Origins and morphogenesis of colorectal neoplasms
WAIMAN WONG
Histopathology Unit, Imperial Cancer Research Fund, London
Department of Histopathology, Imperial College of Science, Technology and Medicine, London, United Kingdom
Division of Gastroenterology and Hepatology, University Department of Medicine, Queen Mary Hospital, University of Hong Kong.
Search for more papers by this authorSERGIO B. GARCIA
Histopathology Unit, Imperial Cancer Research Fund, London
Department of Histopathology, Imperial College of Science, Technology and Medicine, London, United Kingdom
Search for more papers by this authorCorresponding Author
NICHOLAS A. WRIGHT
Histopathology Unit, Imperial Cancer Research Fund, London
Department of Histopathology, Imperial College of Science, Technology and Medicine, London, United Kingdom
Imperial College of Science, Technology and Medicine, Hammersmith Campus, Du Cane Road, London W12 ONN, UK.Search for more papers by this authorWAIMAN WONG
Histopathology Unit, Imperial Cancer Research Fund, London
Department of Histopathology, Imperial College of Science, Technology and Medicine, London, United Kingdom
Division of Gastroenterology and Hepatology, University Department of Medicine, Queen Mary Hospital, University of Hong Kong.
Search for more papers by this authorSERGIO B. GARCIA
Histopathology Unit, Imperial Cancer Research Fund, London
Department of Histopathology, Imperial College of Science, Technology and Medicine, London, United Kingdom
Search for more papers by this authorCorresponding Author
NICHOLAS A. WRIGHT
Histopathology Unit, Imperial Cancer Research Fund, London
Department of Histopathology, Imperial College of Science, Technology and Medicine, London, United Kingdom
Imperial College of Science, Technology and Medicine, Hammersmith Campus, Du Cane Road, London W12 ONN, UK.Search for more papers by this authorAbstract
Gastrointestinal stem cells are considered pivotal in colonic carcinogenesis. There is evidence to suggest that early microadenomas in the colon are polyclonal in origin. Adenomas, once initiated, enlarge by the process of crypt fission. It is also the main mechanism by which neoplastic clones spread through the colorectal epithelium. Both concepts are important for our understanding of the early events in colonic carcinogenesis.
REFERENCES
- Alexander P.. Do cancers arise from a single transformed cell or is monoclonality of tumours a late event in carcinogenesis Br J Cancer, 1985; 51: 453–7.
- Bjerknes M., Cheng H.. Clonal analysis of mouse intestinal epithelial progenitors. Gastroenterology, 1999; 116: 7–14.
- Bjerknes M., Cheng H., Hay K., Gallinger S.. APC mutation and the crypt cycle in murine and human intestine. Am J Pathol, 1997; 150: 833–9.
- Burmer GC, Rabinovitch PS, Haggit RC, Crispin DA, Brentnall TA, Kolli VR, Stevens AC, Rubin CE. Neoplastic progression in ulcerative colitis: histology, DNA content, and loss of a p53 allele. Gastroenterology, 1992; 103: 1602–10.
- Chang WW. Morphological basis of multistep process in experimental colonic carcinogenesis. Virchows Arch. B [Cell Pathol Incl Mol Pathol], 1982; 41: 17–37.
- De Wind N., Dekker M., van Rossum A., van der Valk M., te Riele H.. Mouse models for hereditary non-polyposis colorectal cancer. Cancer Res, 1998; 58: 248–55.
- Fearon ER, Vogelstein B.. A genetic model for colorectal tumorigenesis. Cell, 1990; 61: 759–67.
- Fialkow PJ. Clonal origin of human tumours. Annu Rev Med, 1979; 30: 135–43.
-
Garcia S.,
Park HS,
Novelli M.,
Wright NA.
Field cancerisation, clonality and epithelial stem cells: the spread of mutated clones in epithelial sheets.
J Pathol (in press), 1999.
10.1002/(SICI)1096-9896(199901)187:1<61::AID-PATH247>3.0.CO;2-I CAS PubMed Web of Science® Google Scholar
- Griffiths DF, Davies SJ, Williams D., Williams GT, Williams ED. Demonstration of somatic mutation and colonic crypt clonality by X-linked enzyme histochemistry. Nature, 1988; 333: 461–3.
-
Jasani B.,
Campbell F.,
Navabi H.,
Schmid KW,
Williams GT.
Clonal overexpression of metallothionein is induced by somatic mutation in morphologically normal colonic mucosa.
J Pathol, 1998; 184: 144–7.
10.1002/(SICI)1096-9896(199802)184:2<144::AID-PATH998>3.0.CO;2-J CAS PubMed Web of Science® Google Scholar
-
Kirkland SC.
Clonal origin of columnar, mucous and endocrine cell lineages in human colorectal epithelium.
Cancer, 1988; 61: 1359–63.
10.1002/1097-0142(19880401)61:7<1359::AID-CNCR2820610714>3.0.CO;2-0 CAS PubMed Web of Science® Google Scholar
- Knudson AG. Heredity and human cancer. Am J Pathol, 1974; 77: 77–84.
- Levin DS, Rabinovitch PS, Haggit RC, Blount PL, Dean PJ, Rubin CE, Reid BJ. Distribution of aneuploid cell populations in ulcerative colitis with dysplasia or cancer. Gastroenterology, 1991; 101: 1198–210.
- Loeffler M., Birke A., Winton DJ, Potten C.. Somatic mutation, monoclonality and stochastic models of stem cell organisation in the intestinal crypt. J Theor Biol, 1993; 162: 471–91.
- Merritt AJ, Gould KA, Dove WF. Polyclonal structure of intestinal adenomas in APCMin/+ mice with concomitant loss of APC+ from all tumour lineages. Proc Natl Acad Sci USA, 1997; 94: 13927–31.
- Moolgavkar SH, Luebeck EG. Multistage carcinogenesis: population-based model for colon cancer. J Natl Cancer Inst, 1992; 84: 610–8.
- Novelli MR, Williamson JA, Tomlinson IP, Elia G., Hodgson SV, Talbot IC, Bodmer WF, Wright NA. Polyclonal origin of colonic adenomas in an XO/XY patient with FAR. Science, 1996; 272: 1187–90.
- Park HS, Goodlad RA, Wright NA. Crypt fission in the small intestine and colon. A mechanism for the emergence of G6PD locus-mutated crypts after treatment with mutagens. Am J Pathol, 1995; 147: 1416–27.
- Ponder BAJ, Schmidt GH, Wilkinson MM, Wood MJ, Monk M., Reid A.. Derivation of mouse intestinal crypts from a single progenitor cell. Nature, 1985; 313: 689–91.
- Ponder BA, Wilkinson MM. Direct examination of the clonality of carcinogen-induced colonic epithelial dysplasia in chimeric mice. J Natl Cancer Inst, 1986; 77: 967–76.
- Powell SM, Zilz N., Beazer-Barclay Y., Bryan TM, Hamilton SR, Thibodeau SN, Vogelstein B., Kinzler KW. APC mutations occur early during colorectal tumorigenesis. Nature, 1992; 359: 235–7.
- Rubin H.. Cancer as a dynamic developmental disorder. Cancer Res, 1985; 45: 2935–42.
- St Clair WH, Osborne JW. Crypt fission and crypt number in the small and large bowel of postnatal rats. Cell Tissue Kinet, 1985; 18: 255–62.
- Thompson M., Fleming K., Evans DJ, Fundle R., Surani MA, Wright NA. Gastric endocrine cells share a clonal origin with other gastric cell lineages. Development, 1990; 110: 477–81.
- Totafurno J., Bjerknes M., Cheng H.. The crypt cycle: crypt and villus production in adult intestinal epithelium. Biophys J, 1987; 52: 279–94.
-
Wasan HS,
Park HS,
Liu KC,
Mandir N.,
Winnett A.,
Sasieni P.,
Bodmer WF,
Goodlad RA,
Wright NA.
APC in the regulation of intestinal crypt fission.
J Pathol, 1998; 185: 246–55.
10.1002/(SICI)1096-9896(199807)185:3<246::AID-PATH90>3.0.CO;2-8 CAS PubMed Web of Science® Google Scholar
- Williams ED, Lowes AP, Williams D., Williams GT. A stem cell niche theory of intestinal crypt maintenance based on a study of somatic mutation in colonic mucosa. Am J Pathol, 1992; 141: 773–6.
- Winton DF, Blount MA, Ponder BAJ. A clonal marker induced by mutation in mouse intestinal epithelium. Nature, 1988; 333: 463–6.
- Winton DJ, Ponder BAJ. Stem-cell organization in mouse small intestine. Proc R Soc Lond Biol Sci, 1990; 241: 13–8.
