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Comparison of Snail-1 and Estrogen Receptor Immunoexpression between Fibroadenomas and Phyllodes Tumors

Fairuz Quzwain
  Jurnal Kedokteran Brawijaya, Vol 31, No 2 (2020),  pp.100-104  


Fibroadenomas (FA) and phyllodes tumors (PT) are fibroepithelial lesions in the breast, which until now the relationship between the pathogenesis of both have not been ascertained yet. Epithelial cells are thought to be involved in the regulation of changes in the stromal cells in the PT, so it can be estimated that this process is involved in epithelial-mesenchymal transition (EMT). This study aims to compare of snail family transcriptional repressor 1 (Snail-1) and estrogen receptor (ER) impression as EMT factors among tumor type  (FA, benign PT, boderline PT and malignant PT). This study was an observational analysis with the cross-sectional method. After the histologic grade of the samples was reviewed, immunohistochemistry examination for ER and Snail-1 was performed. Statistical analysis for categorical data was tested by chi-square test. There were 66 samples, consists of 20 FA, 17 benign PT, 16 borderlines PT, and 13 malignant PT. A significant difference in the loss of ER expression in borderline and malignant PT was found compared to FA and benign PT. This is inversely proportional to the snail-1 expression, where the expression was high in borderline PT and malignant PT stromal cells. This could support the consideration of the pathomechanism regulation of epithelial-mesenchymal cell transition changes in FA with PT, where Snail-1 is one of the proteins in the regulation of the EMT and RE processes acting as an inhibiting factor in transcription factors in the mechanism of EMT occurrence.


Estrogen receptor; fibroadenomas; pyhllodes tumors; snail-1

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Hanby AM, Millican-Slater R, and Dessauvagie B. Fibroepithelial Neoplasms of the Breast. Diagnostic Histopathology. 2017; 23(4): 149–158.

Krings G, Bean GR, and Chen YY. Fibroepithelial Lesions; the WHO Spectrum. Seminars in Diagnostic Pathology. 2017; 35(5): 438–452.

Tan J, Ong CK, Lim WK, et al. Genomic Landscapes of Breast Fibroepithelial Tumors. Nature Genetics. 2015; 47(11): 1341–1345.

Zhang Y and Kleer CG. Phyllodes Tumor of the Breast Histopathologic Features, Differential Diagnosis and Molecular/Genetic Updates. Archives of Pathology and Laboratory Medicine. 2016: 140(7); 665-671.

Akrida I, Bravou V, Nikou S, et al. Expression of Epithelial to Mesenchymal Transition-related Transcription Factor ZEB1 in Phyllodes Breast Tumours: An Immunohistochemical Study. Archiv für Pathologische Anatomie und Physiologie und für Klinische Medicin. 2015; 467(1): S11.

Kwon JE, Jung WH, and Koo JS. Molecules Involved In Epithelial-mesenchymal Transition and Epithelial-stromal Interaction in Phyllodes Tumors: Implications for Histologic Grade and Prognosis. Tumor Biology. 2012; 33(3): 787–798.

Smith BN, Burton LJ, Henderson V, et al. Snail Promotes Epithelial Mesenchymal Transition in Breast Cancer Cells in Part Via Activation of Nuclear ERK2. PLoS ONE. 2014; 9(8): e104987.

Tian M and Schiemann WP. TGF-β Stimulation of EMT Programs Elicits Non-genomic ER-α Activity and Anti-estrogen Resistance in Breast Cancer Cells. Journal of Cancer Metastasis and Treatment. 2017; 3(8): 150-160.

Kang BJ, Jo KW, Park TS, et al. Causes and Predictive Factors Associated with “Diagnosis Changed” Outcomes in Patients Notified as Tuberculosis Cases in a Private Tertiary Hospital. Tuberculosis and Respiratory Diseases. 2013; 75(6): 238–243.

Wu Y and Zhou BP. Snail. Cell Adhesion & Migration. 2010; 4(2): 199–203.

Wang Y, Shi J, Chai K, Ying X, and Zhou BP. The Role of Snail in EMT and Tumorigenesis. Current Cancer Drug Targets. 2013; 13(9): 963–972.

Mo XT, Zhou WC, Cui WH, et al. Inositol-requiring Protein 1 - X-box-binding Protein 1 Pathway Promotes Epithelial-mesenchymal Transition Via Mediating Snail Expression in Pulmonary Fibrosis. The International Journal of Biochemistry and Cell Biology. 2015; 65: 230–238.

Poblete CE, Fulla J, Gallardo M, et al. Increased SNAIL Expression and Low Syndecan Levels are Associated with High Gleason Grade in Prostate Cancer. International Journal of Oncology. 2014; 44(3): 647–654.

Fendrich V, Maschuw K, Waldmann J, et al. Epithelial-mesenchymal Transition is a Critical Step in Tumorgenesis of Pancreatic Neuroendocrine Tumors. Cancers (Basel). 2012; 4(1): 281–294.

Wu Y, Sarkissyan M, and Vadgama J. Epithelial-Mesenchymal Transition and Breast Cancer. Journal of Clinical Medicine. 2016; 5(2): 13.

Gurzu S, Turdean S, Kovecsi A, Contac AO, and Jung I. Epithelial-Mesenchymal, Mesenchymal-Epithelial, and Endothelial-Mesenchymal Transitions in Malignant Tumors: An Update. World Journal of Clinical Cases. 2015: 3(5); 393-404.

Shao R, Shi J, Liu H, et al. Epithelial-to-Mesenchymal Transition and Estrogen Receptor α Mediated Epithelial Dedifferentiation Mark the Development of Benign Prostatic Hyperplasia. Prostate. 2014; 74(9): 970–982.

Wik E, Ræder MB, Krakstad C, et al. Lack of Estrogen Receptor-α is Associated with Epithelial-Mesenchymal Transition and PI3K Alterations in Endometrial Carcinoma. Clinical Cancer Research. 2013; 19(5): 1094–1105.

Kim YH, Kim GE, Lee JS, et al. Hormone Receptors Expression in Phyllodes Tumors of the Breast. Analytical and Quantitative Cytology and Histology/The International Academy of Cytology [and] American Society of Cytology. 2012; 34(1): 41–48.

Fairuz and Suryawati B. Hubungan Imunoekspresi ER-α, ER-β, dan PR dengan Gradasi pada Tumor Filodes Payudara. Jurnal Kedokteran Brawijaya. 2017; 29(3): 238–243.

Bouris P, Skandalis SS, Piperigkou Z, et al. Estrogen Receptor Alpha Mediates Epithelial to Mesenchymal Transition, Expression of Specific Matrix Effectors and Functional Properties of Breast Cancer Cells. Matrix Biology: Journal of the International Society for Matrix Biology. 2015; 43: 42–60.



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