Clinical perspective of precancerotic states in gastroenterology and their molecular genetics

Česká verzia

Authors: P. Mináriková ^1,2; M. Zavoral ^1,2
Authors place of work: Interní klinika 1. lékařské fakulty UK a ÚVN Praha, přednosta prof. MUDr. Miroslav Zavoral, Ph. D. ¹; Subkatedra gastroenterologie IPVZ Praha, přednosta prof. MUDr. Miroslav Zavoral, Ph. D. ²
Published in the journal: Vnitř Lék 2010; 56(1): 44-48
Category: Reviews

Summary

Gastrointestinal tract tumours represent an important cause of death in the Czech Republic. Diagnosis of the disease at its advanced stage with progression precluding radical surgical solution is a frequent common denominator. Detection of precancerous states, including congenital genetic defects or premalignant syndromes and malignant lesions may serve as a useful tool for early detection of disease risk or disease onset. Considering the incidence of individual types of tumours, this paper focuses mainly on precancerotic states leading to malignant alterations of oesophagus, colorectum and pancreas. Apart from a concise morphological description of each premalignancy and its malignant transformation, a description of traditional molecular models of development and progression is also provided. Furthermore, we include a brief list of the most important genes contributing to the mechanism of malignant transformation in these three most important tumour diseases.

Key words:
gastrointestinal tract – tumour diseases – genetics – oesophagus – colon – rectum – pancreas – DNA – mutation

Zdroje

1. Wikipedia – the online encyclopedia, http://en.wikipedia.org/wiki/Precancerous.

2. Epidemiologie zhoubných nádorů v České republice v roce 2007, www.svod.cz.

3. Klein CA. Gene expression sigantures, cancer cell evolution and metastatic progression. Cell Cycle 2004; 3: 29–31.

4. Toribara NW, Sleisenger MH. Screening for colorectal cancer. N Engl J Med 1995; 332: 861–867.

5. Barrett N. The lower esophagus lined by columnar epithelium. Surgery 1957; 41: 881–894.

6. Fléjou J. Barrett’s oesophagus: from metaplasia to dysplasia and cancer. Gut 2005; 54 (Suppl 1): i6–i12.

7. Seewald S, Ang TL, Groth S et al. Detection and endoscopic therapy of early esophageal adenocarcinoma. Curr Opin Gastroenterol 2008; 24: 521–529.

8. Kaur BS, Khamnehei N, Iravani M et al. Rofecoxib inhibits cyclooxygenase 2 expression and activity and reduces cell proliferation in Barrett’s esophagus. Gastroenterology 2002; 123: 60–67.

9. Worthley DL, Whitehall VL, Spring KJ et al. Colorectal carcinogenesis: road maps to cancer. World J Gastroenterol 2007; 13: 3784–3791.

10. Lynch HT, Lanspa S, Smyrk T et al. Hereditary nonpolyposis colorectal cancer (Lynch syndromes I & II). Genetics, pathology, natural history, and cancer control, Part I. Cancer Genet Cytogenet 1991; 53: 143–160.

11. Fearon ER, Vogelstein B. A genetic model for colorectal tumorigenesis. Cell 1990; 61: 759–767.

12. Capella G, Cronauer‑Mitra S, Pienado MA et al. Frequency and spectrum of mutations at codons 12 and 13 of the c‑K‑ras gene in human tumors. Environ Health Perspect 1991; 93: 125–131.

13. Jass JR. Colorectal cancer: a multipathway disease. Crit Rev Oncog 2006; 12: 273–287.

14. Wheeler JM. Epigenetics, mismatch repair genes and colorectal cancer. Ann R Coll Surg Engl 2005; 87: 15–20.

15. Watson AJ. Apoptosis and colorectal cancer. Gut 2004; 53: 1701–1709.

16. Osborn NK, Ahlquist DA. Stool screening for colorectal cancer: molecular approaches. Gastroenterology 2005; 128: 192–206.

17. Tsouma A, Aggeli C, Pissimissis N et al. Circulating tumor cells in colorectal cancer: detection methods and clinical significance. Anticancer Res 2008; 28: 3945–3960.

18. Anker P, Mulcahy H, Chen XQ et al. Detection of circulating tumour DNA in the blood (plasma/serum) of cancer patients. Cancer Metastasis Rev 1999; 18: 65–73.

19. Hassan MM, Bondy ML, Wolff RA et al. Risk factors for pancreatic cancer: case‑control study. Am J Gastroenterol 2007; 102: 2696–2707.

20. Otsuki M, Tashiro M. Chronic pancreatitis and pancreatic cancer, lifestyle‑related diseases. Intern Med 2007; 46: 109–113.

21. Hruban RH, Goggins M, Parsons J et al. Progression model for pancreatic cancer. Clin Cancer Res 2000; 6: 2969–2972.

22. Salek C, Benesova L, Zavoral M et al. Evaluation of clinical relevance of examining K-ras, p16 and p53 mutations along with allelic losses at 9p and 18q in EUS‑guided fine needle aspiration samples of patients with chronic pancreatitis and pancreatic cancer. World J Gastroenterol 2007; 13: 3714–3720.

23. Salek C, Minarikova P, Benesova L et al. Mutation status of K‑ras, p53 and allelic losses at 9p and 18q are not prognostic markers in patients with pancreatic cancer. Anticancer Res 2009; 29: 1803–1810.