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Ryoma Kurahashi Tsuyoshi Kadomatsu Masaya Baba Chiaki Hara Hitoshi Itoh Keishi Miyata Motoyoshi Endo Jun Morinaga Kazutoyo Terada Kimi Araki Masatoshi Eto Laura S. Schmidt Tomomi Kamba W. Marston Linehan Yuichi Oike 《Cancer science》2019,110(6):1897-1908
Xp11.2 translocation renal cell carcinoma (Xp11 tRCC) is a rare sporadic pediatric kidney cancer caused by constitutively active TFE3 fusion proteins. Tumors in patients with Xp11 tRCC tend to recur and undergo frequent metastasis, in part due to lack of methods available to detect early‐stage disease. Here we generated transgenic (Tg) mice overexpressing the human PRCC‐TFE3 fusion gene in renal tubular epithelial cells, as an Xp11 tRCC mouse model. At 20 weeks of age, mice showed no histological abnormalities in kidney but by 40 weeks showed Xp11 tRCC development and related morphological and histological changes. MicroRNA (miR)‐204‐5p levels in urinary exosomes of 40‐week‐old Tg mice showing tRCC were significantly elevated compared with levels in control mice. MicroRNA‐204‐5p expression also significantly increased in primary renal cell carcinoma cell lines established both from Tg mouse tumors and from tumor tissue from 2 Xp11 tRCC patients. All of these lines secreted miR‐204‐5p‐containing exosomes. Notably, we also observed increased miR‐204‐5p levels in urinary exosomes in 20‐week‐old renal PRCC‐TFE3 Tg mice prior to tRCC development, and those levels were equivalent to those in 40‐week‐old Tg mice, suggesting that miR‐204‐5p increases follow expression of constitutively active TFE3 fusion proteins in renal tubular epithelial cells prior to overt tRCC development. Finally, we confirmed that miR‐204‐5p expression significantly increases in noncancerous human kidney cells after overexpression of a PRCC‐TFE3 fusion gene. These findings suggest that miR‐204‐5p in urinary exosomes could be a useful biomarker for early diagnosis of patients with Xp11 tRCC. 相似文献
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Kiran Naqvi MD Elias Jabbour MD Jeffrey Skinner BS MHA Kristin Anderson BS Sara Dellasala BS Musa Yilmaz MD Alessandra Ferrajoli MD Prithviraj Bose MD Philip Thompson MBBS Yesid Alvarado MD Nitin Jain MBBS Koichi Takahashi MD Jan Burger MD Zeev Estrov MD Gautam Borthakur MBBS Naveen Pemmaraju MD Shilpa Paul Pharm D Jorge Cortes MD Hagop M. Kantarjian MD 《Cancer》2020,126(1):67-75
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Atsuko Kori Ikumi Hori Tatsushi Tanaka Kohei Aoyama Koichi Ito Ayako Hattori Kyoko Ban Yasushi Okazaki Kei Murayama Shinji Saitoh 《Brain & development》2019,41(9):803-807
An m.10158T>C mutation in MT-ND3, encoding a subunit of respiratory complex I, causes early-onset Leigh syndrome (LS), mitochondrial encephalomyopathy with lactic acid and stroke-like episodes (MELAS) syndrome, and LS and MELAS overlapping syndrome, presumably dependent on the ratio of heteroplasmy. Herein, we report a 4-year-old girl with heteroplasmic m.10158T>C mutation, showing an evolving age-dependent phenotype from LS to MELAS syndromes. She showed mild developmental delay during infancy, which was associated with magnetic resonance imaging lesions in the brain stem and basal ganglia. At the age of 4 years, she developed rapid neurological deterioration and intractable seizures, which was associated with recurrent multiple cerebral lesions as well as basal ganglia lesions. Her cerebral lesions were located predominantly in white matter and appeared at multiple areas simultaneously, unique characteristics that are distinct from typical MELAS. Two patients with LS-MELAS overlapping syndrome with m.10158T>C have been previously reported, however, this is the first patient with m.10158T>C showing significant age-dependent changes in clinical features and neuro-images, implying an age-dependent role of complex I in the developing brain. 相似文献
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Hirokazu Miki Shingen Nakamura Masahiro Oura Hirofumi Hamano Kenji Ikuta Naoto Okada Yasunobu Okamoto Kimiko Sogabe Mamiko Takahashi Masami Iwasa Kengo Udaka Takeshi Harada Kiyoe Kurahashi Shiro Fujii Sumiko Yoshida Kumiko Kagawa Itsuro Endo Ken-ichi Aihara Masahiro Abe 《British journal of haematology》2019,186(2):355-358
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Mai Ishikawa Yukie Endo Akihito Uehara Mariko Suto Masahito Yasuda Sei‐ichiro Motegi Osamu Ishikawa 《The Journal of dermatology》2019,46(2):161-165
Histiocytoses, including Langerhans cell histiocytosis (LCH), juvenile or adult xanthogranuloma (AXG) and Rosai–Dorfman disease (RDD), are rare disorders characterized by the proliferation of cells derived from monocyte/macrophage lineages. A few cases of LCH coexisting with xanthogranuloma or RDD have been reported. The etiology of these diseases remains unclear. However, oncogenic BRAFV600E mutations have been identified in LCH. Here, we report the case of a 26‐year‐old Japanese man with a 3‐month history of a solitary occipital nodule. No abnormality was detected in his other organs, and a total resection of the nodule was performed. Histopathological examination revealed the coexistence of LCH and AXG with prominent emperipolesis characteristic of RDD. Immunohistochemistry showed that most of the large histiocytes were positive for CD68, weakly positive or negative for S100, and negative for CD207 and CD1a, supporting the diagnosis of AXG. The tumor cells with emperipolesis did not show S100‐positive findings characteristic of RDD. The focally aggregated oval histiocytic cells were positive for CD1a, CD207, CD68 and S100, and were compatible with the immunophenotype of LCH cells. In addition, these cells were positive for BRAFV600E mutation. The tumor cells in our patient exhibited a cellular morphology characteristic of multiple histiocytoses in a solitary cutaneous nodule, which may imply an etiological association among LCH, AXG and RDD. To our knowledge, this is the first report of a BRAFV600E mutation‐positive case of LCH coexisting with AXG. Because patients with BRAFV600E mutation have higher risks of multisystemic LCH and recurrence, we should carefully follow up the patient. 相似文献