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
Main Authors: Yamazaki, Kazuto, Yajima, Takayuki, Nagao, Toshitaka, Shinkawa, Hiroki, Kondo, Fukuo, Hanami, Kyota, Asoh, Akira, Sugano, Isamu, Ishida, Yasuo
Format: Journal Article
Language:English
Published: Germany Elsevier GmbH 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.
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 &lt; 0.0001). The patients with higher E2F-1 PI (E2F-1 PI &gt; 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
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  surname: Yamazaki
  fullname: Yamazaki, Kazuto
  email: anskpath@olive.ocn.ne.jp
  organization: Department of Pathology, Teikyo University, Ichihara Hospital, Ichihara, Japan
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  givenname: Takayuki
  surname: Yajima
  fullname: Yajima, Takayuki
  organization: Department of 1st Internal Medicine, Chiba University, School of Medicine, Chiba, Japan
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  givenname: Toshitaka
  surname: Nagao
  fullname: Nagao, Toshitaka
  organization: Department of Surgical Pathology, Tokyo Medical University, Shinjuku, Tokyo, Japan
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  givenname: Hiroki
  surname: Shinkawa
  fullname: Shinkawa, Hiroki
  organization: Department of Pathology, Teikyo University, Ichihara Hospital, Ichihara, Japan
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  givenname: Fukuo
  surname: Kondo
  fullname: Kondo, Fukuo
  organization: Department of Surgical Pathology, Funabashi Central Hospital, Funabashi, Japan
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  givenname: Kyota
  surname: Hanami
  fullname: Hanami, Kyota
  organization: Department of Pathology, Teikyo University, Ichihara Hospital, Ichihara, Japan
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  givenname: Akira
  surname: Asoh
  fullname: Asoh, Akira
  organization: Department of Pathology, Teikyo University, Ichihara Hospital, Ichihara, Japan
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  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
BackLink https://www.ncbi.nlm.nih.gov/pubmed/12650514$$D View this record in MEDLINE/PubMed
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Keywords Pancreatic ductal carcinoma
MIB-1
E2F-1
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Snippet E2F-1 is a transcriptional factor that mediates cell cycle progression from G1 to S phase, thereby influencing tumor progression. However, only a few...
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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
URI https://dx.doi.org/10.1078/0344-0338-00348
https://www.ncbi.nlm.nih.gov/pubmed/12650514
https://www.proquest.com/docview/205507406
https://search.proquest.com/docview/73118497
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