Expression of Transcription Factor E2F-1 in Pancreatic Ductal Carcinoma: An Immunohistochemical Study
E2F-1 is a transcriptional factor that mediates cell cycle progression from G1 to S phase, thereby influencing tumor progression. However, only a few clinicopathologic studies have been carried out using surgically removed specimens for defining its role in tumor biology. Therefore, we studied the e...
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Published in: | Pathology, research and practice Vol. 199; no. 1; pp. 23 - 28 |
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2003
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Abstract | E2F-1 is a transcriptional factor that mediates cell cycle progression from G1 to S phase, thereby influencing tumor progression. However, only a few clinicopathologic studies have been carried out using surgically removed specimens for defining its role in tumor biology. Therefore, we studied the expression of this cell cycle regulator on surgical specimens at the immunohistochemical level, and examined its possible relationship with proliferative index, assessed by analysis of MIB-1 expression, and clinicopathologic factors in pancreatic ductal carcinomas. E2F-1 and MIB-1 were immunostained on 54 surgically removed specimens, and nuclear reactivity was evaluated. The percentage of E2F-1 positive cells (E2F-1 PI) ranged from 3.8% to 71.4%. We found a statistically significant correlation between E2F-1 PI and the histologic grade of tumor differentiation (
p = 0.0133),
i.e. E2F-1 PI was higher in less-differentiated carcinomas. Furthermore, there was a positive correlation between E2F-1 PI and the percentage of MIB-1 PI (
r = 0.763;
p < 0.0001). The patients with higher E2F-1 PI (E2F-1 PI ≥ 38.0 = median) showed a significantly shorter disease-associated survival time in R0 resection cases (
n = 49,
p = 0.015). The present analysis seems to support the theory that E2F-1 is upregulated in cell cycle, and its expression reflects the effector function of G1/S progression as far as pancreatic ductal carcinoma is concerned. |
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AbstractList | E2F-1 is a transcriptional factor that mediates cell cycle progression from G1 to S phase, thereby influencing tumor progression. However, only a few clinicopathologic studies have been carried out using surgically removed specimens for defining its role in tumor biology. Therefore, we studied the expression of this cell cycle regulator on surgical specimens at the immunohistochemical level, and examined its possible relationship with proliferative index, assessed by analysis of MIB-1 expression, and clinicopathologic factors in pancreatic ductal carcinomas. E2F-1 and MIB-1 were immunostained on 54 surgically removed specimens, and nuclear reactivity was evaluated. The percentage of E2F-1 positive cells (E2F-1 PI) ranged from 3.8% to 71.4%. We found a statistically significant correlation between E2F-1 PI and the histologic grade of tumor differentiation (p = 0.0133), i.e. E2F-1 PI was higher in less-differentiated carcinomas. Furthermore, there was a positive correlation between E2F-1 PI and the percentage of MIB-1 PI (r = 0.763; p < 0.0001). The patients with higher E2F-1 PI (E2F-1 PI > or = 38.0 = median) showed a significantly shorter disease-associated survival time in R0 resection cases (n = 49, p = 0.015). The present analysis seems to support the theory that E2F-1 is upregulated in cell cycle, and its expression reflects the effector function of G1/S progression as far as pancreatic ductal carcinoma is concerned. E2F-1 is a transcriptional factor that mediates cell cycle progression from G1 to S phase, thereby influencing tumor progression. However, only a few clinicopathologic studies have been carried out using surgically removed specimens for defining its role in tumor biology. Therefore, we studied the expression of this cell cycle regulator on surgical specimens at the immunohistochemical level, and examined its possible relationship with proliferative index, assessed by analysis of MIB-1 expression, and clinicopathologic factors in pancreatic ductal carcinomas. E2F-1 and MIB-1 were immunostained on 54 surgically removed specimens, and nuclear reactivity was evaluated. The percentage of E2F-1 positive cells (E2F-1 PI) ranged from 3.8% to 71.4%. We found a statistically significant correlation between E2F-1 PI and the histologic grade of tumor differentiation (p = 0.0133), i.e. E2F-1 PI was higher in less-differentiated carcinomas. Furthermore, there was a positive correlation between E2F-1 PI and the percentage of MIB-1 PI (r = 0.763; p < 0.0001). The patients with higher E2F-1 PI (E2F-1 PI > or = 38.0 = median) showed a significantly shorter disease-associated survival time in R0 resection cases (n = 49, p = 0.015). The present analysis seems to support the theory that E2F-1 is upregulated in cell cycle, and its expression reflects the effector function of G1/S progression as far as pancreatic ductal carcinoma is concerned. E2F-1 is a transcriptional factor that mediates cell cycle progression from G1 to S phase, thereby influencing tumor progression. However, only a few clinicopathologic studies have been carried out using surgically removed specimens for defining its role in tumor biology. Therefore, we studied the expression of this cell cycle regulator on surgical specimens at the immunohistochemical level, and examined its possible relationship with proliferative index, assessed by analysis of MIB-1 expression, and clinicopathologic factors in pancreatic ductal carcinomas. E2F-1 and MIB-1 were immunostained on 54 surgically removed specimens, and nuclear reactivity was evaluated. The percentage of E2F-1 positive cells (E2F-1 PI) ranged from 3.8% to 71.4%. We found a statistically significant correlation between E2F-1 PI and the histologic grade of tumor differentiation ( p = 0.0133), i.e. E2F-1 PI was higher in less-differentiated carcinomas. Furthermore, there was a positive correlation between E2F-1 PI and the percentage of MIB-1 PI ( r = 0.763; p < 0.0001). The patients with higher E2F-1 PI (E2F-1 PI ≥ 38.0 = median) showed a significantly shorter disease-associated survival time in R0 resection cases ( n = 49, p = 0.015). The present analysis seems to support the theory that E2F-1 is upregulated in cell cycle, and its expression reflects the effector function of G1/S progression as far as pancreatic ductal carcinoma is concerned. |
Author | Kondo, Fukuo Nagao, Toshitaka Hanami, Kyota Yajima, Takayuki Asoh, Akira Yamazaki, Kazuto Ishida, Yasuo Shinkawa, Hiroki Sugano, Isamu |
Author_xml | – sequence: 1 givenname: Kazuto surname: Yamazaki fullname: Yamazaki, Kazuto email: anskpath@olive.ocn.ne.jp organization: Department of Pathology, Teikyo University, Ichihara Hospital, Ichihara, Japan – sequence: 2 givenname: Takayuki surname: Yajima fullname: Yajima, Takayuki organization: Department of 1st Internal Medicine, Chiba University, School of Medicine, Chiba, Japan – sequence: 3 givenname: Toshitaka surname: Nagao fullname: Nagao, Toshitaka organization: Department of Surgical Pathology, Tokyo Medical University, Shinjuku, Tokyo, Japan – sequence: 4 givenname: Hiroki surname: Shinkawa fullname: Shinkawa, Hiroki organization: Department of Pathology, Teikyo University, Ichihara Hospital, Ichihara, Japan – sequence: 5 givenname: Fukuo surname: Kondo fullname: Kondo, Fukuo organization: Department of Surgical Pathology, Funabashi Central Hospital, Funabashi, Japan – sequence: 6 givenname: Kyota surname: Hanami fullname: Hanami, Kyota organization: Department of Pathology, Teikyo University, Ichihara Hospital, Ichihara, Japan – sequence: 7 givenname: Akira surname: Asoh fullname: Asoh, Akira organization: Department of Pathology, Teikyo University, Ichihara Hospital, Ichihara, Japan – sequence: 8 givenname: Isamu surname: Sugano fullname: Sugano, Isamu organization: Department of Pathology, Teikyo University, Ichihara Hospital, Ichihara, Japan – sequence: 9 givenname: Yasuo surname: Ishida fullname: Ishida, Yasuo organization: Department of Pathology, Teikyo University, Ichihara Hospital, Ichihara, Japan |
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SubjectTerms | Adult Aged Aged, 80 and over Carcinoma, Pancreatic Ductal - metabolism Carcinoma, Pancreatic Ductal - mortality Cell Cycle - physiology Cell Cycle Proteins Cell Division - physiology DNA-Binding Proteins E2F Transcription Factors E2F-1 E2F1 Transcription Factor Female Humans Immunohistochemistry Ki-67 Antigen - biosynthesis Male MIB-1 Middle Aged Neoplasm Invasiveness Neoplasm Proteins - biosynthesis Pancreatic ductal carcinoma Pancreatic Neoplasms - metabolism Pancreatic Neoplasms - mortality Transcription Factors - biosynthesis |
Title | Expression of Transcription Factor E2F-1 in Pancreatic Ductal Carcinoma: An Immunohistochemical Study |
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