Massive B cell lymphoid hyperplasia and its associated factors may play a role in exacerbating inflammation in allergic disorders. We here investigated the chemokines and CD4-positive T cell subset involved in the development of secondary lymphoid follicles (iCALT) in conjunctival tissues in an atopic keratoconjunctivitis mouse model (AKC mouse).NC/Nga mice were divided into three groups: AKC (percutaneous sensitization and instillation of crude house dust mite antigen), AD (percutaneous sensitization only) and C (untreated control). Pathological changes in the conjunctival tissues of each group were investigated using histological and immunohistochemical detection of CD4 and CD20. Furthermore, tissue sections of iCALT (AKC-iCALT subgroup) and conjunctiva without iCALT (AKC-conjunctiva subgroup) were obtained from AKC mice using laser-assisted microdissection. mRNA expression of chemokine and T cell subset-related transcription factors were compared between the AKC-iCALT and AKC-conjunctiva subgroups using polymerase chain reaction (PCR) array and real-time reverse transcription-PCR (RT-PCR) methods.iCALT with central aggregation of CD20-positive B cells and CD4-positive T cell infiltration surrounding B cells was observed in the palpebral conjunctival tissue of the AKC group, but not in that of the AD and C groups. Chemokine and T cell subset-related transcription factor expression was confirmed using real-time RT-PCR, with significant increases in Ccl5, Ccl17, Cxl20, Cxcl3, Ccr7, Foxp3 and T-bet mRNA expression in the AKC-iCALT subgroup compared with those in the AKC-conjunctiva subgroup.We concluded that CCL5, CCL17 and CCL20, as well as T-bet- and Foxp3-positive lymphocytes may be iCALT-related factors and that iCALT-related chemokines are worth evaluating as biomarkers.
Research Articles| February 16 2011 Application of Liquid-Based Preparation to Fine Needle Aspiration Cytology in Breast Cancer Subject Area: Pathology and Cell Biology Kyoko Komatsu; Kyoko Komatsu From the Pathology Laboratory, Nihon University Itabashi Hospital; Departments of Pathology and of Surgery and Endocrinology, Nihon University School of Medicine; and Department of Pathology, Jiseikai Hospital, Tokyo, Japan. Search for other works by this author on: This Site PubMed Google Scholar Yoko Nakanishi; Yoko Nakanishi From the Pathology Laboratory, Nihon University Itabashi Hospital; Departments of Pathology and of Surgery and Endocrinology, Nihon University School of Medicine; and Department of Pathology, Jiseikai Hospital, Tokyo, Japan. Search for other works by this author on: This Site PubMed Google Scholar Toshimi Seki; Toshimi Seki From the Pathology Laboratory, Nihon University Itabashi Hospital; Departments of Pathology and of Surgery and Endocrinology, Nihon University School of Medicine; and Department of Pathology, Jiseikai Hospital, Tokyo, Japan. Search for other works by this author on: This Site PubMed Google Scholar Atsuko Yoshino; Atsuko Yoshino From the Pathology Laboratory, Nihon University Itabashi Hospital; Departments of Pathology and of Surgery and Endocrinology, Nihon University School of Medicine; and Department of Pathology, Jiseikai Hospital, Tokyo, Japan. Search for other works by this author on: This Site PubMed Google Scholar Fumi Fuchinoue; Fumi Fuchinoue From the Pathology Laboratory, Nihon University Itabashi Hospital; Departments of Pathology and of Surgery and Endocrinology, Nihon University School of Medicine; and Department of Pathology, Jiseikai Hospital, Tokyo, Japan. Search for other works by this author on: This Site PubMed Google Scholar Sadao Amano; Sadao Amano From the Pathology Laboratory, Nihon University Itabashi Hospital; Departments of Pathology and of Surgery and Endocrinology, Nihon University School of Medicine; and Department of Pathology, Jiseikai Hospital, Tokyo, Japan. Search for other works by this author on: This Site PubMed Google Scholar Akio Komatsu; Akio Komatsu From the Pathology Laboratory, Nihon University Itabashi Hospital; Departments of Pathology and of Surgery and Endocrinology, Nihon University School of Medicine; and Department of Pathology, Jiseikai Hospital, Tokyo, Japan. Search for other works by this author on: This Site PubMed Google Scholar Masahiko Sugitani; Masahiko Sugitani From the Pathology Laboratory, Nihon University Itabashi Hospital; Departments of Pathology and of Surgery and Endocrinology, Nihon University School of Medicine; and Department of Pathology, Jiseikai Hospital, Tokyo, Japan. Search for other works by this author on: This Site PubMed Google Scholar Norimichi Nemoto Norimichi Nemoto From the Pathology Laboratory, Nihon University Itabashi Hospital; Departments of Pathology and of Surgery and Endocrinology, Nihon University School of Medicine; and Department of Pathology, Jiseikai Hospital, Tokyo, Japan. Search for other works by this author on: This Site PubMed Google Scholar Acta Cytologica (2008) 52 (5): 591–596. https://doi.org/10.1159/000325603 Article history Published Online: February 16 2011 Content Tools Views Icon Views Article contents Figures & tables Video Audio Supplementary Data Peer Review Share Icon Share Facebook Twitter LinkedIn Email Tools Icon Tools Get Permissions Cite Icon Cite Search Site Citation Kyoko Komatsu, Yoko Nakanishi, Toshimi Seki, Atsuko Yoshino, Fumi Fuchinoue, Sadao Amano, Akio Komatsu, Masahiko Sugitani, Norimichi Nemoto; Application of Liquid-Based Preparation to Fine Needle Aspiration Cytology in Breast Cancer. Acta Cytologica 1 October 2008; 52 (5): 591–596. https://doi.org/10.1159/000325603 Download citation file: Ris (Zotero) Reference Manager EasyBib Bookends Mendeley Papers EndNote RefWorks BibTex toolbar search Search Dropdown Menu toolbar search search input Search input auto suggest filter your search All ContentAll JournalsActa Cytologica Search Advanced Search This content is only available via PDF. 2008Copyright / Drug Dosage / DisclaimerCopyright: All rights reserved. No part of this publication may be translated into other languages, reproduced or utilized in any form or by any means, electronic or mechanical, including photocopying, recording, microcopying, or by any information storage and retrieval system, without permission in writing from the publisher.Drug Dosage: The authors and the publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accord with current recommendations and practice at the time of publication. 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A novel nodulin gene, AsNODc22, was isolated from Astragalus sinicus cv. Japan (Renge-sou) by differential screening. The transcript of AsNODc22 was nodule specific, and its size was approximately 0.8 knt. AsNODc22 encoded an unknown ORF containing a putative signal peptide and a pair of similar hepta-peptides (CSAQVSC, CSAQLSC). For immunological study, antiserum against AsNODc22 protein was prepared in mice. By immunoblot analysis, the antiserum detected a nodule specific band at approximately 18 kDa. Immunofluorescence microscopy was used to observe localization of the gene product in the nodule. The signals were seen along the cell wall of bacteria-infected cells, but no significant signals were seen on uninfected cells.
MUC1 glycoprotein is overexpressed and its intracellular localization altered during breast carcinoma tumorigenesis. The present study aimed to clarify the relationship of cytoplasmic localization of MUC1 with the breast cancer subtype and the correlation of 10 molecules associated with cell polarity in breast cancer subtypes. We immunostained 131 formalin-fixed and paraffin-embedded breast cancer specimens with an anti-MUC1 antibody (MUC1/CORE). For 48 of the 131 tumor specimens, laser-assisted microdissection and real-time quantitative RT-PCR were performed to analyze mRNA levels of MUC1 and 10 molecules, β-catenin, E-cadherin, claudin 3, claudin 4, claudin 7, RhoA, cdc42, Rac1, Par3 and Par6. Localization of MUC1 protein varied among breast cancer subtypes, that is, both the apical domain and cytoplasm in luminal A-like tumors (P < 0.01) and both the cytoplasm and cell membrane in luminal B-like (growth factor receptor 2 [HER2]+) tumors (P < 0.05), and no expression was found in triple negative tumors (P < 0.001). Estrogen receptor (ER)+ breast cancers showed higher MUC1 mRNA levels than ER- breast cancers (P < 0.01). The incidence of mutual correlations of expression levels between two of the 10 molecules (55 combinations) was 54.5% in normal breast tissue and 38.2% in luminal A-like specimens, 16.4% in luminal B-like (HER2+), 3.6% in HER2 and 18.2% in triple negative specimens. In conclusion, each breast cancer subtype has characteristic cytoplasmic localization patterns of MUC1 and different degrees of disrupted correlation of the expression levels between the 10 examined molecules in comparison with normal breast tissue.
Breast cancer manifests in diverse forms, with particular reference to various cell types harboring different mutations and gene expression profiles. To elucidate the clonal relationship between cancer cells in tumors composed of both ductal and lobular phenotypes, two combined lobular and ductal carcinoma (CLDC) cases were analyzed, including one mixed ductal‑lobular carcinoma (MDL) lesion, by direct sequencing of the mitochondrial DNA D‑loop, digital PCR targeting of chromosomes 1q and 16q, as well as next‑generation sequencing. DNA was extracted from formalin‑fixed paraffin‑embedded tissue sections of different histological types, including invasive ductal carcinoma, invasive lobular carcinoma, ductal carcinoma in situ, lobular carcinoma in situ, flat epithelial atypia, non‑neoplastic mammary gland and extramammary organs, using laser‑assisted microdissection. Mutations detected by the comprehensive cancer panel were validated by SYBR green allele‑specific quantitative PCR (RRM1, AKT1, PIK3CA, RALGDS, EGFR, TP53, IL21R, DPYD, SGK1, CDH1, TIMP3 and KMT2C). CLDC, which shared the basic genetic alterations of 1q gain or 16q loss, progresses to invasive lobular or ductual carcinoma with the accumulation of further mutations. Cancer cells contained in an MDL lesion shared closely related genetic alterations, suggesting that these cells have the same origin, despite different histological features, namely 'lobular' or 'ductal'. By contrast, multiple lesions located away from the main tumor, diagnosed as CLDC (excluding an MDL lesion) were not always identical with different genetic alterations, despite being diagnosed as ductal carcinoma in situ. Thus, MDL should be defined as a distinct category separate from CLDC, whose components of 'lobular' and 'ductal' may have the same cellular origin.
