Journal of Pathology and Translational Medicine

Hyun Ju Lee

4 Articles

Loss of PTEN Expression is an Independent Poor Prognostic Factor in Non-small Cell Lung Cancer.: Seol Bong Yoo, Xianhua Xu, Hyun Ju Lee, Sanghoon Jheon, Choon Taek Lee, Gheeyoung Choe, Jin Haeng Chung; Korean J Pathol. 2011;45(4):329-335.; DOI: https://doi.org/10.4132/KoreanJPathol.2011.45.4.329

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BACKGROUND
Alterations in the phosphatase and tensin homolog (PTEN) are correlated with tumor progression. Downregulation of PTEN is related to drug resistance of epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors in non-small cell lung cancer (NSCLC). The aim of this study was to evaluate the prognostic significance of PTEN in patients with NSCLC and its correlation with EGFR.
METHODS
Two hundred eighty eight surgically resected NSCLC samples, including 168 adenocarcinomas (ADCs), 99 squamous cell carcinomas (SCCs) and 21 other NSCLCs were analyzed for the PTEN. The results were correlated with other clinicopathological variables including EGFR amplification and mutation.
RESULTS
Loss of PTEN was detected in 42.4% of NSCLCs, specifically 28.6% of ADCs, 66.7% of SCCs, and 38.1% of others. Loss of PTEN was significantly associated with SCC, smoking, male gender, and higher stage. In a multivariate analysis, loss of PTEN was significantly associated with short progression-free survival (p=0.037). No association between PTEN and EGFR was observed.
CONCLUSIONS
These results suggest that loss of PTEN results in shorter progression-free survival in patients with NSCLC, and loss of PTEN is more associated with SCC, smoking, male gender, and higher T stage by the 7th tumor, node and metastasis staging system but not EGFR status.

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Molecular mechanisms underlying the regulation of tumour suppressor genes in lung cancer
Jia Yee Lee, Richie R. Bhandare, Sai H.S. Boddu, Afzal B. Shaik, Lakshmana Prabu Saktivel, Gaurav Gupta, Poonam Negi, Muna Barakat, Sachin Kumar Singh, Kamal Dua, Dinesh Kumar Chellappan
Biomedicine & Pharmacotherapy.2024; 173: 116275. CrossRef
Alterations in the PI3K Pathway Drive Resistance to MET Inhibitors in NSCLC Harboring MET Exon 14 Skipping Mutations
Philippe Jamme, Marie Fernandes, Marie-Christine Copin, Clotilde Descarpentries, Fabienne Escande, Angela Morabito, Valérie Grégoire, Matthieu Jamme, Simon Baldacci, David Tulasne, Zoulika Kherrouche, Alexis B. Cortot
Journal of Thoracic Oncology.2020; 15(5): 741. CrossRef
PTEN Tumor-Suppressor: The Dam of Stemness in Cancer
Francesca Luongo, Francesca Colonna, Federica Calapà, Sara Vitale, Micol E. Fiori, Ruggero De Maria
Cancers.2019; 11(8): 1076. CrossRef
PTEN in Lung Cancer: Dealing with the Problem, Building on New Knowledge and Turning the Game Around
Anastasios Gkountakos, Giulia Sartori, Italia Falcone, Geny Piro, Ludovica Ciuffreda, Carmine Carbone, Giampaolo Tortora, Aldo Scarpa, Emilio Bria, Michele Milella, Rafael Rosell, Vincenzo Corbo, Sara Pilotto
Cancers.2019; 11(8): 1141. CrossRef
PTEN expression is a prognostic marker for patients with non-small cell lung cancer: a systematic review and meta-analysis of the literature
Jian Xiao, Cheng-Ping Hu, Bi-Xiu He, Xi Chen, Xiao-Xiao Lu, Ming-Xuan Xie, Wei Li, Shu-Ya He, Shao-Jin You, Qiong Chen
Oncotarget.2016; 7(36): 57832. CrossRef
Alteration of the E-cadherin/β-Catenin Complex Predicts Poor Response to Epidermal Growth Factor Receptor-Tyrosine Kinase Inhibitor (EGFR-TKI) Treatment
Seol Bong Yoo, Yu Jung Kim, Hyojin Kim, Yan Jin, Ping-Li Sun, Sanghoon Jheon, Jong Seok Lee, Jin-Haeng Chung
Annals of Surgical Oncology.2013; 20(S3): 545. CrossRef
High concordance of EGFR mutation status between histologic and corresponding cytologic specimens of lung adenocarcinomas
Ping‐Li Sun, Yan Jin, Hyojin Kim, Choon‐Taek Lee, Sanghoon Jheon, Jin‐Haeng Chung
Cancer Cytopathology.2013; 121(6): 311. CrossRef
Impact of HER2 and PTEN Simultaneous Deregulation in Non-small Cell Lung Carcinoma: Correlation with Biological Behavior
Ioannis Panagiotou, Stavros N. Georgiannos, Evangelos Tsiambas, Andreas Karameris, Marios Konstantinou, Andreas C. Lazaris, Nikolaos Kavantzas, George Vilaras, Efstratios Patsouris
Asian Pacific Journal of Cancer Prevention.2012; 13(12): 6311. CrossRef
Expression of the Mammalian Target of Rapamycin Pathway Markers in Lung Adenocarcinoma and Squamous Cell Carcinoma
Hyun-Soo Kim, Gou Young Kim, Sung-Jig Lim, Youn Wha Kim
Pathobiology.2012; 79(2): 84. CrossRef

CD44 and MMP14 Expression Associated with WHO Grade of the Astrocytoma and the Prognostic Implications.: Jaekyung Myung, Bogun Jang, Heae Surng Park, Woongjae Yon, Hyun Ju Lee, Sung Hye Park; Korean J Pathol. 2010;44(1):35-41.; DOI: https://doi.org/10.4132/KoreanJPathol.2010.44.1.35

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Abstract PDF: BACKGROUND
CD44 is a cell surface receptor that has been implicated in tumor cell invasion and metastasis in a range of tumors of various organs, including breast, ovary, colon, lung, and brain. CD44 stimulates the invasive ability by interacting with matrix metalloproteinase 14 (MMP14). The expression of MMP14 on the cell surface is thought to trigger multiple proteinase cascades and to stimulate cell migration.
METHODS
A total 54 astrocytoma patients were eligible for this study. We performed a retrospective clinicopathological review and CD44 and MMP14 immunohistochemistry.
RESULTS
The expressions of CD44 and MMP14 were significantly correlated with the World Health Organization (WHO) grade. On univariate analysis, the WHO grade and the expression of CD44 were the significant prognostic factors affecting overall survival (OS) and disease progression free survival (DPFS). On the multivariate analysis by the Cox regression model, the only WHO grade was shown to be a significant independent prognostic factor for predicting the DPFS and OS.
CONCLUSIONS
In this study, the CD44 and MMP14 expressions were related to the WHO grade of astrocytoma. The CD44 expression status was a prognostic factor for DPFS and OS on univariate analysis, but it was not an independent prognostic factor on the multivariate analysis.

Differential Expression of Glut1 in Pulmonary Neuroendocrine Tumors: Correlation with Histological Grade.: Hyun Ju Lee, Seol Bong Yoo, Won Woo Lee, Doo Hyun Chung, Jeong Wook Seo, Jin Haeng Chung; Korean J Pathol. 2009;43(3):201-205.; DOI: https://doi.org/10.4132/KoreanJPathol.2009.43.3.201

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Abstract PDF

BACKGROUND
Increased glucose uptake, a process that is mediated by glucose transporter (Glut1) proteins, is an important metabolic feature in a variety of cancer cells. The overexpression of Glut1 in human cancers is known to be related to a variety of histopathological parameters, including histological grade, proliferation rate, and lymphatic invasion. The principal objective of this study was to evaluate Glut1 expression in the spectrum of pulmonary neuroendocrine (NE) tumors including typical carcinoid tumor (TC), atypical carcinoid tumor (AC), large cell neuroendocrine carcinoma (LCNEC), and small cell carcinoma (SCC), and to characterize the relationship between Glut1 expression and the histologic grade of NE tumors.
METHODS
19 TC, 7 AC, 13 LCNEC, and 6 SCC patients were included in this study. The percentages of Glut1-positive tumor cells in these patients were determined. For statistical analysis, Glut1 expression was subdivided into a Glut1-low expression group (0-30%) and a Glut1-high expression group (31-90%).
RESULTS
In our subgroup analyses, the histological grade of pulmonary neuroendocrine (NE) tumors was significantly correlated with Glut1 expression; TC (n=19, 3.6+/-4.2%), AC (n=7, 20.0+/-4.9%), LCNEC (n=13, 60.0+/-21.1%), and SCC (n=6, 74.2+/-16.9%). Glut1-high expression was significantly associated with high-grade NE tumors such as LCNEC and SCC (n=19, 62.6+/-21.0%) (p=0.000).
CONCLUSIONS
The results of this study appear to indicate that Glut1 overexpression is a consistent feature of high-grade NE lung tumors.

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GLUT1: A novel tool reflecting proliferative activity of lung neuroendocrine tumors?
Nazim Benzerdjeb, Pascal Berna, Henri Sevestre
Pathology International.2017; 67(1): 32. CrossRef
Oncocytic carcinoid tumor of the lung with intense F-18 fluorodeoxyglucose (FDG) uptake in positron emission tomography–computed tomography (PET/CT)
Yuki Tanabe, Yoshifumi Sugawara, Rieko Nishimura, Kohei Hosokawa, Makoto Kajihara, Teruhiko Shimizu, Tadaaki Takahashi, Shinya Sakai, Shigeki Sawada, Motohiro Yamashita, Haruhiko Ohtani
Annals of Nuclear Medicine.2013; 27(8): 781. CrossRef

Mineralizing Pulmonary Elastosis Associated with a Giant Cell Carcinoma.: Min Kyung Kim, Kwang Il Kim, Min Joo Kim, Young Woo Suh, Il Hun Seo, Hyun Ju Lee, Han Gyeom Kim; Korean J Pathol. 1998;32(9):691-693.

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Abstract: Mineralizing pulmonary elastosis is a result of chronic alveolar hemorrhage forming iron encrustation of a pulmonary elastic tissue. It has been reported as a complication of some diseases such as bronchiectasis, idiopathic pulmonary hemosiderosis, and cardiac failure. It is extremely rare to occur with a giant cell carcinoma as we experienced. A 59 year-old man visited our hospital for cough and blood tinged sputum. A chest CT scan revealed 10 9 6 cm sized round mass in the left upper lobe. He had lobectomy of left upper lobe, but died of respiratory failure at the postoperative eighteenth day. The lung showed a necrotic tumor and a yellow tan consolidation around the mass. Microscopically, the tumor was composed of nests or syncytia of large bizarre cells and tumor giant cells, and was diagnosed as a giant cell carcinoma. Interestingly, in the surrounding lung parenchyma there were a lot of foreign body type giant cells phagocytizing iron encrustated elastic fibers, which were easily identified by elastic van Gieson and prussian blue stains. Those degenerated elastic fibers appeared in pulmonary interstitial tissue as well as blood vessel walls. The authors concluded tumoral hemorrhage and necrosis resulted in mineralizing pulmonary elastosis.

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