79 Patients in Japan

Author

Otsuru, Mitsunobu, primary, Yanamoto, Souichi, additional, Yamada, Shin-ichi, additional, Nakashiro, Kohichi, additional, Harazono, Yosuke, additional, Kohgo, Tomoyuki, additional, Nakamura, Moriyoshi, additional, Nomura, Takeshi, additional, Kasamatsu, Atsushi, additional, Tanaka, Susumu, additional, Kirita, Tadaaki, additional, Kioi, Mitomu, additional, Ogawa, Masaru, additional, Sasaki, Masashi, additional, Ota, Yoshihide, additional, and Umeda, Masahiro, additional

Published
2023
Full Text
View/download PDF

29. Osteoblastoma in the mandible of an older adult patient without FOSgene rearrangement: A case report and literature review

Author

Harazono, Yosuke, Yoshitake, Hiroyuki, Fukawa, Yuki, Ikeda, Tohru, and Yoda, Tetsuya

Abstract

Osteoblastoma is a benign bone tumor with predominance in those < 20 years of age and rarely occurs in the maxillofacial region. The identification of FOSgene rearrangements in osteoblastomas has been reported, however, a small subset of osteoblastomas do not show FOSgene rearrangements. There are no reports discussing the relationship between age and FOSgene rearrangement in osteoblastomas. We report the case of a 66-year-old female patient with histological features of osteoblastoma in the mandible without FOSgene rearrangement. According to a review of previously reported cases of osteoblastoma, FOSgene rearrangement is significantly less common in patients > 40 years of age (P = 0.041). Osteoblastomas occurring in older adult patients may exhibit pathogeneses different from those of young patients. Further data, including the relationship between age and FOSgene rearrangement, is necessary to clarify the pathogenesis of osteoblastoma.

Published
2024
Full Text
View/download PDF

37. miR-655 Is an EMT-Suppressive MicroRNA Targeting ZEB1 and TGFBR2

Author

Harazono, Yosuke, Muramatsu, Tomoki, Endo, Hironori, Uzawa, Narikazu, Kawano, Tatsuyuki, Harada, Kiyoshi, Inazawa, Johji, and Kozaki, Ken-ichi

Subjects
*MICRORNA, *EPITHELIAL cells, *MESENCHYMAL stem cells, *CANCER invasiveness, *CANCER cells, *PANCREATIC cancer, *GENE expression, *CELLULAR signal transduction
Abstract

Recently, the epithelial-to-mesenchymal transition (EMT) has been demonstrated to contribute to normal and disease processes including cancer progression. To explore EMT-suppressive microRNAs (miRNAs), we established a cell-based reporter system using a stable clone derived from a pancreatic cancer cell line, Panc1, transfected with a reporter construct containing a promoter sequence of CDH1/E-cadherin in the 5′ upstream region of the ZsGreen1 reporter gene. Then, we performed function-based screening with 470 synthetic double-stranded RNAs (dsRNAs) mimicking human mature miRNAs using the system and identified miR-655 as a novel EMT-suppressive miRNA. Overexpression of miR-655 not only induced the upregulation of E-cadherin and downregulation of typical EMT-inducers but also suppressed migration and invasion of mesenchymal-like cancer cells accompanied by a morphological shift toward the epithelial phenotype. In addition, we found a significant correlation between miR-655 expression and a better prognosis in esophageal squamous cell carcinoma (ESCC). Moreover, ZEB1 and TGFBR2, which are essential components of the TGF-b signaling pathway, were identified as direct targets of miR-655, suggesting that the activation of the TGF-b-ZEB1-E-cadherin axis by aberrant downregulation of miR-655 may accelerate cancer progression. [ABSTRACT FROM AUTHOR]

Published
2013
Full Text
View/download PDF

38. TP63mutation mapping information in TP63mutation-associated syndromes

Author

Harazono, Yosuke, Morita, Kei-ichi, Tonouchi, Erina, Anzai, Eri, Takahara, Namiaki, Kohmoto, Tomohiro, Imoto, Issei, and Yoda, Tetsuya

Abstract

The transcription factor tumour protein 63, encoded by the TP63gene, is a regulator of epidermal development. Heterozygous mutations in TP63cause a variety of human ectodermal dysplasia disorders, including ankyloblepharon-ectodermal defects-cleft lip/palate syndrome, ectrodactyly, ectodermal dysplasia, cleft lip/palate syndrome, split hand/foot malformation 4, Rapp-Hodgkin syndrome, limb mammary syndrome, and acro-dermato-ungual-lacrimal-tooth syndrome. There are genotype-phenotype correlations in some of these syndromes, and the number of cases with overlapping symptoms has been increasing. The phenotypic spectrum and expressivity of TP63mutation-associated syndromes complicate its clinical diagnosis and classification. Here, we present an updated review of TP63mutation mapping information, together with a comprehensive overview of TP63mutation-associated syndromes. We show that several cases with the same mutation have been previously diagnosed with different syndromes. This study will be useful for the diagnosis and classification of TP63mutation-associated syndromes.

Published
2022
Full Text
View/download PDF

Catalog

Books, media, physical & digital resources
See catalog results