9 results on '"Tateishi Y"'
Search Results
2. The first case of gastric leiomyosarcoma developed through malignant transformation of leiomyoma.
- Author
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Yamamoto A, Tateishi Y, Aikou S, Seto Y, and Ushiku T
- Subjects
- Aged, Humans, Leiomyoma diagnosis, Leiomyosarcoma diagnosis, Male, Stomach Neoplasms diagnosis, Cell Transformation, Neoplastic pathology, Leiomyoma pathology, Leiomyosarcoma pathology, Stomach Neoplasms pathology
- Abstract
Malignant transformation of gastric leiomyoma has not been reported, and therefore it is considered to have virtually no malignant potential. We report a case of gastric leiomyosarcoma arising from leiomyoma. The patient is a 72-year-old man with a submucosal mass measuring 20 mm in diameter, which was incidentally identified by an endoscopic surveillance. A biopsy suggested a diagnosis of leiomyosarcoma, and local excision was performed. Pathological examination revealed that the tumor was composed of two distinct components: typical leiomyoma-like area in the periphery and leiomyosarcoma component exhibiting higher cellularity, prominent nuclear atypia, necrosis, and increased mitosis. Immunohistochemically, in the latter, p53 overexpression, increased Ki-67 labeling index, and attenuated expression of smooth muscle markers were noted. This is the first report to demonstrate the presence of leiomyoma-leiomyosarcoma sequence in the stomach that is well recognized in the uterus. Our observation highlights the potential occurrence of malignant transformation of gastrointestinal leiomyoma., (© 2021 Japanese Society of Pathology and John Wiley & Sons Australia, Ltd.)
- Published
- 2021
- Full Text
- View/download PDF
3. Pulmonary melanocytic nevus - A case report with a mutation analysis of common driver oncogenes.
- Author
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Tanaka M, Matsumura M, Okudela K, Mitsui H, Tateishi Y, Umeda S, Suzuki T, Koike C, Kataoka T, Kawano N, Kojima Y, Osawa H, and Ohashi K
- Subjects
- DNA Mutational Analysis, Female, Humans, Lung Neoplasms pathology, Middle Aged, Mutation, Nevus, Pigmented pathology, Lung Neoplasms genetics, Nevus, Pigmented genetics, Proto-Oncogene Proteins B-raf genetics
- Abstract
Nevi are benign melanocytic tumors, and some nevi are considered to develop into malignant melanomas. Most nevi arise in the skin, but nevi occasionally occur in the conjunctiva, esophageal mucosa, or at other sites. Pulmonary melanocytic nevi are extremely rare, and only one case has been reported in the literature. Here, we present a case of pulmonary melanocytic nevus, involving a BRAF gene mutation (V600E), and we discuss the potential significance of this condition as a precursor to pulmonary malignant melanoma., (© 2019 Japanese Society of Pathology and John Wiley & Sons Australia, Ltd.)
- Published
- 2019
- Full Text
- View/download PDF
4. A molecular pathological study of four cases of ciliated muconodular papillary tumors of the lung.
- Author
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Kataoka T, Okudela K, Matsumura M, Mitsui H, Suzuki T, Koike C, Sawazumi T, Umeda S, Tateishi Y, Yamanaka S, Ishikawa Y, Arai H, Tajiri M, and Ohashi K
- Subjects
- Aged, Biomarkers, Tumor analysis, DNA Mutational Analysis, Female, Humans, Male, Middle Aged, Mutation, Pathology, Molecular, Lung Neoplasms genetics, Lung Neoplasms pathology, Papilloma genetics, Papilloma pathology
- Abstract
Ciliated muconodular papillary tumors (CMPTs) are a recently categorized benign or low-grade malignant neoplasm that develops in the peripheral lung. Only about 40 cases have been reported to date, and the clinicopathological characteristics have yet to be defined in detail. Here, we present four cases of CMPTs with a focus on their immunohistochemical profiles and driver gene mutations. These tumors were a papillary proliferation of a mixture of ciliated, mucous, and basal cells located in the peripheral lung. Ciliated, mucous and basal cells were positive for TTF-1 when using the clone SPT24, but negative for HNF-4α. Basal cells were positive for p40. Mucous cells in some tumors were positive for MUC5AC and MUC6. The Ki-67 index was less than 5%, and strong expression of p53 was not detected. Three of the four tumors had a BRAF (V600E) driver mutation, an EGFR (del E746-T751/S752V) driver mutation, or driver mutations in both EGFR (E709G) and KRAS (G12V). These mutation types are rare for any histological type of lung cancer. The present results confirmed that CMPT is a neoplasm with immunohistochemical features and driver gene mutations that are distinct from those of common lung tumors., (© 2018 Japanese Society of Pathology and John Wiley & Sons Australia, Ltd.)
- Published
- 2018
- Full Text
- View/download PDF
5. Alterations in cathepsin L expression in lung cancers.
- Author
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Okudela K, Mitsui H, Woo T, Arai H, Suzuki T, Matsumura M, Kojima Y, Umeda S, Tateishi Y, Masuda M, and Ohashi K
- Subjects
- Adenocarcinoma of Lung, Cell Line, Tumor, Epithelial Cells pathology, Humans, Lung physiopathology, Adenocarcinoma physiopathology, Cathepsin L genetics, Gene Expression Regulation, Neoplastic, Lung Neoplasms physiopathology
- Abstract
We herein investigated the potential role of cathepsin L in lung carcinogenesis. Lung cancer cell lines and surgically resected tumors were examined for the expression of the cathepsin L protein and copy number alterations in its gene locus. Cathepsin L was stably expressed in bronchiolar epithelial cells. Neoplastic cells expressed cathepsin L at various levels, whereas its expression was completely lost in most of the lung cancer cell lines (63.6%, 7/11) examined. Furthermore, expression levels were lower in a large fraction of lung tumors (69.5%, 139/200) than in bronchiolar epithelia. The expression of cathepsin L was lost in some tumors (16.0%, 32/200). In adenocarcinomas, expression levels were significantly lower in high-grade tumors than in low-grade tumors (one-way ANOVA, P < 0.0500). Copy number alterations were found in 18.0% (36 [32 gain + 4 loss] /200) of lung tumors. No relationship existed between cathepsin L protein expression levels and the copy number of its gene locus (Spearman's rank-order correlation, P = 0.3096). Collectively, these results suggest that the down-regulated expression of cathepsin L, which is caused by an undefined mechanism other than copy number alterations, is involved in the progression of lung adenocarcinomas., (© 2016 Japanese Society of Pathology and John Wiley & Sons Australia, Ltd.)
- Published
- 2016
- Full Text
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6. The potential role of microRNA-31 expression in early colorectal cancer.
- Author
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Tateishi Y, Okudela K, Mitsui H, Umeda S, Suzuki T, Kojima Y, Watanabe K, Kawano N, Endo I, and Ohashi K
- Subjects
- Adult, Aged, Aged, 80 and over, Biomarkers, Tumor genetics, Colorectal Neoplasms diagnosis, Female, Humans, Lymphatic Metastasis, Male, Middle Aged, Neoplasm Staging methods, Real-Time Polymerase Chain Reaction methods, Colorectal Neoplasms genetics, Colorectal Neoplasms pathology, Gene Expression Regulation, Neoplastic genetics, MicroRNAs genetics
- Abstract
The expression of microRNA-31 (miR-31) has been implicated in the progression of some human malignancies including colorectal cancer. However, the clinical significance of the expression of miR-31 in submucosally invasive (T1) colorectal cancer remains unclear. The aim of the present study was to delineate the relationship between clinicopathological features and the oncogenic modulator miR-31 in submucosally invasive colorectal cancer. We investigated the expression of miR-31 in 50 submucosally invasive colorectal cancer specimens, along with the corresponding non-tumoral mucosa specimens, using a real-time quantitative reverse transcription-polymerase chain reaction (qRT-PCR). The relationships between miR-31 expression levels and clinicopathological characteristics were assessed. The miR-31 host gene locus was investigated using fluorescence in situ hybridization. qRT-PCR revealed that the expression of miR-31 was higher in colorectal cancer tissue than in non-tumoral tissue (P = 0.0002). The up-regulated expression of miR-31 may play an oncogenic role in the early stage of carcinogenesis in colorectal cancers., (© 2015 Japanese Society of Pathology and Wiley Publishing Asia Pty Ltd.)
- Published
- 2015
- Full Text
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7. Leptomeningeal melanomatosis associated with neurocutaneous melanosis: an autopsy case report.
- Author
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Matsumura M, Okudela K, Tateishi Y, Umeda S, Mitsui H, Suzuki T, Nakayama T, Inayama Y, and Ohashi K
- Subjects
- Adult, Autopsy, Humans, Male, Melanosis pathology, Meningeal Neoplasms pathology, Neurocutaneous Syndromes pathology
- Abstract
An autopsy case of leptomeningeal melanomatosis associated with neurocutaneous melanosis (NCM) involving a 44-year-old male is reported. The autopsy showed that the leptomeningeal surface of the brain and the spinal cord were covered with a diffuse black lesion. A histological examination detected diffusely distributed, proliferating, melanin-containing cells and demonstrated that the lesion consisted of three different components; i.e. regions of melanomatosis, melanocytosis, and melanocyte hyperplasia. In the leptomeningeal melanomatosis component, tumor cells with pleomorphic nuclei and prominent nucleoli had infiltrated into the cerebral parenchyma via Virchow-Robin spaces. The Ki-67 labeling index and the nuclear accumulation of p53 and p16 protein were immunohistochemically examined in each component. The Ki-67 labeling indices of the melanomatosis, melanocytosis, and melanocyte hyperplasia components were 8.7%, 0.8%, and 0%, respectively. Immunostaining of nuclear p16 produced a negative result in the melanomatosis component, but positive results in the melanocytosis and melanocyte hyperplasia components, whereas nuclear p53 expression was not detected in any of the components. This case suggests that p16(INK4) /CDKN2 may play a significant role in progression of leptomeningeal melanocytic neoplasms. We also reviewed previously reported cases of leptomeningeal neoplasms associated with NCM and discussed the relationship between the biological behavior and proliferative activity of such lesions., (© 2014 Japanese Society of Pathology and Wiley Publishing Asia Pty Ltd.)
- Published
- 2015
- Full Text
- View/download PDF
8. Hepatocyte nuclear factor-1 α inactivated hepatocellular adenomas in patient with congenital absence of the portal vein: a case report.
- Author
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Tateishi Y, Furuya M, Kondo F, Torii I, Nojiri K, Tanaka Y, Umeda S, Okudela K, Inayama Y, Endo I, and Ohashi K
- Subjects
- Adenoma, Liver Cell blood supply, Adult, Female, Hepatocyte Nuclear Factor 1-alpha genetics, Humans, Immunohistochemistry, Liver Neoplasms blood supply, Adenoma, Liver Cell genetics, Adenoma, Liver Cell pathology, Liver Neoplasms genetics, Liver Neoplasms pathology, Portal Vein abnormalities
- Abstract
Hepatocellular adenomas (HCAs) have been recognized recently as a heterogeneous group, and are subclassified according to genotype as well as morphological characteristics. We report a case of a 35-year-old Japanese woman who exhibited hepatocyte nuclear factor (HNF)-1α-inactivated HCA in the background of the congenital absence of the portal vein (CAPV). On a dynamic contrast computed tomography (CT) scan, the hypovascular tumor enlarged from 1 cm to 3 cm and another tumor emerged in the course of 7 years. Because the possibility of hepatocellular carcinoma (HCC) with multiple metastases was not excluded, partial hepatectomy was performed. On a cut section, two well-demarcated tumors were observed and one tumor had a central fibrous scar. The histological features of these tumors were similar to those of focal nodular hyperplasia (FNH) with a central scar and HCA; however, these tumors were diagnosed as HNF-1α-inactivated HCA by immunohistochemistry according to the criteria of the current World Health Organization (WHO) classification. In non-tumorous liver tissue, an abnormal architecture of the vessels and a vague nodular appearance of lobuli were observed, which were likely to be those of nodular regenerated hyperplasia (NRH). We discuss its pathogenesis and relationship with CAPV., (© 2013 The Authors. Pathology International © 2013 Japanese Society of Pathology and Wiley Publishing Asia Pty Ltd.)
- Published
- 2013
- Full Text
- View/download PDF
9. Gastric carcinoma with osteoclast-like giant cells. Lymphoepithelioma-like carcinoma with Epstein-Barr virus infection is the predominant type.
- Author
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Ushiku T, Shinozaki A, Uozaki H, Iwasaki Y, Tateishi Y, Funata N, Seto Y, and Fukayama M
- Subjects
- Adenocarcinoma complications, Adenocarcinoma virology, Aged, Aged, 80 and over, Carcinoma, Neuroendocrine virology, Epstein-Barr Virus Infections complications, Epstein-Barr Virus Infections virology, Giant Cells virology, Herpesvirus 4, Human genetics, Humans, In Situ Hybridization, Male, Middle Aged, Stomach Neoplasms complications, Stomach Neoplasms virology, Adenocarcinoma pathology, Carcinoma, Neuroendocrine pathology, Epstein-Barr Virus Infections pathology, Giant Cells pathology, Stomach Neoplasms pathology
- Abstract
Osteoclast-like giant cells (OGC) are rare in gastric carcinomas. Histopathological study of seven gastric carcinomas with OGC demonstrated three distinct types: lymphoepithelioma-like carcinoma (LELC), non-LELC, and giant cell tumor (GCT) types. LELC is a poorly differentiated adenocarcinoma with prominent lymphoid stroma. The LELC type (n = 4) showed similar histology to LELC of the stomach, except that they were accompanied by OGC and granulomatous reaction. Epstein-Barr virus (EBV) infection was demonstrated by EBV-encoded RNA (EBER) in situ hybridization (ISH) in all the neoplastic cells. The non-LELC type (n = 2) consisted of EBV-negative carcinoma cells with inflammatory infiltrates. OGC and granulomas were frequently observed in the glandular lumens with accumulated mucus. The GCT type (n = 1) was a neuroendocrine carcinoma, containing many OGC with metaplastic bone formation, which showed typical morphological features of OGC in GCT of the bone. In all three types, OGC expressed CD68, but not cytokeratin, indicating that OGC had a reactive histiocytic lineage. Both LELC and non-LELC types are included in the differential diagnosis of isolated granulomatous gastritis, and EBER-ISH was useful for the identification of LELC type. Both LELC and no-LELC types were also suggested to have better prognoses, but the behavior of the GCT type needs to be further characterized.
- Published
- 2010
- Full Text
- View/download PDF
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