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Identification of Significant Prognostic Tissue Markers Associated with Survival in Upper Urinary Tract Urothelial Carcinoma Patients Treated with Radical Nephroureterectomy: A Retrospective Immunohistochemical Analysis Using Tissue Microarray
Sung Han Kim, Weon Seo Park, Boram Park, Jinsoo Chung, Jae Young Joung, Kang Hyun Lee, Ho Kyung Seo
Cancer Res Treat. 2020;52(1):128-138.   Published online June 19, 2019
DOI: https://doi.org/10.4143/crt.2019.119
AbstractAbstract PDFSupplementary MaterialPubReaderePub
Purpose
The purpose of this study was to identify prognostic tissue markers for several survival outcomes after radical nephroureterectomy among patients with upper urinary tract urothelial carcinoma using tissue microarray and immunohistochemistry.
Materials and Methods
Retrospectively, data of 162 non-metastatic patients with upper urinary tract urothelial carcinoma after radical nephroureterectomy between 2004 and 2016 were reviewed to determine intravesical recurrence-free survival (IVRFS), disease-free survival (DFS), and overall survival (OS). The expression of 27 tissue markers on a tissue microarray of radical nephroureterectomy samples and prognostic values of clinicopathological parameters were evaluated using immunohistochemistry and Cox proportional hazard models after adjusting for significant prognostic clinicopathological variables. The expression of all tissue markers was categorized into a binary group with continuous H-scores (0-300).
Results
Median follow-up was 53.4 months (range, 3.6 to 176.5 months); and, 58 (35.8%), 48 (29.6%), and 19 (11.7%) bladder recurrence, disease progression, and all cause death, respectively, were identified. After adjusting for significant clinicopathological factors including intravesical instillation for bladder recurrence-free survival, pathologic T category and intravesical instillation for disease progression-free survival , and pathologic T category for OS (p < 0.05), IVRFS was associated with epithelial cadherin (hazard ratio [HR], 0.49), epidermal growth factor receptor/erythroblastosis oncogene B (c-erb) (HR, 2.59), and retinoblastoma protein loss (HR, 1.85); DFS was associated with cyclin D1 (HR, 2.16) and high-molecular-weight cytokeratin (HR, 0.42); OS was associated with E-cadherin (HR, 0.34) and programmed cell death 1 ligand (HR, 13.42) (p < 0.05).
Conclusion
Several significant tissue markers were associated with survival outcomes in upper urinary tract urothelial carcinoma patients treated with radical nephroureterectomy.

Citations

Citations to this article as recorded by  
  • A multi‐institutional retrospective study of open versus laparoscopic nephroureterectomy focused on the intravesical recurrence
    Soichiro Shimura, Kazumasa Matsumoto, Masaomi Ikeda, Shigenori Moroo, Dai Koguchi, Yoshinori Taoka, Takahiro Hirayama, Yasukiyo Murakami, Takuji Utsunomiya, Daisuke Matsuda, Norihiko Okuno, Akira Irie, Masatsugu Iwamura
    Asia-Pacific Journal of Clinical Oncology.2023; 19(1): 71.     CrossRef
  • Upper Tract Urinary Carcinoma: A Unique Immuno-Molecular Entity and a Clinical Challenge in the Current Therapeutic Scenario
    Giulia Mazzaschi, Giulia Claire Giudice, Matilde Corianò, Davide Campobasso, Fabiana Perrone, Michele Maffezzoli, Irene Testi, Luca Isella, Umberto Maestroni, Sebastiano Buti
    Technology in Cancer Research & Treatment.2023;[Epub]     CrossRef
  • Prognostic value of programmed death ligand‐1 and programmed death‐1 expression in patients with upper tract urothelial carcinoma
    Luca Campedel, Eva Compérat, Géraldine Cancel‐Tassin, Justine Varinot, Christian Pfister, Clara Delcourt, Françoise Gobet, Mathieu Roumiguié, Pierre‐Marie Patard, Gwendoline Daniel, Pierre Bigot, Julie Carrouget, Caroline Eymerit, Stéphane Larré, Priscill
    BJU International.2023; 132(5): 581.     CrossRef
  • The Prevalence and Prognostic Role of PD-L1 in Upper Tract Urothelial Carcinoma Patients Underwent Radical Nephroureterectomy: A Systematic Review and Meta-Analysis
    Yi Lu, Jiaqi Kang, Zhiwen Luo, Yuxuan Song, Jia Tian, Zhongjia Li, Xiao Wang, Li Liu, Yongjiao Yang, Xiaoqiang Liu
    Frontiers in Oncology.2020;[Epub]     CrossRef
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High-Throughput Multiplex Immunohistochemical Imaging of the Tumor and Its Microenvironment
Jiwon Koh, Yoonjin Kwak, Jin Kim, Woo Ho Kim
Cancer Res Treat. 2020;52(1):98-108.   Published online May 27, 2019
DOI: https://doi.org/10.4143/crt.2019.195
AbstractAbstract PDFPubReaderePub
Purpose
The aim of this study was to develop a formalin-fixed paraffin-embedded (FFPE) tissue based multiplex immunochemistry (mIHC) method for high-throughput comprehensive tissue imaging and demonstrate its feasibility, validity, and usefulness.
Materials and Methods
The mIHC protocol was developed and tested on tissue microarray slides made from archived gastric cancer (GC) tissue samples. On a single FFPE slide, cyclic immunochemistry for multiple markers of immune cells and cytokeratin for tumor cells was performed; hematoxylin staining was used for demarcation of nuclei. Whole slides were digitally scanned after each cycle. For interpretation of mIHC results, we performed computer-assisted image analysis using publicly available software.
Results
Using mIHC, we were able to characterize the tumor microenvironment (TME) of GCs with accurate visualization of various immune cells harboring complex immunophenotypes. Spatial information regarding intratumoral and peritumoral TME could be demonstrated by digital segmentation of image guided by cytokeratin staining results. We further extended the application of mIHC by showing that subcellular localization of molecules can be achieved by image analysis of mIHC results.
Conclusion
We developed a robust method for high-throughput multiplex imaging of FFPE tissue slides. The feasibility and adaptability of mIHC suggest that it is an efficient method for in situ single-cell characterization and analysis.

Citations

Citations to this article as recorded by  
  • Exploring Multiplex Immunohistochemistry (mIHC) Techniques and Histopathology Image Analysis: Current Practice and Potential for Clinical Incorporation
    Aria Kaiyuan Sun, Song Fan, Siu Wai Choi
    Cancer Medicine.2025;[Epub]     CrossRef
  • The immunologic phenotype of thrombi is associated with future vascular events after cerebral infarction
    Wookjin Yang, Soon Auck Hong, Jeong-Min Kim, Hae-Bong Jeong, Taek-Kyun Nam, Hyun Ho Choi, Suh Min Kim, Kwang-Yeol Park, Hye Ryoun Kim
    Journal of NeuroInterventional Surgery.2024; 16(4): 352.     CrossRef
  • The tumor immune microenvironment remodeling and response to HER2‐targeted therapy in HER2‐positive advanced gastric cancer
    Lei Jiang, Xingwang Zhao, Yilin Li, Yajie Hu, Yu Sun, Shengde Liu, Zizhen Zhang, Yanyan Li, Xujiao Feng, Jiajia Yuan, Jian Li, Xiaotian Zhang, Yang Chen, Lin Shen
    IUBMB Life.2024; 76(7): 420.     CrossRef
  • HCR spectral imaging: 10-plex, quantitative, high-resolution RNA and protein imaging in highly autofluorescent samples
    Samuel J. Schulte, Mark E. Fornace, John K. Hall, Grace J. Shin, Niles A. Pierce
    Development.2024;[Epub]     CrossRef
  • iRhom2 deficiency reduces sepsis-induced mortality associated with the attenuation of lung macrophages in mice
    Jihye Kim, Jee Hyun Kim, Younghoon Kim, Jooyoung Lee, Hyun Jung Lee, Seong-Joon Koh, Jong Pil Im, Joo Sung Kim
    Histochemistry and Cell Biology.2024; 162(5): 415.     CrossRef
  • Immunohistochemistry for assessing toxicity and mechanism of action of anticancer drugs during preclinical trials. From theory to practice
    M. A. Dodokhova, M. A. Akimenko, O. V. Voronova, M. S. Alkhusein-Kulyaginova, N. A. Kornienko, M. V. Gulyan, D. N. Gyulmamedov, M.-M. Kh. Alasheva, E. Sh. Kazimagomedova, D. B. Shpakovsky, E. R. Milaeva, I. M. Kotieva
    Fundamental and Clinical Medicine.2024; 9(3): 74.     CrossRef
  • Nontoxic Fluorescent Nanoprobes for Multiplexed Detection and 3D Imaging of Tumor Markers in Breast Cancer
    Pavel Sokolov, Galina Nifontova, Pavel Samokhvalov, Alexander Karaulov, Alyona Sukhanova, Igor Nabiev
    Pharmaceutics.2023; 15(3): 946.     CrossRef
  • Automatic generation of pathological benchmark dataset from hyperspectral images of double stained tissues
    Jiansheng Wang, Xintian Mao, Yan Wang, Xiang Tao, Junhao Chu, Qingli Li
    Optics & Laser Technology.2023; 163: 109331.     CrossRef
  • Heterogeneity of the Tumor Microenvironment Across Molecular Subtypes of Breast Cancer
    Dharambir Kashyap, Amanjit Bal, Santosh Irinike, Siddhant Khare, Shalmoli Bhattacharya, Ashim Das, Gurpreet Singh
    Applied Immunohistochemistry & Molecular Morphology.2023; 31(8): 533.     CrossRef
  • Exploring the Complex and Multifaceted Interplay between Melanoma Cells and the Tumor Microenvironment
    Magdalena Kuras
    International Journal of Molecular Sciences.2023; 24(18): 14403.     CrossRef
  • New insights into the tumour immune microenvironment of nasopharyngeal carcinoma
    Aisling Forder, Greg L. Stewart, Nikita Telkar, Wan L. Lam, Cathie Garnis
    Current Research in Immunology.2022; 3: 222.     CrossRef
  • Let us not forget about our past contributions to the field of prostatic neoplasms: To some extent what we value now was already there
    Rodolfo Montironi, Alessia Cimadamore, Marina Scarpelli, Liang Cheng, Antonio Lopez-Beltran, Gregor Mikuz
    Pathology - Research and Practice.2021; 219: 153377.     CrossRef
  • Programmed Death Ligand 1-Expressing Classical Dendritic Cells Mitigate -Induced Gastritis
    Du-Min Go, Seung Hyun Lee, Su-Hyung Lee, Sang-Ho Woo, Kibyeong Kim, Kyeongdae Kim, Kyu Seong Park, Jong-Hwan Park, Sang-Jun Ha, Woo Ho Kim, Jae-Hoon Choi, Dae-Yong Kim
    Cellular and Molecular Gastroenterology and Hepatology.2021; 12(2): 715.     CrossRef
  • Expression of the immune checkpoint receptors PD-1, LAG3, and TIM3 in the immune context of stage II and III gastric cancer by using single and chromogenic multiplex immunohistochemistry
    Yujun Park, An Na Seo, Jiwon Koh, Soo Kyoung Nam, Yoonjin Kwak, Sang-Hoon Ahn, Do Joong Park, Hyung-Ho Kim, Hye Seung Lee
    OncoImmunology.2021;[Epub]     CrossRef
  • Prognostic significance of natural killer cell-associated markers in gastric cancer: quantitative analysis using multiplex immunohistochemistry
    Hee Young Na, Yujun Park, Soo Kyung Nam, Jiwon Koh, Yoonjin Kwak, Sang-Hoon Ahn, Do Joong Park, Hyung-Ho Kim, Kyu Sang Lee, Hye Seung Lee
    Journal of Translational Medicine.2021;[Epub]     CrossRef
  • Cellular and Extracellular Components in Tumor Microenvironment and Their Application in Early Diagnosis of Cancers
    Rui Wei, Si Liu, Shutian Zhang, Li Min, Shengtao Zhu
    Analytical Cellular Pathology.2020; 2020: 1.     CrossRef
  • Towards a Systems Immunology Approach to Unravel Responses to Cancer Immunotherapy
    Laura Bracci, Alessandra Fragale, Lucia Gabriele, Federica Moschella
    Frontiers in Immunology.2020;[Epub]     CrossRef
  • 9,617 View
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  • 17 Web of Science
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Plasma Macrophage Migration Inhibitory Factor and CCL3 as Potential Biomarkers for Distinguishing Patients with Nasopharyngeal Carcinoma from High-Risk Individuals Who Have Positive Epstein-Barr Virus Capsid Antigen-Specific IgA
Ning Xue, Jian-Hua Lin, Shan Xing, Dan Liu, Shi-Bing Li, Yan-Zhen Lai, Xue-Ping Wang, Min-Jie Mao, Qian Zhong, Mu-Sheng Zeng, Wan-Li Liu
Cancer Res Treat. 2019;51(1):378-390.   Published online May 29, 2018
DOI: https://doi.org/10.4143/crt.2018.070
AbstractAbstract PDFSupplementary MaterialPubReaderePub
Purpose
The purpose of this study was to identify novel plasma biomarkers for distinguishing nasopharyngeal carcinoma (NPC) patients from healthy individuals who have positive Epstein-Barr virus (EBV) viral capsid antigen (VCA-IgA).
Materials and Methods
One hundred seventy-four plasma cytokines were analyzed by a Cytokine Array in eight healthy individuals with positive EBV VCA-IgA and eight patients with NPC. Real-time polymerase chain reaction, Western blotting, enzyme-linked immunosorbent assay (ELISA), and immunohistochemistry were employed to detect the expression levels of macrophage migration inhibitory factor (MIF) and CC chemokine ligand 3 (CCL3) in NPC cell lines and tumor tissues. Plasma MIF and CCL3 were measured by ELISA in 138 NPC patients, 127 EBV VCA-IgA negative (VN) and 100 EBV VCA-IgA positive healthy donors (VP). Plasma EBV VCA-IgA was determined by immunoenzymatic techniques.
Results
Thirty-four of the 174 cytokines varied significantly between the VP and NPC group. Plasma MIF and CCL3 were significantly elevated in NPC patients compared with VN and VP. Combination of MIF and CCL3 could be used for the differential diagnosis of NPC from VN cohort (area under the curve [AUC], 0.913; sensitivity, 90.00%; specificity, 80.30%), and combination of MIF, CCL3, and VCA-IgA could be used for the differential diagnosis of NPC from VP cohort (AUC, 0.920; sensitivity, 90.00%; specificity, 84.00%), from (VN+VP) cohort (AUC, 0.961; sensitivity, 90.00%; specificity, 92.00%). Overexpressions of MIF and CCL3 were observed in NPC plasma, NPC cell lines and NPC tissues.
Conclusion
Plasma MIF, CCL3, and VCA-IgA combination significantly improves the diagnostic specificity of NPC in high-risk individuals.

Citations

Citations to this article as recorded by  
  • Nasopharyngeal carcinoma-associated inflammatory cytokines: ongoing biomarkers
    Chuwen Liang, Jun Kan, Jingli Wang, Wei Lu, Xiaoyan Mo, Bei Zhang
    Frontiers in Immunology.2024;[Epub]     CrossRef
  • Genetic Variants of the MIF Gene and Susceptibility of Rectal Cancer
    Dongyu Chuo, Dapeng Lin, Mingdi Yin, Yuze Chen
    Pharmacogenomics and Personalized Medicine.2021; Volume 14: 55.     CrossRef
  • microRNA-451 (miR-451) Regulates the Apoptosis of Non-Small Cell Lung Cancer Cells by Targeting Macrophage Migration Promoting Factors
    Caihong Wei, Dan Guo, Huayun Pu
    Journal of Biomaterials and Tissue Engineering.2021; 11(7): 1388.     CrossRef
  • 8,721 View
  • 186 Download
  • 3 Web of Science
  • 3 Crossref
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Upregulation of MicroRNA-1246 Is Associated with BRAF Inhibitor Resistance in Melanoma Cells with Mutant BRAF
Jae-Hyeon Kim, Jun-Ho Ahn, Michael Lee
Cancer Res Treat. 2017;49(4):947-959.   Published online January 3, 2017
DOI: https://doi.org/10.4143/crt.2016.280
AbstractAbstract PDFSupplementary MaterialPubReaderePub
Purpose
Intrinsic and acquired resistance limit the therapeutic benefits of inhibitors of oncogenic BRAF in melanoma. To identify microRNAs (miRNAs) associated with resistance to a BRAF inhibitor, we compared miRNA expression levels in three cell lines with different BRAF inhibitor sensitivity.
Materials and Methods
miRNA microarray analysis was conducted to compare miRNA expression levels. Real-time quantitative reverse-transcription polymerase chain reaction (qRT-PCR) was performed to confirm the expression of differentially expressed miRNAs. The cellular effects of miR-1246 were further examined by MTT assay, immunoblotting analysis, cell cycle analysis, flow cytometric assay of apoptosis, and autophagy assay.
Results
The miRNA microarray analysis and qRT-PCR identified five miRNAs (miR-3617, miR-92a-1, miR-1246, miR-193b-3p, and miR-17-3p) with expression that was consistently altered in two BRAF inhibitor-resistant cell lines. Among the five miRNAs, a miR-1246 mimic significantly reduced the antiproliferative effects of the BRAF inhibitor PLX4720 in BRAF inhibitor–resistant A375P (A375P/Mdr) cells, suggesting that miR-1246 upregulation confers acquired resistance to BRAF inhibition. In particular, apoptosis was identified as a major type of cell death in miR-1246–transfected cells; however, necrosis predominated in mimic-control-transfected cells, indicating that the resistance to PLX4720 in miR-1246 mimic-transfected cells is predominantly due to a reduction in necrosis. Furthermore, we found that miR-1246 promoted G2/M arrest through autophagy as a way to escape cell death by necrosis and apoptosis in response to PLX4720. The promotion of BRAF inhibitor resistance by miR-1246 was associated with lowered levels of p-ERK.
Conclusion
These results suggest that miR-1246 may be a potential therapeutic target in melanoma with acquired resistance to BRAF inhibitors.

Citations

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    International Journal of Biological Macromolecules.2023; 230: 123127.     CrossRef
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    Cancers.2022; 14(15): 3706.     CrossRef
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    Cancers.2022; 14(24): 6198.     CrossRef
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    Meet Patel, Adam Eckburg, Shahina Gantiwala, Zachary Hart, Joshua Dein, Katie Lam, Neelu Puri
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    Lisa Linck-Paulus, Lisa Lämmerhirt, Daniel Völler, Katharina Meyer, Julia C. Engelmann, Rainer Spang, Norbert Eichner, Gunter Meister, Silke Kuphal, Anja Katrin Bosserhoff
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    Cell Death Discovery.2021;[Epub]     CrossRef
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    Simona Caporali, Adriana Amaro, Lauretta Levati, Ester Alvino, Pedro Miguel Lacal, Simona Mastroeni, Federica Ruffini, Laura Bonmassar, Gian Carlo Antonini Cappellini, Nadia Felli, Alessandra Carè, Ulrich Pfeffer, Stefania D’Atri
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    Douglas Donnelly, Phyu P. Aung, George Jour
    Seminars in Cancer Biology.2019; 59: 165.     CrossRef
  • Upregulation of S100A9 contributes to the acquired resistance to BRAF inhibitors
    Sung-Hee Hwang, Jun-Ho Ahn, Michael Lee
    Genes & Genomics.2019; 41(11): 1273.     CrossRef
  • Targeting CDC7 sensitizes resistance melanoma cells to BRAFV600E-specific inhibitor by blocking the CDC7/MCM2-7 pathway
    Shaimaa A. Gad, Hamdy E. A. Ali, Rofaida Gaballa, Rania M. Abdelsalam, Mourad Zerfaoui, Hamed I. Ali, Salwa H. Salama, Sanaa A. Kenawy, Emad Kandil, Zakaria Y. Abd Elmageed
    Scientific Reports.2019;[Epub]     CrossRef
  • The Role of Autophagy in the Resistance to BRAF Inhibition in BRAF-Mutated Melanoma
    Xiao Liu, Jinfeng Wu, Haihong Qin, Jinhua Xu
    Targeted Oncology.2018; 13(4): 437.     CrossRef
  • Targeting signal-transducer-and-activator-of-transcription 3 sensitizes human cutaneous melanoma cells to BRAF inhibitor
    Xiaohui Wang, Huajun Qu, Yinghe Dong, Guozhi Wang, Yuchen Zhen, Linxia Zhang
    Cancer Biomarkers.2018; 23(1): 67.     CrossRef
  • Exosome-packaged miR-1246 contributes to bystander DNA damage by targeting LIG4
    Li-Jun Mo, Man Song, Qiao-Hua Huang, Hua Guan, Xiao-Dan Liu, Da-Fei Xie, Bo Huang, Rui-Xue Huang, Ping-Kun Zhou
    British Journal of Cancer.2018; 119(4): 492.     CrossRef
  • An oasis in the desert of cancer chemotherapeutic resistance: The enlightenment from reciprocal crosstalk between signaling pathways of UPR and autophagy in cancers
    Yuhang Zhang, Xianjun Qu, Lingfan Jiang
    Biomedicine & Pharmacotherapy.2017; 92: 972.     CrossRef
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  • 37 Web of Science
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Maspin Suppresses Survival of Lung Cancer Cells through Modulation of Akt Pathway
Eunsook Nam, Chaehwa Park
Cancer Res Treat. 2010;42(1):42-47.   Published online March 31, 2010
DOI: https://doi.org/10.4143/crt.2010.42.1.42
AbstractAbstract PDFPubReaderePub
Purpose

Maspin is a tumor suppressor protein that has been reported to stimulate the cell death of cancer and inhibit the metastasis of cancer. The present study aimed to explore the survival pathway by which maspin modulates the resistance of human lung cancer cells to chemotherapeutic drugs, and the consequences of maspin gene therapy in an animal model.

Materials and Methods

NCI-H157 and A549 cells were transfected with either a mock vector (pCMVTaq4C), maspin (pCMV-maspin), siControl or siMaspin. RT-PCR and Western blot analysis were performed to study the expressions of survival proteins in lung cancer. cDNA microarray analysis was carried out to compare the maspin-modulated gene expression between the xenograft tumors derived from the lung cancer cells that were stably transfected with pCMVTaq4C or pCMV-maspin. Maspin gene therapy was performed by intra-tumoral injections of pCMVTaq4C or pCMV-maspin into the pre-established subcutaneous tumors in nude mice.

Results

Maspin significantly decreased the survival to doxorubicin and etoposide, whereas did not affect the survival to cisplatin in the NCI-H157 cells. Interestingly, transfection with a maspin plasmid resulted in a significant reduction of the phosphorylation of Akt in the NCI-H157 cells, whereas knockdown of maspin increased the phosphorylation of Akt in the A549 cells. Microarray analysis of the xenograft tumors revealed a specific gene expression profile, demonstrating that maspin is associated with the differential expressions of PTEN and IGF2R. Direct transfer of pCMV-maspin into the tumor significantly retarded the tumor growth in the animal experiments (p=0.0048).

Conclusion

Lung cancer cells lacking maspin could be resistant to chemotherapeutic drugs such as doxorubicin or etoposide, at least in part by maintaining Akt phosphorylation.

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An Attempt for Combining Microarray Data Sets by Adjusting Gene Expressions
Ki-Yeol Kim, Se Hyun Kim, Dong Hyuk Ki, Jaeheon Jeong, Ha Jin Jeong, Hei-Cheul Jeung, Hyun Cheol Chung, Sun Young Rha
Cancer Res Treat. 2007;39(2):74-81.   Published online June 30, 2007
DOI: https://doi.org/10.4143/crt.2007.39.2.74
AbstractAbstract PDFPubReaderePub
Purpose

The diverse experimental environments in microarray technology, such as the different platforms or different RNA sources, can cause biases in the analysis of multiple microarrays. These systematic effects present a substantial obstacle for the analysis of microarray data, and the resulting information may be inconsistent and unreliable. Therefore, we introduced a simple integration method for combining microaray data sets that are derived from different experimental conditions, and we expected that more reliable information can be detected from the combined data set rather than from the separated data sets.

Materials and Methods

This method is based on the distributions of the gene expression ratios among the different microarray data sets and it transforms, gene by gene, the gene expression ratios into the form of the reference data set. The efficiency of the proposed integration method was evaluated using two microarray data sets, which were derived from different RNA sources, and a newly defined measure, the mixture score.

Results

The proposed integration method intermixed the two data sets that were obtained from different RNA sources, which in turn reduced the experimental bias between the two data sets, and the mixture score increased by 24.2%. A data set combined by the proposed method preserved the inter-group relationship of the separated data sets.

Conclusion

The proposed method worked well in adjusting systematic biases, including the source effect. The ability to use an effectively integrated microarray data set yields more reliable results due to the larger sample size and this also decreases the chance of false negatives.

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Characterization of RhoA-mediated Chemoresistance in Gastric Cancer Cells
Won Ki Kang, Inkyoung Lee, Chaehwa Park
Cancer Res Treat. 2005;37(4):251-256.   Published online August 31, 2005
DOI: https://doi.org/10.4143/crt.2005.37.4.251
AbstractAbstract PDFPubReaderePub
Purpose

RhoA is a critical transducer of extracellular signals, which leads to organization of actin cytoskeleton, motility, adhesion and gene regulation. The present study aimed to explore whether RhoA influences the susceptibility of gastric cancer cells to chemotherapeutic drugs.

Materials and Methods

SNU638 cells were transfected with a mock vector (pcDNA3.1), RhoA (pcDNA/RhoA), or constitutively active RhoA (pcDNA/caRhoA). MTT assay and Western blot analysis were performed to study the growth response to several chemotherapeutic drugs in the gastric cancer cell line, SNU638, with different RhoA levels.

Results

RhoA significantly enhanced the resistance to lovastatin, 5-FU, taxol and vincristine, but did not affect the sensitivity to cisplatin or etoposide in SNU638. In the Western blot analysis, RhoA decreased the PARP cleavage, which was accompanied by a concurrent reductionin cell death. The gene expression profile after a cDNA microarray analysis demonstrated that RhoA was associated with the differential expression of 19 genes, including those involved in anti-oxidant defense, glucose metabolism, anti-apoptosis and protein turnover.

Conclusion

Gastric cancer cells with a high expression of RhoA could be resistant to chemotherapeutic drugs, such as taxol or vincristine, implying that treatment strategies aimed at inactivation of RhoA might be promising for improving the efficacy of these chemotherapeutic drugs.

Citations

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cDNA Microarray Analysis of Differential Gene Expression in Gastric Cancer Cells Sensitive and Resistant to 5-Fluorouracil and Cisplatin
Myung-Ju Ahn, Young-Do Yoo, Ki-Hwan Lee, Joon-Ik Ahn, Dong-Hyun Yu, Hye-Sook Lee, Ho-Suck Oh, Jung-Hye Choi, Yong-Sung Lee
Cancer Res Treat. 2005;37(1):54-62.   Published online February 28, 2005
DOI: https://doi.org/10.4143/crt.2005.37.1.54
AbstractAbstract PDFPubReaderePub
Purpose

Gastric cancer is one of the most prevalent cancers worldwide. 5-fluorouracil (5-FU) and cisplatin are the most commonly used drugs for the treatment of gastric cancer. However, a significant number of tumors often fail to respond to chemotherapy.

Materials and Methods

To better understand the molecular mechanisms underlying drug resistance in gastric cancer the gene expression in gastric cancer cells, which were either sensitive or resistant to 5-FU and cisplatin, were examined using cDNA microarray analysis. To confirm the differential gene expression, as determined using the microarray, semiquantitative RT-PCR was performed on a subset of differentially expressed cDNAs.

Results

69 and 45 genes, which were either up-regulated (9 and 22 genes) or down-regulated (60 and 25 genes), were identified in 5-FU- and cisplatin-resistant cells, respectively. Several genes, such as adaptor-related protein complex 1 and baculoviral IAP repeat-containing 3, were up-regulated in both drug-resistant cell types. Several genes, such as the ras homolog gene family, tropomyosin, tumor rejection antigen, protein disulfide isomerase-related protein, melanocortin 1 receptor, defensin, cyclophilin B, dual specificity phosphatase 8 and hepatocyte nuclear factor 3, were down-regulated in both drugresistant cell types.

Conclusion

These findings show that cDNA microarray analysis can be used to obtain gene expression profiles that reflect the effect of anticancer drugs on gastric cancer cells. Such data may lead to the assigning of signature expression profiles of drug-resistant tumors, which may help predict responses to drugs and assist in the design of tailored therapeutic regimens to overcome drug resistance.

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Comparison of As2O3 and As4O6 in the Detection of SiHa Cervical Cancer Cell Growth Inhibition Pathway
Yong Wook Kim, Su Mi Bae, Keun Ho Lee, Joon Mo Lee, Sung Eun Namkoong, Insu P. Lee, Chong Kook Kim, Jeong-Sun Seo, Jeong-Im Sin, Yong-Wan Kim, Woong Shick Ahn
Cancer Res Treat. 2004;36(4):255-262.   Published online August 31, 2004
DOI: https://doi.org/10.4143/crt.2004.36.4.255
Retraction in: Cancer Res Treat 2007;39(1):47
  • 7,545 View
  • 45 Download
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Review Article
Microarray Applications in Cancer Research
Il-Jin Kim, Hio Chung Kang, Jae-Gahb Park
Cancer Res Treat. 2004;36(4):207-213.   Published online August 31, 2004
DOI: https://doi.org/10.4143/crt.2004.36.4.207
AbstractAbstract PDFPubReaderePub

DNA microarray technology permits simultaneous analysis of thousands of DNA sequences for genomic research and diagnostics applications. Microarray technology represents the most recent and exciting advance in the application of hybridization-based technology for biological sciences analysis. This review focuses on the classification (oligonucleotide vs. cDNA) and application (mutation-genotyping vs. gene expression) of microarrays. Oligonucleotide microarrays can be used both in mutation-genotyping and gene expression analysis, while cDNA microarrays can only be used in gene expression analysis. We review microarray mutation analysis, including examining the use of three oligonucleotide microarrays developed in our laboratory to determine mutations in RET, β-catenin and K-ras genes. We also discuss the use of the Affymetrix GeneChip in mutation analysis. We review microarray gene expression analysis, including the classifying of such studies into four categories: class comparison, class prediction, class discovery and identification of biomarkers.

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Original Articles
The Differential Gene Expression Profiles between Sensitive and Resistant Breast Cancer Cells to Adriamycin by cDNA Microarray
Myung-Ju Ahn, Ki-Hwan Lee, Joon-Ik Ahn, Dong-Hyun Yu, Hye-Sook Lee, Jung-Hye Choi, Joung Soon Jang, Jong Min Bae, Yong-Sung Lee
Cancer Res Treat. 2004;36(1):43-49.   Published online February 29, 2004
DOI: https://doi.org/10.4143/crt.2004.36.1.43
AbstractAbstract PDFPubReaderePub
Purpose

Adriamycin® is one of the most commonly used drugs in the treatment of breast cancer. This study was performed to understand the molecular mechanisms of drug resistance in breast cancer cells.

Materials and Methods

We have analyzed the MCF-7 breast cell line and its adriamycin-resistant variants, MCF-7/ADR using human 10 K element cDNA microarrays.

Results

We defined 68 genes that were up-regulated (14 genes) or down-regulated (54 genes) in adriamycin resistant breast cancer cells. Several genes, such as G protein-coupled receptor kinase 5, phospholipase A2, guanylate cyclase 1, vimentin, matrix metalloproteinase 1 are up-regulated in drug resistant cells. Several genes, such as interferon, alpha-inducible protein 27, forkhead box M1, mitogen-activated protein kinase 6, regulator of mitotic spindle assembly 1 and tumor necrosis factor superfamily are down-regulated in adriamycin resistant cells. The altered expression of genes observed in microarray was verified by RT-PCR.

Conclusion

These findings show that cDNA microarray analysis can be used to obtain gene expression profiles reflecting the effect of anticancer drugs on breast cancer cells. Such data may lead to the assigning of signature expression profiles of drug-resistant tumors which may help predict responses to drugs and assist in the design of tailored therapeutic regimens to overcome drug resistance.

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    Myung-Ju Ahn, Young-Do Yoo, Ki-Hwan Lee, Joon-Ik Ahn, Dong-Hyun Yu, Hye-Sook Lee, Ho-Suck Oh, Jung-Hye Choi, Yong-Sung Lee
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Expression Profiling of the Cellular Processes in Uterine Leiomyomas: Omic Approaches and IGF-2 Association with Leiomyosarcomas
Su Mi Bae, Yong-Wan Kim, Joon Mo Lee, Sung Eun Namkoong, Chong Kook Kim, Woong Shick Ahn
Cancer Res Treat. 2004;36(1):31-42.   Published online February 29, 2004
DOI: https://doi.org/10.4143/crt.2004.36.1.31
AbstractAbstract PDFPubReaderePub
Purpose

This study utilized both cDNA microarray and 2D protein gel electrophoresis technology to investigate the multiple interactions of the genes and proteins involved in the pathophysiology of uterine leiomyomas. Also, Gene Ontology (GO) analysis was used to systematically characterize the global expression profiles, which were found to correlate with the leiomyosarcomas.

Materials and Methods

The uterine leiomyoma biopsies were obtained from patients in the Department of Obstetrics and Gynecology, The Catholic University of Korea. Differentially expressed transcriptome and proteome, in 6 paired leiomyoma and normal myometrium, were profiled. The total RNAs from the leiomyoma and normal myometrium were labeled with Cy5 and Cy3. All specimens were punch-biopsy-obtained, and frozen in liquid nitrogen.

Results

Screening of up to 17,000 genes identified 71 that were either up-regulated or down-regulated (21 and 50, respectively). The gene expression profiles were classified into 420 mutually dependent functional sets, resulting in 611 cellular processes, according to the gene ontology. Also, the protein analysis, using 2D gel electrophoresis, identified 33 proteins (17 up-regulated and 16 down-regulated) with more than 500 total spots, which were classified into 302 cellular processes. O f these functional profilings, transcriptomes and proteoms down-regulations were shown in the cell adhesion, cell m otility, organogenesis, enzyme regulator, structural molecule activity and responses to external stimulus functional activities, which are supposed to play important roles in the pathophysiology. In contrast, up-regulation was only shown in the nucleic acid binding activity. The CDKN2A, ADH1A, DCX, IGF2, CRABP2 and KIF5C were found to increase the reliability of this study, and correlate with the leiomyosarcomas.

Conclusion

Potentially significant pathogenetic cellular processes showed that down-regulated functional profiling has an important impact on the discovery of the pathogenic pathways in leiomyomas and leiomyosarcomas. GO analysis can also overcome the complexity of the expression profiles of cDNA microarrays and 2D protein analyses, via a cellular process level approach. Thereby, a valuable prognostic candidate gene, with real relevance to disease-specific pathogenesis, can be found at cellular process levels.

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  • H3K4me3 mediates uterine leiomyoma pathogenesis via neuronal processes, synapsis components, proliferation, and Wnt/β-catenin and TGF-β pathways
    María Cristina Carbajo-García, Elena Juarez-Barber, Marina Segura-Benítez, Amparo Faus, Alexandra Trelis, Javier Monleón, Greta Carmona-Antoñanzas, Antonio Pellicer, James M. Flanagan, Hortensia Ferrero
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  • Differential Expression of MED12-Associated Coding RNA Transcripts in Uterine Leiomyomas
    Tsai-Der Chuang, Jianjun Gao, Derek Quintanilla, Hayden McSwiggin, Drake Boos, Wei Yan, Omid Khorram
    International Journal of Molecular Sciences.2023; 24(4): 3742.     CrossRef
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    Özge KÖMÜRCÜ KARUSERCİ, Esra GÜZEL TANOĞLU, Halime Hanım PENÇE, Mete Gürol UĞUR
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    Zorawar Singh
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    Liping Xia, Yan Liu, Yan Fu, Shengyi Dongye, Dewei Wang
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    BLENDI URA, FEDERICA SCRIMIN, FABRIZIO ZANCONATI, GIORGIO ARRIGONI, LORENZO MONASTA, ANDREA ROMANO, RUBINA BANCO, MARINA ZWEYER, DANIELA MILANI, GIUSEPPE RICCI
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cDNA Microarray Experiment: Design Issues in Early Stage and the Need of Normalization
Byung Soo Kim, Sunho Lee, Sun Young Rha, Hyun Cheol Chung
Cancer Res Treat. 2003;35(6):533-540.   Published online December 31, 2003
DOI: https://doi.org/10.4143/crt.2003.35.6.533
AbstractAbstract PDF
PURPOSE
The cDNA microarray has become a useful tool for observing the expression of thousands of genes simultaneously. However, obtaining good quality microarray data is not easy due to the inherent noise at various stages of the experiment. Therefore, it is essential to understand the source of the variation in the microarray experiment and its size as an initial step of the data analyses. MATERIALS AND METHODS: The total RNA extracted from HT-1080 fibrosarcoma and normal rat tissues were hybridized to the cDNA microarrays with 0.5 K human and 5 K rat genes, respectively. A homotypic reaction and dye swap experiments were used to identify the sources of the variation. RESULTS: The relative fluorescent intensities of the microarray, if unnormalized, have a large variation, particularly in the lower intensity region. The distribution of the log intensity ratios also exhibit some departure from a band around zero, which is the distribution pattern expected when the majority of genes in the microarray are not regulated. Normalization of the log ratios is usually required as a means of preprocessing the data. We claim that a within-print tip group, an intensity-dependent normalization through a loess fit adjustment will be useful for this purpose, particularly in the initial stages of the microarray experiment. CONCLUSION: For proper data analysis, an understanding the source of the variation and preprocessing of data with a suitable normalization method will be important. It is important to have an interactive cooperation between a researcher and a statistician from the early stages of the study design and to the final stages of data analysis.

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  • Whole genome analysis for liver metastasis gene signatures in colorectal cancer
    Dong Hyuk Ki, Hei‐Cheul Jeung, Chan Hee Park, Seung Hee Kang, Gui Youn Lee, Won Suk Lee, Nam Kyu Kim, Hyun Chul Chung, Sun Young Rha
    International Journal of Cancer.2007; 121(9): 2005.     CrossRef
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cDNA Microarray Analysis of Gene Expression Profiles Associated with Cervical Cancer
Joo Hee Yoon, Joon Mo Lee, Sung Eun Namkoong, Su Mi Bae, Yong Wan Kim, Sei Jun Han, Young Lae Cho, Gye Hyun Nam, Chong Kook Kim, Jeong Sun Seo, Woong Shick Ahn
Cancer Res Treat. 2003;35(5):451-459.   Published online October 31, 2003
DOI: https://doi.org/10.4143/crt.2003.35.5.451
AbstractAbstract PDF
PURPOSE
The molecular pathology of cervical cancers associated with human papillomavirus infection is presently unclear. In an effort to clarify this issue, the gene expression profiles and pathogenic cellular processes of cervical cancer lesions were investigated. MATERIALS AND METHODS: Cervical cancer biopsies were obtained from patients at the Department of Obstetrics and Gynecology, The Catholic University of Korea. The disease status was assigned according to the International Federation of Gynecology and Obstetrics. The tissue samples of 11 patients (invasive cancer stage Ib- IIIa) were investigated by a cDNA microarray of 4, 700 genes, hierarchical clustering and the Gene Ontology (GO). Total RNA from cervical cancer and non-lesional tissues were labeled with Cy5 and Cy3. The HaCaT human epithelial keratinocyte cell line was used as a negative control cell. The stages of invasive cancer were Ib to IIIb. All specimens were obtained by punch-biopsies and frozen in liquid nitrogen until required. RESULTS: 74 genes, showing more than a 2 fold difference in their expressions, were identified in at least 8 of the 11 patients. Of these genes, 33 were up-regulated and 41 were down-regulated. The gene expression profiles were classified into 345 mutually dependent function sets, resulting in 611 cellular processes according to their GO. The GO analysis showed that cervical carcinogenesis underwent complete down-regulation of cell death, protein biosynthesis and nucleic acid metabolism. The genes related to nucleic acid binding and structural molecule activity were also significantly down-regulated. In contrast, significant up-regulation was shown in the skeletal development, immune response and extracellular activity. CONCLUSION: These data are suggestive of potentially significant pathogenetic cellular processes, and showed that the down-regulated functional profiling has an important impact on the discovery of pathogenic pathways in cervical carcinogenesis. GO analysis can also overcome the complexity of the expression profiles of the cDNA microarray via a cellular process level approach. Thereby, a valuable prognostic candidate gene, with real relevance to disease-specific pathogenesis, can be found at the cellular process levels.

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    Przemysław Podstawski, Marcin Samiec, Maria Skrzyszowska, Tomasz Szmatoła, Ewelina Semik-Gurgul, Katarzyna Ropka-Molik
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    Simon A. Rudge, Michael J.O. Wakelam
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    Ju Youn Park, Jae Ho Chang, Myong Jo Kim, Ju Sung Kim, Soo-Ki Kim
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    Tom D. Bunney, Matilda Katan
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    Lisa M. Ooms, Kristy A. Horan, Parvin Rahman, Gillian Seaton, Rajendra Gurung, Dharini S. Kethesparan, Christina A. Mitchell
    Biochemical Journal.2009; 419(1): 29.     CrossRef
  • Altered MicroRNA Expression in Cervical Carcinomas
    Jeong-Won Lee, Chel Hun Choi, Jung-Joo Choi, Young-Ae Park, Seung-Jun Kim, Seung Yong Hwang, Woo Young Kim, Tae-Joong Kim, Je-Ho Lee, Byoung-Gie Kim, Duk-Soo Bae
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  • Identification of hemoglobin‐α and ‐β subunits as potential serum biomarkers for the diagnosis and prognosis of ovarian cancer
    Ahn Woong‐Shick, Park Sung‐Pil, Bae Su‐Mi, Lee Joon‐Mo, Namkoong Sung‐Eun, Nam Gye‐Hyun, Cho Young‐Lae, Choi Ho‐Sun, Jun Heung‐Jae, Kim Chong‐Kook, Kim Young‐Wan, Han Byoung‐Don, Jin Hyun‐Sun
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  • The Differential Gene Expression Profiles between Sensitive and Resistant Breast Cancer Cells to Adriamycin by cDNA Microarray
    Myung-Ju Ahn, Ki-Hwan Lee, Joon-Ik Ahn, Dong-Hyun Yu, Hye-Sook Lee, Jung-Hye Choi, Joung Soon Jang, Jong Min Bae, Yong-Sung Lee
    Cancer Research and Treatment.2004; 36(1): 43.     CrossRef
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Gene Expression Profiling of Non-Small Cell Lung Cancer
Mee Sook Roh, Hyuk Chan Kwon, Jin Sook Jeong, Dae Cheol Kim, Choon Hee Son, Soo Keol Lee, Phil Jo Choi, Jae Ik Lee, Ki Nam Lee, Hyo Jin Kim, Jin Han Yoon, Tae Ho Hwang
Cancer Res Treat. 2003;35(2):154-160.   Published online April 30, 2003
DOI: https://doi.org/10.4143/crt.2003.35.2.154
AbstractAbstract PDF
PURPOSE
cDNA microarray provided a powerful alternative, with an unprecedented view scope, in monitoring gene expression levels, and led to the discovery of regulatory pathways involved in complicated biological processes. This study was performed to gain better understanding of the molecular mechanisms underlying the carcinogenesis and progression of lung cancer. MATERIALS AND METHODS: Using a cDNA microarray, representing 4, 600 cDNA clusters, we studied the expression profiles in 10 non-small cell lung cancer (NSCLC) samples and the adjacent noncancerous lung tissues form the same patients. The alterations in the levels of gene expression were confirmed by reverse-transcription PCR in 10 randomly selected genes.
RESULTS
Genes that were differently expressed in the cancerous and noncancerous tissues were identified. One hundred and nine genes (of which 68 were known) and 69 cDNAs (of which 32 were known) were up- and down-regulated in>70% of the NSCLC samples, respectively. In the cancerous tissues, the genes related to the cell cycle, metabolism, cell structure and signal transduction, were mostly up-regulated. Furthermore, we identified a few putative tumor suppressor genes that had previously been proposed by other workers. CONCLUSIONS: These results provide, not only a new molecular basis for understanding the biological properties of NSCLC, but also useful resources for the future development of diagnostic markers and therapeutic targets for NSCLC.

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  • Expression of double‐stranded RNA‐activated protein kinase in small‐size peripheral adenocarcinoma of the lung
    Mee Sook Roh, Ju Young Kwak, Su Jin Kim, Hyun Wook Lee, Hyuk Chan Kwon, Tae Ho Hwang, Phil Jo Choi, Young Seoub Hong
    Pathology International.2005; 55(11): 688.     CrossRef
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Interrelation of Cyclin D1, Cyclin E, and p27Kip1 Expression on Tissue Arrays of Breast Cancer
Se Hwan Han, Kyeong Mee Park, Byung Noe Bae, Suk Yong Ryu, Ki Hwan Kim, Hong Joo Kim, Young Duck Kim, Hong Yong Kim
Cancer Res Treat. 2002;34(5):388-393.   Published online October 31, 2002
DOI: https://doi.org/10.4143/crt.2002.34.5.388
AbstractAbstract PDF
PURPOSE
To evaluate the clinical impact of the altered expression of cell cycle regulators in stage I and II breast cancers.
MATERIALS AND METHODS
The interaction between cyclin D1/E and p27Kip1 expressions were analyzed using tissue microarray (TMA) technology in 133 breast cancers. Data from the immunohistochemical assays of 3 molecules were merged, and analyzed, with a Ki67 labeling index of the same tumors.
RESULTS
Cyclin D1 was expressed in 72 breast carcinomas (54.1%) and cyclin E in 60 (45.1%) out of the 133 breast carcinomas. Expressions of cyclin D1 and cyclin E were inversely related to each other, and significantly associated with the estrogen receptor (ER) expression and differentiation of the breast carcinoma. The expression of cyclin E was significantly decreased in tumors expressing cyclin D1 (p=0.022). There was a trend for cyclin D1 expression to increase in tumors expressing p27Kip1 (p=0.053), but the expression of cyclin E did not correlate with p27Kip1 expression. The Ki67 labeling index was markedly increased in tumors expressing cyclin E, whereas it was significantly decreased in the cyclin D1 or p27Kip1 expressing-tumors. From survival analysis, cyclin E expression was the only significant variable for the prediction of poor survival.
CONCLUSION
The abnormal expressions of cell cycle regulatory molecules are prevalent, and interrelated with each other in breast cancer. Integration of TMA technology allowed a high-throughput analysis for correlating molecular the in situ findings, with the clinico-pathologic information. Among the three molecules studied, the cyclin E had a prognostic implication for stage I and II breast cancer.

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  • Novel insights into biomarkers of progression in Desmoid tumor
    Baiqi Liu, Zefang Sun, Rui Zhou, Dingcheng Shen, Shuai Zhu, Lu Chen, Gengwen Huang
    Frontiers in Oncology.2023;[Epub]     CrossRef
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