» Articles » PMID: 9771410

Colonic Epithelial Cell Proliferation in Hereditary Non-polyposis Colorectal Cancer

Overview
Journal Gut
Specialty Gastroenterology
Date 1998 Oct 15
PMID 9771410
Citations 4
Authors
Affiliations
Soon will be listed here.
Abstract

Background: Despite the recent discovery of four genes responsible for up to 90% of all cases of hereditary non-polyposis colorectal cancer (HNPCC), there will still be families in whom predictive testing is not possible. A phenotypic biomarker would therefore be useful. An upwards shift of the proliferative compartment in colonic crypts is reported to be one of the earliest changes in premalignant mucosa.

Aims: To assess the role of crypt cell proliferation as a phenotypic biomarker in HNPCC.

Patients: Thirty five patients at 50% risk of carrying the HNPCC gene (21 of whom subsequently underwent predictive testing and hence gene carrier status was known) and 18 controls.

Methods: Crypt cell proliferation was measured at five sites in the colon using two different techniques. Labelling index was determined using the monoclonal antibody MIB1 and whole crypt mitotic index was measured using the microdissection and crypt squash technique. The distribution of proliferating cells within the crypts was also assessed.

Results: There were no significant differences in the total labelling index or mean number of mitoses per crypt, nor in the distribution of proliferating cells within the crypt, between the study and control groups at any site. When the 21 patients in whom gene carrier status was known were analysed separately there were no significant differences in the measured indices of proliferation between the HNPCC gene carriers and non-gene carriers.

Conclusion: Crypt cell proliferation is not a discriminative marker of gene carriage in HNPCC.

Citing Articles

Aberrant crypt foci: the case for inclusion as a biomarker for colon cancer.

Wargovich M, Brown V, Morris J Cancers (Basel). 2013; 2(3):1705-16.

PMID: 24281183 PMC: 3837333. DOI: 10.3390/cancers2031705.


Commonly used bowel preparations have significant and different effects upon cell proliferation in the colon: a pilot study.

Croucher L, Bury J, Williams E, Riley S, Corfe B BMC Gastroenterol. 2008; 8:54.

PMID: 19014572 PMC: 2588612. DOI: 10.1186/1471-230X-8-54.


Severe imbalance of cell proliferation and apoptosis in the left colon and in the rectosigmoid tract in subjects with a history of large adenomas.

Anti M, Armuzzi A, Morini S, Iascone E, Pignataro G, Coco C Gut. 2001; 48(2):238-46.

PMID: 11156647 PMC: 1728212. DOI: 10.1136/gut.48.2.238.


Colonic crypt cell proliferation state assessed by whole crypt microdissection in sporadic neoplasia and familial adenomatous polyposis.

Mills S, Mathers J, Chapman P, Burn J, Gunn A Gut. 2000; 48(1):41-6.

PMID: 11115821 PMC: 1728170. DOI: 10.1136/gut.48.1.41.

References
1.
Sigdestad C, Bauman J, Lesher S . Diurnal fluctuations in the number of cells in mitosis and DNA synthesis in the jejunum of the mouse. Exp Cell Res. 1969; 58(1):159-62. DOI: 10.1016/0014-4827(69)90126-8. View

2.
Jass J, Ajioka Y, Radojkovic M, Allison L, LANE M . Failure to detect colonic mucosal hyperproliferation in mutation positive members of a family with hereditary non-polyposis colorectal cancer. Histopathology. 1997; 30(3):201-7. DOI: 10.1046/j.1365-2559.1997.d01-589.x. View

3.
Maskens A, DESCHNER E . Tritiated thymidine incorporation into epithelial cells of normal-appearing colorectal mucosa of cancer patients. J Natl Cancer Inst. 1977; 58(5):1221-4. DOI: 10.1093/jnci/58.5.1221. View

4.
DESCHNER E, Winawer S, LONG F, Boyle C . Early detection of colonic neoplasia in patients at high risk. Cancer. 1977; 40(5 Suppl):2625-31. DOI: 10.1002/1097-0142(197711)40:5+<2625::aid-cncr2820400936>3.0.co;2-v. View

5.
Bayer B, BEAVEN M . Evidence that indomethacin reversibly inhibits cell growth in the G1 phase of the cell cycle. Biochem Pharmacol. 1979; 28(3):441-3. DOI: 10.1016/0006-2952(79)90112-6. View