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High MET gene copy number leads to shorter survival in patients with non-small cell lung cancer.
Go, Heounjeong,Jeon, Yoon Kyung,Park, Hyo Jin,Sung, Sook-Whan,Seo, Jeong-Wook,Chung, Doo Hyun Lippincott Williams Wilkins 2010 JOURNAL OF THORACIC ONCOLOGY Vol.5 No.3
<P>Activation of MET, either by increased gene copy number (GCN) or mutation, has been detected in various cancers. We investigate the clinicopathologic features of MET gene copy in nonsmall cell lung cancer (NSCLC).</P>
Jeon, Yoon K,Go, Heounjeong,Nam, Soo J,Keam, Bhumsuk,Kim, Tae M,Jung, Kyeong C,Kang, Hyoung J,Lee, Dong S,Huh, Joo R,Park, Seong H Williams Wilkins 2012 Modern pathology Vol.25 No.9
<P>The promyelocytic leukemia zinc-finger (PLZF) is essential for the development of innate T cells (as represented by natural killer T cells) for acquisition of their unique innate immune properties. We evaluated the PLZF protein expression in a variety of immature and mature lymphoid malignancies. PLZF was preferentially expressed in T-lymphoblastic lymphoma/acute lymphoblastic leukemia (T-LBL/ALL) in 50% of the 54 cases. Among 51 cases of peripheral T-cell lymphoma not otherwise specified, only one (2%) expressed PLZF. One mycosis fungoides case expressed PLZF in lymph node involved by tumor. Otherwise, PLZF was not detected in any other type of lymphoma. In T-LBL/ALL, PLZF expression was more common in CD4/CD8 double-negative (67%) or CD8 single-positive subtypes (73%) than in CD4/CD8 double-positive (13%) and CD4 single-positive subtypes (0%) (P=0.001). Importantly, PLZF and CD1a expression were mutually exclusive in T-LBL/ALL (P=0.001). This was also the case for T-cell receptor βF1 expression (P=0.000). Most (96%) of the PLZF-positive T-LBL/ALL cases showed initial bone marrow involvement compared with 39% of PLZF-negative cases (P=0.000). Based on these findings, we suggest that T-LBL/ALLs that express PLZF arise from early immature double-negative thymocytes when the T-cell receptor β chain has not yet expressed or innate T-cell precursors, and strongly imply bone marrow involvement.</P>
( Yu Mee Wee ),( Heounjeong Go ),( Monica Young Choi ),( Hey Rim Jung ),( Yong Mee Cho ),( Young Hoon Kim ),( Duck Jong Han ),( Sung Shin ) 생화학분자생물학회(구 한국생화학분자생물학회) 2019 BMB Reports Vol.52 No.9
Despite reports suggesting that tissue-resident natural killer (trNK) cells cause ischemic kidney injury, their contribution to the development of tubulointerstitial fibrosis has not been determined. This study hypothesized that the depletion of trNK cells may ameliorate renal fibrosis by affecting transglutaminase 2/syndecan-4 interactions. Aristolochic acid nephropathy (AAN) was induced in C57BL/6 mice as an experimental model of kidney fibrosis. The mice were treated with anti-asialo GM1 (ASGM1) or anti-NK1.1 antibodies to deplete NK cells. Although both ASGM1 and NK1.1 antibodies suppressed renal NKp46<sup>+</sup>DX5<sup>+</sup> NK cells, renal NKp46<sup>+</sup>DX5<sup>-</sup> cells were resistant to suppression by ASGM1 or NK1.1 antibodies during the development of tubulointerstitial fibrosis in the AAN-induced mouse model. Western blot analysis showed that both antibodies increased the expression of fibronectin, transglutaminase 2, and syndecan-4. These findings indicate that trNK cells played an exacerbating role in tubulointerstitial fibrosis by activating transglutaminase 2 and syndecan-4 in the AAN-induced mouse model. [BMB Reports 2019; 52(9): 554-559]
Pellino 1 promotes lymphomagenesis by deregulating BCL6 polyubiquitination.
Park, Hye-Young,Go, Heounjeong,Song, Ha Rim,Kim, Suhyeon,Ha, Geun-Hyoung,Jeon, Yoon-Kyung,Kim, Ji-Eun,Lee, Ho,Cho, Hyeseong,Kang, Ho Chul,Chung, Hee-Young,Kim, Chul-Woo,Chung, Doo Hyun,Lee, Chang-Woo American Society for Clinical Investigation 2014 The Journal of clinical investigation Vol.124 No.11
<P>The signal-responsive E3 ubiquitin ligase pellino 1 (PELI1) regulates TLR and T cell receptor (TCR) signaling and contributes to the maintenance of autoimmunity; however, little is known about the consequence of mutations that result in upregulation of PELI1. Here, we developed transgenic mice that constitutively express human PELI1 and determined that these mice have a shorter lifespan due to tumor formation. Constitutive expression of PELI1 resulted in ligand-independent hyperactivation of B cells and facilitated the development of a wide range of lymphoid tumors, with prominent B cell infiltration observed across multiple organs. PELI1 directly interacted with the oncoprotein B cell chronic lymphocytic leukemia (BCL6) and induced lysine 63-mediated BCL6 polyubiquitination. In samples from patients with diffuse large B cell lymphomas (DLBCLs), PELI1 expression levels positively correlated with BCL6 expression, and PELI1 overexpression was closely associated with poor prognosis in DLBCLs. Together, these results suggest that increased PELI1 expression and subsequent induction of BCL6 promotes lymphomagenesis and that this pathway may be a potential target for therapeutic strategies to treat B cell lymphomas.</P>
Kim, Yeon‐,Joo,Go, Heounjeong,Wu, Hong‐,Gyun,Jeon, Yoon Kyung,Park, Suk Won,Lee, Seung Hee Wiley Subscription Services, Inc., A Wiley Company 2011 Head & neck Vol.33 No.10
<P><B>Abstract</B></P><P><B>Background</B></P><P>We evaluated the predictive significance of 14 reported markers using immunohistochemical study in nasopharyngeal carcinoma.</P><P><B>Methods</B></P><P>Immunohistochemical stainings were done in 38 patients for Met, cyclooxygenase‐2 (COX‐2), nm23‐H1, epidermal growth factor receptor (EGFR), p63, early growth response factor 1 (Egr1), chromosome segregation 1‐like (CSE1L), cathepsin‐D (aspartyl protease), <I>C‐erb</I>B2, p53, signal transducers and activators of transcription (STAT3/STAT5), CD138 (Syndecan‐1), and LIN28 with the usual methods.</P><P><B>Results</B></P><P>The median follow‐up time was 30 months (11–83 months). High Met and CD138 expression were statistically significant negative prognostic factors on survival. The expression of Egr1 had a positive prognostic effect on survival. The combined score of these 3 markers, Met plus CD138 minus Egr1, was a strong prognostic factor. The median survival curve was distinctly separated in accord with this combined score. No prognostic value was revealed in COX‐2, nm23‐H1, EGFR, p63, CSE1L, cathepsin‐D, C‐<I>erb</I>B2, p53, STAT3, STAT5, and LIN28.</P><P><B>Conclusions</B></P><P>The combined score of these markers could be used to stratify biomolecular risk groups. © 2010 Wiley Periodicals, Inc. Head Neck, 2010</P>
Hee Sang Hwang,박윤용,Su-Jin Shin,Heounjeong Go,Ja-Min Park,Sun Young Yoon,Jae Lyun Lee,Yong Mee Cho 대한의학회 2020 Journal of Korean medical science Vol.35 No.5
Background: Mechanism and predictive biomarkers for tyrosine kinase inhibitor (TKI) resistance of advanced clear cell renal cell carcinoma (ccRCC) have not been fully evaluated. Methods: We performed gene expression profiling on samples from an acquired TKI resistance cohort that consisted of 10 cases of TKI-treated ccRCC patients with matched tumor tissues harvested at pre-treatment and TKI-resistant post-treatment periods. In addition, a public microarray dataset from patient-derived xenograft model for TKI-treated ccRCC (GSE76068) was retrieved. Commonly altered pathways between the datasets were investigated by Ingenuity Pathway Analysis using commonly regulated differently expressed genes (DEGs). The significance of candidate DEG on intrinsic TKI resistance was assessed through immunohistochemistry in a separate cohort of 101 TKI-treated ccRCC cases. Results: TNFRSF1A gene expression and tumor necrosis factor (TNF)-α pathway were upregulated in ccRCCs with acquired TKI resistance in both microarray datasets. Also, high expression (> 10% of labeled tumor cells) of TNF receptor 1 (TNFR1), the protein product of TNFRSF1A gene, was correlated with sarcomatoid dedifferentiation and was an independent predictive factor of clinically unfavorable response and shorter survivals in separated TKI- treated ccRCC cohort. Conclusion: TNF-α signaling may play a role in TKI resistance, and TNFR1 expression may serve as a predictive biomarker for clinically unfavorable TKI responses in ccRCC.
Yoon, Sun Och,Kim, Wook Youn,Go, Heounjeong,Paik, Jin Ho,Kim, Ji Eun,Kim, Young A.,Huh, Joo R.,Jeon, Yoon Kyung,Kim, Chul-Woo Lippincott Williams Wilkins, Inc. 2010 The American journal of surgical pathology Vol.34 No.5
Class III &bgr;-tubulin (TUBB3) expression in carcinoma is associated with resistance to tubulin-binding chemotherapeutic agents. Recently, follicular dendritic cells (FDCs) were reported to express TUBB3 under physiologic conditions. We investigated TUBB3 expression in a wide range of lymphoproliferative disorders using immunohistochemistry. Dual immunostaining for Bcl-6 and TUBB3 revealed that some germinal center B cells also express TUBB3 in addition to FDCs. In Hodgkin lymphomas (HLs), 47.1% (40/85) expressed TUBB3 in the tumor cells with an all-or-none pattern. TUBB3 expression in HL was more common in mixed cellularity type than nodular sclerosis type (P=0.032). Among non-HLs, 79.3% (23/29) of anaplastic large cell lymphoma (ALCL), 8% (2/25) of extranodal natural killer/T-cell lymphoma, and 75% (21/28) of Burkitt lymphoma showed TUBB3 expression with an all-or-none pattern. Of diffuse large B-cell lymphoma, 15.2% (32/210) expressed TUBB3 in a heterogeneous pattern. In ALCL, TUBB3 expression was more common in systemic ALCL than in primary cutaneous ALCL (P=0.046). Diffuse large B-cell lymphomas with a germinal center B-like subgroup exhibited TUBB3 expression more frequently than non−GCB-like subgroup (P=0.01). Otherwise, none of the 18 angioimmunoblastic T-cell lymphomas; 18 peripheral T-cell lymphomas, not otherwise specified; 12 follicular lymphomas; 62 marginal zone lymphomas; 7 mantle cell lymphomas; 8 small lymphocytic lymphomas; or 2 FDC sarcomas expressed TUBB3. In angioimmunoblastic T-cell lymphoma and Castleman disease, TUBB3 was positive in immunoblasts corresponding to Epstein-Barr virus-infected or Kaposi sarcoma herpes virus-infected cells. A variety of neoplastic and non-neoplastic lymphoproliferative disorders exhibited characteristic TUBB3 expression patterns; these results suggest potential for diagnostic utility, some insight into the pathobiology of TUBB3 expression, and potential therapeutic implications.