Sporadic colorectal cancer in elderly people.
OBJECTIVE
The mechanism of the development of cancer in old age is not well understood in various cancers, especially colorectal cancer. Colorectal cancer in elderly patients often shows a high frequency of proximal colon cancer. Microsatellite instability cancers are often found in the proximal colon and show a lower incidence of p53 abnormality. While the aberrant expression of p53 is more frequent in the distal colon. To investigate the carcinogenesis of colorectal cancer in elderly patients, we studied the genetic background of these patients regarding microsatellite instability and the aberrant expression of p53.


METHODS
In the present study, we examined the clinicopathological features and the frequency of p53 abnormality in elderly patients compared to younger patients, and the frequency of microsatellite instability in elderly patients. In microsatellite instability cancer, immunoreactivity of hMSH2 and hMLH1 were also examined.


RESULTS
Colorectal cancer in elderly patients is associated with proximal location of the cancer (p = 0.008). Microsatellite instability was observed in only 1 case (2.8%). The immunoreactivity of hMLH1 showed negative staining in malignant glands. The frequency of aberrant expression of p53 showed no significant difference between two groups.


CONCLUSIONS
We found colorectal cancer more frequently in proximal colon in elderly patients than in younger patients, and microsatellite instability frequency in elderly patients (2.8%) was lower than reported microsatellite instability frequency in sporadic colorectal cancer patients. Moreover, the frequency of aberrant expression of p53 did not differ between the two groups. In the present study, microsatellite instability appeared to be less important for the carcinogenesis of colorectal cancer in elderly patients as compared to younger patients.
Koketsu
Shinichiro
S
Department of Surgical Oncology, Graduate School of Medicine, University of Tokyo, 7-3-1 Hongo, Bunkyo-Ku, Tokyo, Japan 113-8655. koketsu-tky@umin.ac.jp
Watanabe
Toshiaki
T
Tada
Tomohiro
T
Kanazawa
Takamitsu
T
Ueda
Eiji
E
Nagawa
Hirokazu
H
D048868:Adaptor Proteins, Signal Transducing; D000367:Age Factors; D000368:Aged; D002352:Carrier Proteins; D002471:Cell Transformation, Neoplastic / Q000235:genetics* / Q000473:pathology; D016922:Cellular Senescence / Q000235:genetics*; D043171:Chromosomal Instability / Q000235:genetics*; D002869:Chromosome Aberrations; D015179:Colorectal Neoplasms / Q000235:genetics* / Q000473:pathology; D004268:DNA-Binding Proteins / Q000235:genetics; D005260:Female; D015972:Gene Expression Regulation, Neoplastic / Q000502:physiology; D005787:Gene Frequency / Q000235:genetics; D006801:Humans; D007413:Intestinal Mucosa / Q000473:pathology; D008198:Lymph Nodes / Q000473:pathology; D008297:Male; D018895:Microsatellite Repeats / Q000235:genetics*; D000070957:MutL Protein Homolog 1; D051718:MutS Homolog 2 Protein; D009363:Neoplasm Proteins / Q000235:genetics; D009367:Neoplasm Staging; D009687:Nuclear Proteins; D011518:Proto-Oncogene Proteins / Q000235:genetics; D016159:Tumor Suppressor Protein p53 / Q000235:genetics*
D048868:Adaptor Proteins, Signal Transducing; D002352:Carrier Proteins; D004268:DNA-Binding Proteins; C501486:MLH1 protein, human; D009363:Neoplasm Proteins; D009687:Nuclear Proteins; D011518:Proto-Oncogene Proteins; D016159:Tumor Suppressor Protein p53; C497172:MSH2 protein, human; D000070957:MutL Protein Homolog 1; D051718:MutS Homolog 2 Protein