본문 바로가기
HOME> 저널/프로시딩 > 저널/프로시딩 검색상세

저널/프로시딩 상세정보

권호별목차 / 소장처보기

H : 소장처정보

T : 목차정보

Human pathology 28건

  1. [해외논문]   In This Issue   SCI SCIE


    Human pathology v.69 ,pp. iv - v , 2017 , 0046-8177 ,

    초록

    원문보기

    원문보기
    무료다운로드 유료다운로드

    회원님의 원문열람 권한에 따라 열람이 불가능 할 수 있으며 권한이 없는 경우 해당 사이트의 정책에 따라 회원가입 및 유료구매가 필요할 수 있습니다.이동하는 사이트에서의 모든 정보이용은 NDSL과 무관합니다.

    NDSL에서는 해당 원문을 복사서비스하고 있습니다. 아래의 원문복사신청 또는 장바구니담기를 통하여 원문복사서비스 이용이 가능합니다.

    이미지

    Fig. 1 이미지
  2. [해외논문]   Masthead   SCI SCIE


    Human pathology v.69 ,pp. IFC - IFC , 2017 , 0046-8177 ,

    초록

    원문보기

    원문보기
    무료다운로드 유료다운로드

    회원님의 원문열람 권한에 따라 열람이 불가능 할 수 있으며 권한이 없는 경우 해당 사이트의 정책에 따라 회원가입 및 유료구매가 필요할 수 있습니다.이동하는 사이트에서의 모든 정보이용은 NDSL과 무관합니다.

    NDSL에서는 해당 원문을 복사서비스하고 있습니다. 아래의 원문복사신청 또는 장바구니담기를 통하여 원문복사서비스 이용이 가능합니다.

    이미지

    Fig. 1 이미지
  3. [해외논문]   Editorial board   SCI SCIE


    Human pathology v.69 ,pp. iii - iii , 2017 , 0046-8177 ,

    초록

    원문보기

    원문보기
    무료다운로드 유료다운로드

    회원님의 원문열람 권한에 따라 열람이 불가능 할 수 있으며 권한이 없는 경우 해당 사이트의 정책에 따라 회원가입 및 유료구매가 필요할 수 있습니다.이동하는 사이트에서의 모든 정보이용은 NDSL과 무관합니다.

    NDSL에서는 해당 원문을 복사서비스하고 있습니다. 아래의 원문복사신청 또는 장바구니담기를 통하여 원문복사서비스 이용이 가능합니다.

    이미지

    Fig. 1 이미지
  4. [해외논문]   Masthead  


    Human pathology v.69 ,pp. IFC , 2017 , 0046-8177 ,

    초록

    원문보기

    원문보기
    무료다운로드 유료다운로드

    회원님의 원문열람 권한에 따라 열람이 불가능 할 수 있으며 권한이 없는 경우 해당 사이트의 정책에 따라 회원가입 및 유료구매가 필요할 수 있습니다.이동하는 사이트에서의 모든 정보이용은 NDSL과 무관합니다.

    NDSL에서는 해당 원문을 복사서비스하고 있습니다. 아래의 원문복사신청 또는 장바구니담기를 통하여 원문복사서비스 이용이 가능합니다.

    이미지

    Fig. 1 이미지
  5. [해외논문]   Table of Contents   SCI SCIE


    Human pathology v.69 ,pp. i - ii , 2017 , 0046-8177 ,

    초록

    원문보기

    원문보기
    무료다운로드 유료다운로드

    회원님의 원문열람 권한에 따라 열람이 불가능 할 수 있으며 권한이 없는 경우 해당 사이트의 정책에 따라 회원가입 및 유료구매가 필요할 수 있습니다.이동하는 사이트에서의 모든 정보이용은 NDSL과 무관합니다.

    NDSL에서는 해당 원문을 복사서비스하고 있습니다. 아래의 원문복사신청 또는 장바구니담기를 통하여 원문복사서비스 이용이 가능합니다.

    이미지

    Fig. 1 이미지
  6. [해외논문]   Genetic profile of ductal adenocarcinoma of the prostate   SCI SCIE

    Seipel, Amanda H. (Department of Oncology-Pathology, Karolinska Institutet, 171 76 Stockholm, Sweden ) , Whitington, Thomas (Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, 171 77 Stockholm, Sweden ) , Delahunt, Brett (Department of Pathology and Molecular Medicine, Wellington School of Medicine and Health Sciences, University of Otago, Wellington 6021, New Zealand ) , Samaratunga, Hemamali (Aquesta Pathology, Brisbane, Queensland 4066, Australia ) , Mayrhofer, Markus (Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, 171 77 Stockholm, Sweden ) , Wiklund, Peter (Department of Urology, Division of Surgery, Karolinska University Hospital, 171 76 Stockholm, Sweden ) , Grö (Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, 171 77 Stockholm, Sweden ) , nberg, Henrik (Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, 171 77 Stockholm, Sweden ) , Lindberg, Johan (Department of Oncology-Pathology, Karolinska Institutet, 171 76 Stockholm, Sweden) , Egevad, Lars
    Human pathology v.69 ,pp. 1 - 7 , 2017 , 0046-8177 ,

    초록

    Summary Despite being discovered almost 50 years ago, little is known regarding the genetic profile of ductal adenocarcinoma of the prostate (DAC). In recent years, progress has been made in the understanding of the genetics of acinar adenocarcinomas, and at least 7 genetically different subtypes have been identified. DAC is known to present at an advanced stage with a high rate of extraprostatic extension and seminal vesicle invasion, and a decreased interval to biochemical recurrence and the development of metastatic disease when compared with acinar adenocarcinoma. Our aim was to investigate the genetic profile of DAC to determine whether there is a genomic rationale for the aggressive behavior associated with this tumor type. Frozen tissue from 11 cases of DAC with paired benign tissue was analyzed. After DNA extraction, copy-number alteration analysis was performed, as well as identification of mutations and indels. We compared the fraction of the DAC genome with copy-number alteration to previous results from 74 primary acinar adenocarcinomas of the prostate. The alteration rate in DAC was comparable to that of acinar adenocarcinoma of high Gleason score. DAC harbored somatic changes seen in advanced and/or metastatic castration-resistant acinar adenocarcinoma, which likely accounts for its aggressive biological behavior. Highlights The genetic profile of ductal adenocarcinoma of the prostate was investigated. The genetic alteration rate was comparable to high-grade acinar adenocarcinoma. The involved genes were similar to those affected in advanced prostate cancer. Our findings may explain the aggressive behavior of ductal adenocarcinom.

    원문보기

    원문보기
    무료다운로드 유료다운로드

    회원님의 원문열람 권한에 따라 열람이 불가능 할 수 있으며 권한이 없는 경우 해당 사이트의 정책에 따라 회원가입 및 유료구매가 필요할 수 있습니다.이동하는 사이트에서의 모든 정보이용은 NDSL과 무관합니다.

    NDSL에서는 해당 원문을 복사서비스하고 있습니다. 아래의 원문복사신청 또는 장바구니담기를 통하여 원문복사서비스 이용이 가능합니다.

    이미지

    Fig. 1 이미지
  7. [해외논문]   Association of expression of the hedgehog signal with Merkel cell polyomavirus infection and prognosis of Merkel cell carcinoma   SCI SCIE

    Kuromi, Teruyuki (Division of Molecular Pathology, Department of Pathology, Tottori University Faculty of Medicine, Yonago, 683-8503, Japan ) , Matsushita, Michiko (Division of Molecular Pathology, Department of Pathology, Tottori University Faculty of Medicine, Yonago, 683-8503, Japan ) , Iwasaki, Takeshi (Department of Anatomic Pathology, Graduate School of Medical Sciences, Kyushu University, Higashi-ku, Fukuoka, 812-8582, Japan ) , Nonaka, Daisuke (Department of Histopathology, the Christie NHS Foundation Trust, Manchester, M20 4BX, United Kingdom ) , Kuwamoto, Satoshi (Division of Molecular Pathology, Department of Pathology, Tottori University Faculty of Medicine, Yonago, 683-8503, Japan ) , Nagata, Keiko (Division of Molecular Pathology, Department of Pathology, Tottori University Faculty of Medicine, Yonago, 683-8503, Japan ) , Kato, Masako (Division of Molecular Pathology, Department of Pathology, Tottori University Faculty of Medicine, Yonago, 683-8503, Japan ) , Akizuki, Gen (Division of Molecular Pathology, Department of Pathology, Tottori University Faculty of Medicine, Yonago, 683-8503, Japan ) , Kitamura, Yukisato (Department of Pathobiolo) , Hayashi, Kazuhiko
    Human pathology v.69 ,pp. 8 - 14 , 2017 , 0046-8177 ,

    초록

    Summary Merkel cell carcinoma (MCC) is an aggressive neuroendocrine skin cancer that mostly occurs in the elderly. Merkel cell polyomavirus (MCPyV) is detected in approximately 80% of MCCs and is associated with carcinogenesis. Hedgehog signaling pathway plays a role in human embryogenesis and organogenesis. In addition, reactivation of this pathway later in life can cause tumors. Twenty-nineMCPyV-positive and 21 MCPyV-negative MCCs were immunohistochemically stained with primary antibodies for hedgehog signaling (SHH, IHH, PTCH1, SMO, GLI1, GLI2, and GLI3) and evaluated using H-score. Polymerase chain reaction and sequence analysis for SHH and GLI1 exons were also performed. Expression of SHH was higher in MCPyV-positive MCCs than in MCPyV-negative MCCs ( P P = .034, P = .001, P = .042, and P = .036, respectively). Higher expression of SHH and MCPyV infection were associated with improved MCC-specific survival ( P = .037 and P = .002, respectively). The mutation analysis of prognosis-related GLI1 and SHH genes in our study revealed a low frequency of mutations in the 10 exons examined, except GLI1 exon 5 (18/22 cases), all having the same silent mutation of c.576G>A. Only 2 mutations with amino acid changes were detected in MCPyV-negative MCCs only: 1 missense mutation in GLI1 exon 4 and 1 nonsense mutation in SHH -3B. Expression of SHH and GLI1 may be useful prognostic markers of MCC because increased expression was associated with better prognosis. The high rate of c.576G>A silent mutation in GLI1 exon 5 was a feature of MCC. Highlights Higher expressions of SHH and GLI1 were associated with better prognosis in MCCs. SHH and GLI1 signals may be useful prognostic markers of MCCs. High rate of the same silent mutation (c.576G>A) in GLI1 exon 5 was a feature of MCCs.

    원문보기

    원문보기
    무료다운로드 유료다운로드

    회원님의 원문열람 권한에 따라 열람이 불가능 할 수 있으며 권한이 없는 경우 해당 사이트의 정책에 따라 회원가입 및 유료구매가 필요할 수 있습니다.이동하는 사이트에서의 모든 정보이용은 NDSL과 무관합니다.

    NDSL에서는 해당 원문을 복사서비스하고 있습니다. 아래의 원문복사신청 또는 장바구니담기를 통하여 원문복사서비스 이용이 가능합니다.

    이미지

    Fig. 1 이미지
  8. [해외논문]   Molecular classification of adult diffuse gliomas: conflicting IDH1/IDH2, ATRX, and 1p/19q results   SCI SCIE

    Ballester, Leomar Y. (Department of Pathology and Genomic Medicine, Houston Methodist Hospital, Houston, TX 77030 ) , Huse, Jason T. (Department of Pathology, The University of Texas MD Anderson Cancer Center, Houston, TX 77030 ) , Tang, Guilin (Department of Hematopathology, The University of Texas MD Anderson Cancer Center, Houston, TX 77030 ) , Fuller, Gregory N. (Department of Pathology, The University of Texas MD Anderson Cancer Center, Houston, TX 77030)
    Human pathology v.69 ,pp. 15 - 22 , 2017 , 0046-8177 ,

    초록

    Summary Until recently, the diagnosis of brain tumors was primarily based on microscopic examination of hematoxylin and eosin–stained tissue sections. The updated World Health Organization (WHO) Classification of Tumours of the Central Nervous System incorporates genetic alterations into the classification system, with the goal of creating more homogenous disease categories with greater prognostic value. Hence, under the new classification system, the diagnosis of diffuse gliomas incorporates the evaluation of mutations in the IDH1 and IDH2 genes and simultaneous deletion of chromosomes 1p and 19q. For example, although under the 2007 WHO classification system, oligodendrogliomas could be diagnosed based solely on the presence of characteristic histologic features, the newly molecularly defined entity of “oligodendroglioma, IDH-mutant and 1p/19q codeleted” requires the presence of both an IDH1 or IDH2 mutation and 1p/19q codeletion. Given that diagnosis requires evaluation of critical genetic alterations, molecular diagnostics is becoming an increasingly important aspect of clinical oncologic neuropathology practice. As molecular testing is applied more frequently to the diagnosis of brain tumors, inconsistent or conflicting molecular information will create diagnostic challenges. Here we present 6 cases of diffuse glioma that presented a diagnostic challenge due to conflicting molecular testing results. These cases exemplify some of the potential complications that arise when introducing the new 2016 central nervous system WHO classification system diagnostic criteria into routine clinical practice. We aim to alert the general practice pathology community to these potential conflicts to help mitigate the risk of potential misdiagnosis. Highlights Conflicting molecular test results create challenges in the classification of diffuse gliomas. IDH1/IDH2 mutation and complete loss of 1p/19q is a molecular signature for oligodendrogliomas. FISH to evaluate 1p/19q status can be positive in the setting of partial deletions of 1p and 19q. CMA can help distinguish partial deletions of 1p and 19q from complete loss. Loss of ATRX expression is a common alteration in astrocytomas.

    원문보기

    원문보기
    무료다운로드 유료다운로드

    회원님의 원문열람 권한에 따라 열람이 불가능 할 수 있으며 권한이 없는 경우 해당 사이트의 정책에 따라 회원가입 및 유료구매가 필요할 수 있습니다.이동하는 사이트에서의 모든 정보이용은 NDSL과 무관합니다.

    NDSL에서는 해당 원문을 복사서비스하고 있습니다. 아래의 원문복사신청 또는 장바구니담기를 통하여 원문복사서비스 이용이 가능합니다.

    이미지

    Fig. 1 이미지
  9. [해외논문]   Mitochondrial DNA “common deletion” in post–fine needle aspiration infarcted oncocytic thyroid tumors   SCI SCIE

    Conti, Luca (Department of Medical Sciences, University of Torino, Città) , Vatrano, Simona (della Salute e della Scienza Hospital, 10126 Torino, Italy ) , Bertero, Luca (Department of Oncology, University of Torino, San Luigi Hospital, 10043 Orbassano (Torino), Italy ) , Masu, Lavinia (Department of Medical Sciences, University of Torino, Città) , Pacchioni, Donatella (della Salute e della Scienza Hospital, 10126 Torino, Italy ) , Daniele, Lorenzo (Department of Medical Sciences, University of Torino, Città) , De Rosa, Giovanni (della Salute e della Scienza Hospital, 10126 Torino, Italy ) , Cassoni, Paola (Pathology Unit, Città) , Volante, Marco (della Salute e della Scienza Hospital, 10126 Torino, Italy ) , Papotti, Mauro (Pathology Unit, Mauriziano Hospital, 10128 Torino, Italy )
    Human pathology v.69 ,pp. 23 - 30 , 2017 , 0046-8177 ,

    초록

    Summary Thyroid fine needle aspiration (FNA) can rarely induce morphological changes potentially hindering the histopathological diagnosis, especially in Hurthle cell tumors (HCTs), which may easily undergo post-FNA infarction or necrosis. HCTs contain mitochondrion (mt)−rich cells that may bear mtDNA mutations, the most frequent being the so-called common deletion (CD). The aim of this study was to determine the presence and extent of the mtDNA CD in a series of thyroid HCTs that underwent extensive infarction following FNA procedure in comparison with a control series of HCTs lacking post-FNA ischemic/hemorrhagic alterations. Of 257 HCTs with available matched FNA and surgical specimens, 8 cases showed extensive (≥80%) infarction or necrosis in the resected nodule (4 adenomas, 1 carcinoma, 3 HCTs undefined for malignancy). Noninfarcted tumors in the control series included 9 adenomas, 1 carcinoma, and 1 follicular tumor of uncertain malignant potential. These lesions were significantly ( P = .03) larger than infarcted nodules. The mtDNA CD was identified using semiquantitative real-time polymerase chain reaction in 2 of 8 (25%) infarcted tumors. In HCTs lacking infarction/necrosis of the control series, the CD was significantly ( P = .05) more common (8/11 cases, 72.7%). In 7 of the 10 deleted cases, the CD was present also in the adjacent nonneoplastic parenchyma. In conclusion, the rare oncocytic tumors undergoing extensive infarction are smaller than those lacking ischemic changes and bear the mtDNA CD in a significantly lower proportion compared with control noninfarcted HCTs. This may suggest that mtDNA deletion confers a survival advantage to oncocytic cells in stress conditions, including FNA procedures. Highlights Mitochondrial DNA “common deletion” is evaluated in oncocytic thyroid tumors. “Common deletion” is more frequent in noninfarcted oncocytic tumors than in infarcted. “Common deletion” is frequently present also in the adjacent nonneoplastic parenchyma. Infarcted oncocytic tumors are smaller than noninfarcted.

    원문보기

    원문보기
    무료다운로드 유료다운로드

    회원님의 원문열람 권한에 따라 열람이 불가능 할 수 있으며 권한이 없는 경우 해당 사이트의 정책에 따라 회원가입 및 유료구매가 필요할 수 있습니다.이동하는 사이트에서의 모든 정보이용은 NDSL과 무관합니다.

    NDSL에서는 해당 원문을 복사서비스하고 있습니다. 아래의 원문복사신청 또는 장바구니담기를 통하여 원문복사서비스 이용이 가능합니다.

    이미지

    Fig. 1 이미지
  10. [해외논문]   Prognostic implication of NQO1 overexpression in hepatocellular carcinoma   SCI SCIE

    Lin, Lijuan (Institute of Molecular Medicine, Medical College of Eastern Liaoning University, Dandong 118000, China ) , Sun, Jie (Department of Pathology, Yanbian University, Yanji 133002, China ) , Tan, Yan (Institute of Molecular Medicine, Medical College of Eastern Liaoning University, Dandong 118000, China ) , Li, Zhenling (Department of Pathology, Yanbian University, Yanji 133002, China ) , Kong, Fanyong (Institute of Molecular Medicine, Medical College of Eastern Liaoning University, Dandong 118000, China ) , Shen, Yue (Institute of Molecular Medicine, Medical College of Eastern Liaoning University, Dandong 118000, China ) , Liu, Chao (Department of Pathology, Yanbian University, Yanji 133002, China ) , Chen, Litian (Department of Liver Transplantation Surgery, Xin Hua Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200092, China)
    Human pathology v.69 ,pp. 31 - 37 , 2017 , 0046-8177 ,

    초록

    To explore the role of NQO1 overexpression for prognostic implication in hepatocellular carcinoma (HCC), NQO1 mRNA levels were detected in HCC fresh tissue samples of HCC and nontumor tissues, respectively. One hundred fifty-six cases of HCC meeting strict follow-up criteria were selected for immunohistochemical staining of NQO1 protein. Correlations between NQO1 overexpression and clinicopathological features of HCC were evaluated using χ 2 tests, survival rates were calculated using the Kaplan-Meier method, and the relationship between prognostic factors and patient 5-year survival was analyzed using Cox proportional hazards analysis. In results, the levels of NQO1 mRNA were significantly up-regulated in 14 fresh tissue samples of HCC. Immunohistochemical analysis showed that the NQO1 expression and overexpression rates were significantly higher in HCC samples compared with either adjacent nontumor tissues or normal liver tissues. NQO1 overexpression correlated to tumor size, venous infiltration and late pTNM stage of HCC. NQO1 overexpression was also related to low disease-free survival and 5-year survival rates. In the late‐stage group, disease-free and 5-year survival rates of patients with NQO1 overexpression were significantly lower than those of patients without NQO1 expression. Further analysis using a Cox proportional hazards regression model revealed that NQO1 expression emerged as a significant independent hazard factor for the 5-year survival rate of patients with HCC. Therefore, NQO1 plays an important role in the progression of HCC. NQO1 may potentially be used as an independent biomarker for prognostic evaluation of HCC. Highlights The roles of NQO1 on the progression of hepatocellular carcinoma are still unclear. NQO1 is frequently up-regulated in hepatocellular carcinoma. NQO1 is a potential effective predictor for poor prognosis in patients with HCC. NQO1 expression levels should help identify high-risk HCC patients. These findings provide potential diagnostic and therapeutic targets.

    원문보기

    원문보기
    무료다운로드 유료다운로드

    회원님의 원문열람 권한에 따라 열람이 불가능 할 수 있으며 권한이 없는 경우 해당 사이트의 정책에 따라 회원가입 및 유료구매가 필요할 수 있습니다.이동하는 사이트에서의 모든 정보이용은 NDSL과 무관합니다.

    NDSL에서는 해당 원문을 복사서비스하고 있습니다. 아래의 원문복사신청 또는 장바구니담기를 통하여 원문복사서비스 이용이 가능합니다.

    이미지

    Fig. 1 이미지

논문관련 이미지