c-myc amplification is frequent in esophageal adenocarcinoma and correlated with the upregulation of VEGF-A expression1

Neoplasia

Volumn 8, Issue 9, 2006, Pages 702-707

  Von Rahden, Burkhard H A ^a,b,d   Stein, Hubert J ^a,b   Pühringer Oppermann, Franziska ^b   Sarbia, Mario ^b,c  

^a PARACELSUS MEDICAL UNIVERSITY   (Austria)

^b TECHNICAL UNIVERSITY OF MUNICH   (Germany)

^c Unfallkrankenhaus ^*  (Germany)

^d TECHNICAL UNIVERSITY OF MUNICH   (Germany)

Author keywords

Angiogenesis; Barrett cancer; c myc; Esophageal adenocarcinoma; VEGF

Indexed keywords

CYCLOOXYGENASE 1; CYCLOOXYGENASE 2; VASCULOTROPIN A; VASCULOTROPIN C;

ADULT; AGED; ARTICLE; BARRETT ESOPHAGUS; CANCER SURGERY; CANCER SURVIVAL; CONTROLLED STUDY; CORRELATION ANALYSIS; ESOPHAGEAL ADENOCARCINOMA; FEMALE; GENE AMPLIFICATION; GENE EXPRESSION; HUMAN; HUMAN TISSUE; IN SITU HYBRIDIZATION; MAJOR CLINICAL STUDY; MALE; ONCOGENE C MYC; PRIORITY JOURNAL; PROTEIN EXPRESSION; STATISTICAL SIGNIFICANCE; TISSUE MICROARRAY; UPREGULATION;

EID: 33749063055     PISSN: 15228002     EISSN: 14765586     Source Type: Journal    
DOI: 10.1593/neo.06277     Document Type: Article

References (23)

1. Spechler SJ (2002). Clinical practice. Barrett's esophagus. N Engl J Med 346, 836-842.
2. Devesa SS, Blot WJ, and Fraumeni JF (1998). Changing patterns in the incidence of esophageal and gastric carcinoma in the United States. Cancer 83, 2049-2053.
3. Siewert JR, Stein HJ, Feith M, Brücher BLDM, Bartels H, and Fink U (2001). Tumor cell type is an independent prognostic parameter in esophageal cancer: lessons learned from more than 1000 consecutive resections at a single institution in the Western world. Ann Surg 234, 360-369.
4. Stein HJ, von Rahden BHA, and Siewert JR (2004). Survival after surgery of cancer of the esophagus. Langenbecks Arch Surg 390, 280-285.
5. Morales CP, Souza RF, and Spechler SJ (2002). Hallmarks of cancer progression in Barrett's oesophagus. Lancet 360, 1587-1589.
6. Walch AK, Zitzelsberger HF, Bruch J, Keller G, Angermeier D, Aubele MM, Mueller J, Stein H, Braselmann H, Siewert JR, et al. (2000). Chromosomal imbalances in Barrett's adenocarcinoma and the metaplasia - dysplasia-carcinoma sequence. Am J Pathol 156, 555-566.
7. Sarbia M, Arjumand J, Wolter M, Reifenberger G, Heep H, and Gabbert HE (2001). Frequent c-myc amplification in high-grade dysplasia and adenocarcinoma in Barrett esophagus. Am J Clin Pathol 115, 835-840.
8. Miller CT, Moy JR, Lin L, Schipper M, Normolle D, Brenner DE, Iannettoni MD, Orringer MB, and Beer DG (2003). Gene amplification in esophageal adenocarcinomas and Barrett's with high-grade dysplasia. Clin Cancer Res 9, 4819-4825.
9. Tselepis C, Morris CD, Wakelin D, Hardy R, Perry I, Luong QT, Harper E, Harrison R, Attwood SE, and Jankowski JA (2003). Upregulation of the oncogene c-myc in Barrett's adenocarcinoma: induction of c-myc by acidified bile acid in vitro. Gut 52, 174-180.
10. Hamilton SR and Aaltonen LA (Eds). (2000). Pathology and Genetics of Tumors of the Digestive System. Tumors of Small Intestine, IARC Press: Lyon, pp 69-91.
11. Adhikary S and Eilers M (2005). Transcriptional regulation and transformation by Myc proteins. Nat Rev Mol Cell Biol 6, 635-645.
12. Pelengaris S, Khan M, and Evan GI (2002). Suppression of Myc-induced apoptosis in beta cells exposes multiple oncogenic properties of Myc and triggers carcinogenic progression. Cell 109, 321-334.
13. Baudino TA, McKay C, Pendeville-Samain H, Nilsson JA, Maclean KH, White EL, Davis AC, Ihle JN, and Cleveland JL (2002). c-Myc is essential for vasculogenesis and angiogenesis during development and tumor progression. Genes Dev 16, 2530-2543.
14. von Rahden BHA, Stein HJ, Pühringer F, Langer R, Koch I, Siewert JR, Höfler H, and Sarbia M (2005). Coexpression of cyclooxygenases (COX-1, COX-2) and vascular endothelial growth factors (VEGF-A, VEGF-C) in esophageal adenocarcinoma. Cancer Res 65, 5038-5044.
15. Smith DR and Goh HS (1996). Overexpression of the c-myc protooncogene in colorectal carcinoma is associated with a reduced mortality that is abrogated by point mutation of the p53 tumor suppressor gene. Clin Cancer Res 2, 1049-1053.
16. Pelengaris S and Khan M (2003). The c-MYC oncoprotein as a treatment target in cancer and other disorders of cell growth. Expert Opin Ther Targets 7, 623-642.
17. Sobin LH and Wittekind Ch (Eds). (2002). TNM Classification of Malignant Tumors, 6th ed, New York: Wiley-Liss.
18. Arnould L, Denoux Y, MacGrogan G, Penault-Llorca F, Fiche M, Treilleux I, Mathieu MC, Vincent-Salomon A, Vilain MO, and Couturier J (2003). Agreement between chromogenic in situ hybridisation (CISH) and FISH in the determination of HER2 status in breast cancer. Br J Cancer 88, 1587-1591.
19. Bhargava R, Oppenheimer O, Gerald W, Jhanwar SC, and Chen B (2005). Identification of MYCN gene amplification in neuroblastoma using chromogenic in situ hybridization (CISH): an alternative and practical method. Diagn Mol Pathol 14, 72-76.
20. Moskaluk CA, Hu J, and Perlman EJ (1998). Comparative genomic hybridization of esophageal and gastroesophageal adenocarcinomas shows consensus areas of DNA gain and loss. Genes Chromosomes Cancer 22, 305-311.
21. van Dekken H, Geelen E, Dinjens WN, Wijnhoven BP, Tilanus HW, Tanke HJ, and Rosenberg C (1999). Comparative genomic hybridization of cancer of the gastroesophageal junction: deletion of 14Q31-32.1 discriminates between esophageal (Barrett's) and gastric cardia adenocarcinomas. Cancer Res 59, 748-752.
22. Jenkins GJ, Harries K, Doak SH, Wilmes A, Griffiths AP, Baxter JN, and Parry JM (2004). The bile acid deoxycholic acid (DCA) at neutral pH activates NF-kappaB and induces IL-8 expression in oesophageal cells in vitro. Carcinogenesis 25, 317-323.
23. Stamp DH (2006). Bile acids aided by acid suppression therapy may be associated with the development of esophageal cancers in westernized societies. Med Hypotheses 66, 154-157.