PMID- 9683778
OWN - NLM
STAT- MEDLINE
DCOM- 19980904
LR  - 20190516
IS  - 1019-6439 (Print)
IS  - 1019-6439 (Linking)
VI  - 13
IP  - 3
DP  - 1998 Sep
TI  - Effect of cyclin D1 and associated proteins on proliferation of esophageal 
      squamous cell carcinoma.
PG  - 455-60
AB  - Cyclin D1, which functionally competes with the tumor suppressor genes 
      retinoblastoma (Rb) and p16INK4, is widely recognized as an oncogene. P27KIP1, 
      which inhibits the cyclin D1-CDK4 complex, is also a putative tumor suppressor 
      gene. In order to evaluate the regulatory interaction of these molecules, a 
      retrospective series of tissues from 66 patients with esophageal squamous cell 
      carcinoma was evaluated immunohistochemically for the expressions of cyclin D1, 
      Rb, p16INK4 and p27KIP1. The expressions of these molecules were correlated with 
      the proliferation cell nuclear antigen (PCNA) index as an indicator of cell 
      proliferation. Cyclin D1 was overexpressed (++) in 28 cases (42%), Rb was lost 
      (-) in 19 cases (24%), p16INK4 was lost (-) in 37 cases (56%) and p27KIP1 was 
      lost (-) in 27 cases (41%). Taken together, disorder of at least one or more of 
      these molecules was observed in 62 cases (92%). Expression of cyclin D1 and 
      p16INK4 was negatively correlated (p<0.03), while expression of cyclin D1 and 
      p27KIP1 was positively correlated (p<0.0004). We found strong overall correlation 
      between expression of cyclin D1 and the PCNA index (p<0.0001), however expression 
      of p16INK4 and p27KIP1 was significantly correlated with the PCNA index in tumors 
      devoid of cyclin D1 overexpression (p<0.03 and p<0.02 respectively). Thus, it was 
      found that cyclin D1 plays a major role and closely related to abnormal cell 
      proliferation in esophageal cancer, however assessment of p16INK4 and p27KIP1 
      status, particularly in tumors devoid of cyclin D1 overexpression, is necessary 
      for comprehensive evaluation of cancer cell proliferation. Furthermore, 
      expression of cyclin D1 is correlated with that of p16INK4 and p27KIP1 in 
      squamous cell carcinoma of the esophagus.
FAU - Shamma, A
AU  - Shamma A
AD  - Department of Surgery II, Osaka University, Medical School, Suita, Osaka 565, 
      Japan.
FAU - Doki, Y
AU  - Doki Y
FAU - Shiozaki, H
AU  - Shiozaki H
FAU - Tsujinaka, T
AU  - Tsujinaka T
FAU - Inoue, M
AU  - Inoue M
FAU - Yano, M
AU  - Yano M
FAU - Kimura, Y
AU  - Kimura Y
FAU - Yamamoto, M
AU  - Yamamoto M
FAU - Monden, M
AU  - Monden M
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - Greece
TA  - Int J Oncol
JT  - International journal of oncology
JID - 9306042
RN  - 0 (Cell Cycle Proteins)
RN  - 0 (Cyclin-Dependent Kinase Inhibitor p16)
RN  - 0 (Microtubule-Associated Proteins)
RN  - 0 (Neoplasm Proteins)
RN  - 0 (Proliferating Cell Nuclear Antigen)
RN  - 0 (Retinoblastoma Protein)
RN  - 0 (Tumor Suppressor Proteins)
RN  - 136601-57-5 (Cyclin D1)
RN  - 147604-94-2 (Cyclin-Dependent Kinase Inhibitor p27)
SB  - IM
MH  - Aged
MH  - Aged, 80 and over
MH  - Carcinoma, Squamous Cell/*metabolism/*pathology
MH  - Cell Cycle Proteins/biosynthesis/*physiology
MH  - Cell Division/physiology
MH  - Cyclin D1/biosynthesis/*physiology
MH  - Cyclin-Dependent Kinase Inhibitor p16/biosynthesis/physiology
MH  - Cyclin-Dependent Kinase Inhibitor p27
MH  - Esophageal Neoplasms/*metabolism/*pathology
MH  - Female
MH  - Humans
MH  - Male
MH  - Microtubule-Associated Proteins/biosynthesis/physiology
MH  - Middle Aged
MH  - Neoplasm Proteins/biosynthesis/*physiology
MH  - Proliferating Cell Nuclear Antigen/analysis
MH  - Retinoblastoma Protein/biosynthesis/physiology
MH  - Retrospective Studies
MH  - *Tumor Suppressor Proteins
EDAT- 1998/07/31 00:00
MHDA- 1998/07/31 00:01
CRDT- 1998/07/31 00:00
PHST- 1998/07/31 00:00 [pubmed]
PHST- 1998/07/31 00:01 [medline]
PHST- 1998/07/31 00:00 [entrez]
AID - 10.3892/ijo.13.3.455 [doi]
PST - ppublish
SO  - Int J Oncol. 1998 Sep;13(3):455-60. doi: 10.3892/ijo.13.3.455.