Expression of insulin-like growth factor-1 receptor, p-AKT and p-ERK1/2 protein in extramammary Paget's disease

H. Liu, Y. Moroi, S. Yasumoto, H. Kokuba, S. Imafuku, T. Koga, T. Masuda, Y. Tu, M. Furue, K. Urabe

Research output: Contribution to journalArticle

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Abstract

Background: The insulin-like growth factor-1 (IGF-1) receptor (R)-induced phosphatidylinositol 3-kinase (PI3K)/AKT and mitogen-activated protein kinase (MAPK)/ERK signal transduction cascade, which have critical roles in prevention of apoptosis and regulation of cell cycle progression, plays an important role in tumorigenesis. The expression of IGF-1R, AKT and ERK1/2 has been described in some human malignancies, but not in extramammary Paget's disease (EMPD). Objectives: To study the expression of IGF-1R, p-AKT and p-ERK1/2 in EMPD and to evaluate the relationships among them. Methods: Thirty-six tissue samples of 34 patients with primary EMPD were subjected to immunohistochemical staining for IGF-1R, p-AKT and p-ERK1/2. Results: Of thirty-six EMPD tissue samples, 34, 34 and 28 were positive for IGF-IR, p-AKT and p-ERK1/2 expression, respectively; 27, 23 and 17 of the 36 specimens stained positive for IGF-IR, p-AKT and p-ERK1/2 in more than half of Paget's cells, respectively. There were significant correlations between the IGF-1R and p-AKT expression as well as between IGF-1R and p-ERK1/2 expression. Taken together, these results indicate that IGF-1R is overexpressed, and AKT and ERK1/2 are frequently phosphorylated in EMPD. Conclusions: Our study shows that the expression of IGF-1R and the induction of p-AKT and the p-ERK1/2 pathway may play an important role in the pathogenesis of EMPD. The IGF-IR system might be a potential therapeutic target in EMPD.

Original languageEnglish
Pages (from-to)586-591
Number of pages6
JournalBritish Journal of Dermatology
Volume155
Issue number3
DOIs
Publication statusPublished - Sep 1 2006

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Extramammary Paget's Disease
Somatomedin Receptors
Proteins
Phosphatidylinositol 3-Kinase
MAP Kinase Signaling System
Mitogen-Activated Protein Kinases
Signal Transduction
Cell Cycle
Carcinogenesis
Apoptosis
Staining and Labeling

All Science Journal Classification (ASJC) codes

  • Dermatology

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Expression of insulin-like growth factor-1 receptor, p-AKT and p-ERK1/2 protein in extramammary Paget's disease. / Liu, H.; Moroi, Y.; Yasumoto, S.; Kokuba, H.; Imafuku, S.; Koga, T.; Masuda, T.; Tu, Y.; Furue, M.; Urabe, K.

In: British Journal of Dermatology, Vol. 155, No. 3, 01.09.2006, p. 586-591.

Research output: Contribution to journalArticle

Liu, H, Moroi, Y, Yasumoto, S, Kokuba, H, Imafuku, S, Koga, T, Masuda, T, Tu, Y, Furue, M & Urabe, K 2006, 'Expression of insulin-like growth factor-1 receptor, p-AKT and p-ERK1/2 protein in extramammary Paget's disease', British Journal of Dermatology, vol. 155, no. 3, pp. 586-591. https://doi.org/10.1111/j.1365-2133.2006.07366.x
Liu, H. ; Moroi, Y. ; Yasumoto, S. ; Kokuba, H. ; Imafuku, S. ; Koga, T. ; Masuda, T. ; Tu, Y. ; Furue, M. ; Urabe, K. / Expression of insulin-like growth factor-1 receptor, p-AKT and p-ERK1/2 protein in extramammary Paget's disease. In: British Journal of Dermatology. 2006 ; Vol. 155, No. 3. pp. 586-591.
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T1 - Expression of insulin-like growth factor-1 receptor, p-AKT and p-ERK1/2 protein in extramammary Paget's disease

AU - Liu, H.

AU - Moroi, Y.

AU - Yasumoto, S.

AU - Kokuba, H.

AU - Imafuku, S.

AU - Koga, T.

AU - Masuda, T.

AU - Tu, Y.

AU - Furue, M.

AU - Urabe, K.

PY - 2006/9/1

Y1 - 2006/9/1

N2 - Background: The insulin-like growth factor-1 (IGF-1) receptor (R)-induced phosphatidylinositol 3-kinase (PI3K)/AKT and mitogen-activated protein kinase (MAPK)/ERK signal transduction cascade, which have critical roles in prevention of apoptosis and regulation of cell cycle progression, plays an important role in tumorigenesis. The expression of IGF-1R, AKT and ERK1/2 has been described in some human malignancies, but not in extramammary Paget's disease (EMPD). Objectives: To study the expression of IGF-1R, p-AKT and p-ERK1/2 in EMPD and to evaluate the relationships among them. Methods: Thirty-six tissue samples of 34 patients with primary EMPD were subjected to immunohistochemical staining for IGF-1R, p-AKT and p-ERK1/2. Results: Of thirty-six EMPD tissue samples, 34, 34 and 28 were positive for IGF-IR, p-AKT and p-ERK1/2 expression, respectively; 27, 23 and 17 of the 36 specimens stained positive for IGF-IR, p-AKT and p-ERK1/2 in more than half of Paget's cells, respectively. There were significant correlations between the IGF-1R and p-AKT expression as well as between IGF-1R and p-ERK1/2 expression. Taken together, these results indicate that IGF-1R is overexpressed, and AKT and ERK1/2 are frequently phosphorylated in EMPD. Conclusions: Our study shows that the expression of IGF-1R and the induction of p-AKT and the p-ERK1/2 pathway may play an important role in the pathogenesis of EMPD. The IGF-IR system might be a potential therapeutic target in EMPD.

AB - Background: The insulin-like growth factor-1 (IGF-1) receptor (R)-induced phosphatidylinositol 3-kinase (PI3K)/AKT and mitogen-activated protein kinase (MAPK)/ERK signal transduction cascade, which have critical roles in prevention of apoptosis and regulation of cell cycle progression, plays an important role in tumorigenesis. The expression of IGF-1R, AKT and ERK1/2 has been described in some human malignancies, but not in extramammary Paget's disease (EMPD). Objectives: To study the expression of IGF-1R, p-AKT and p-ERK1/2 in EMPD and to evaluate the relationships among them. Methods: Thirty-six tissue samples of 34 patients with primary EMPD were subjected to immunohistochemical staining for IGF-1R, p-AKT and p-ERK1/2. Results: Of thirty-six EMPD tissue samples, 34, 34 and 28 were positive for IGF-IR, p-AKT and p-ERK1/2 expression, respectively; 27, 23 and 17 of the 36 specimens stained positive for IGF-IR, p-AKT and p-ERK1/2 in more than half of Paget's cells, respectively. There were significant correlations between the IGF-1R and p-AKT expression as well as between IGF-1R and p-ERK1/2 expression. Taken together, these results indicate that IGF-1R is overexpressed, and AKT and ERK1/2 are frequently phosphorylated in EMPD. Conclusions: Our study shows that the expression of IGF-1R and the induction of p-AKT and the p-ERK1/2 pathway may play an important role in the pathogenesis of EMPD. The IGF-IR system might be a potential therapeutic target in EMPD.

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