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Mairinger FD, Walter RF, Werner R, et al. Activation of angiogenesis differs strongly between pulmonary carcinoids and neuroendocrine carinomas and is crucial for carcinoid tumourgenesis. J Cancer. 2014;5(6):465-71doi: 10.7150/jca.9235.
Mairinger, F. D., Walter, R. F., Werner, R., Christoph, D. C., Ting, S., Vollbrecht, C., Zarogoulidis, K., Huang, H., Li, Q., Schmid, K. W., Wohlschlaeger, J., & Zarogoulidis, P. (2014). Activation of angiogenesis differs strongly between pulmonary carcinoids and neuroendocrine carinomas and is crucial for carcinoid tumourgenesis. Journal of Cancer, 5(6), 465-71. https://doi.org/10.7150/jca.9235
Mairinger, Fabian D, et al. "Activation of angiogenesis differs strongly between pulmonary carcinoids and neuroendocrine carinomas and is crucial for carcinoid tumourgenesis." Journal of Cancer vol. 5,6 (2014): 465-71. doi: https://doi.org/10.7150/jca.9235
Mairinger FD, Walter RF, Werner R, Christoph DC, Ting S, Vollbrecht C, Zarogoulidis K, Huang H, Li Q, Schmid KW, Wohlschlaeger J, Zarogoulidis P. Activation of angiogenesis differs strongly between pulmonary carcinoids and neuroendocrine carinomas and is crucial for carcinoid tumourgenesis. J Cancer. 2014 May 15;5(6):465-71. doi: 10.7150/jca.9235. eCollection 2014. PMID: 24959299; PMCID: PMC4066358.
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J Cancer. 2014 May 15;5(6):465-71. doi: 10.7150/jca.9235. eCollection 2014.

Activation of angiogenesis differs strongly between pulmonary carcinoids and neuroendocrine carinomas and is crucial for carcinoid tumourgenesis.

Journal of Cancer

Fabian D Mairinger, Robert F H Walter, Robert Werner, Daniel C Christoph, Saskia Ting, Claudia Vollbrecht, Konstantinos Zarogoulidis, Haidong Huang, Qiang Li, Kurt W Schmid, Jeremias Wohlschlaeger, Paul Zarogoulidis

Affiliations

  1. 1. Institute of Pathology, University Hospital Essen, University of Duisburg-Essen, Essen, Germany;
  2. 1. Institute of Pathology, University Hospital Essen, University of Duisburg-Essen, Essen, Germany; ; 2. Ruhrlandklinik, West German Lung Center, University Hospital Essen, University of Duisburg-Essen, Essen, Germany;
  3. 3. Department of medical Oncology, University Hospital Essen, University of Duisburg-Essen, Essen, Germany;
  4. 4. Institute of Pathology, University Hospital Cologne, Cologne, Germany.
  5. 5. Pulmonary Department-Oncology Unit, ``G. Papanikolaou`` General Hospital, Aristotle University of Thessaloniki, Thessaloniki, Greece.
  6. 6. Department of Respiratory Diseases, Changhai Hospital/First Affiliated Hospital of the Second Military Medical University, Shanghai, People's Republic of China, China.

PMID: 24959299 PMCID: PMC4066358 DOI: 10.7150/jca.9235

Abstract

BACKGROUND: Lung cancer still remains the leading cause of cancer for men after prostate cancer and breast cancer for women. Angiogenesis is considered a major microenvironment modifier.

MATERIAL AND METHODS: Demographic data and study design; The study is based on a collective of twenty representative specimens of each tumour entity (Typical Carcinoid, Atypical Carcinoid, Large-Cell Neuroendocrine Carcinoma , Small Cell Lung Cancer) for mRNA expression analysis. The following methods were performed: RNA Extraction and RNA Integrity Assessment, NanoString CodeSet Design and Expression Quantification, NanoString Data Processing and Statistical Analysis.

RESULTS: KDR rendered significant association to aggressiveness of the tumour and decreases with increasing malignancy (p=0.049). A decreased expression of HIF1A and KDR mRNA as associated with a higher risk of tumour invasion in vessels (HIF1A: p=0.034; KDR: p=0.029). FIGF and HIF1A expression levels are significantly associated with progression-free survival (FIGF: p= 0.021; HIF1A: p= 0.049). CRHR2 and FLT4 are stronger expressed in female than in male patients (CRHR2: p=0.024, FLT4: p=0.004). FIGF expression is still significant between LCNEC and SCLC (p=0.023). FLT4 and KDR show highly significant association to one of the analysed groups (FLT4: p=0.001; KDR: p=0.006). Additionally, HIF1A expression differs significantly between these focus cohorts (p=0.018).

CONCLUSION: We should consider for clinical practice application which factors affect most the tumour growth and distal metastasis, thereafter investigate easy to administer drugs with low side effects. Probably a cluster system of therapy should be established where a drug targets simultaneously different pathways of the same origin.

Keywords: CRHR2.; FIGF; FLT4; HIF1A; KDR; carcinoid; lung cancer

References

  1. Hum Pathol. 2000 Oct;31(10):1255-65 - PubMed
  2. Cancer Res Treat. 2013 Dec;45(4):325-33 - PubMed
  3. Med Oncol. 2014 Apr;31(4):877 - PubMed
  4. Mol Clin Oncol. 2013 Mar;1(2):331-336 - PubMed
  5. J Carcinog. 2010 Aug 03;9: - PubMed
  6. Eur J Cardiothorac Surg. 2007 Feb;31(2):192-7 - PubMed
  7. Lancet Oncol. 2014 Feb;15(2):143-55 - PubMed
  8. Bioorg Med Chem Lett. 2013 Dec 15;23(24):6650-5 - PubMed
  9. Chest Surg Clin N Am. 2003 Feb;13(1):111-28 - PubMed
  10. Curr Gene Ther. 2014;14(2):75-85 - PubMed
  11. Arch Pathol Lab Med. 2010 Nov;134(11):1628-38 - PubMed
  12. Hum Pathol. 1998 Mar;29(3):272-9 - PubMed
  13. Dan Med Bull. 2000 Nov;47(5):328-39 - PubMed
  14. Biochim Biophys Acta. 2012 Dec;1826(2):255-71 - PubMed
  15. Mol Cancer Ther. 2013 Jun;12(6):992-1001 - PubMed
  16. J Clin Oncol. 2006 Jan 1;24(1):70-6 - PubMed
  17. Ann Thorac Surg. 2004 May;77(5):1781-5 - PubMed
  18. Eur J Cancer. 2009 Sep;45 Suppl 1:251-66 - PubMed
  19. J Cancer Res Ther. 2013 Oct-Dec;9(4):701-5 - PubMed
  20. Semin Respir Crit Care Med. 2014 Feb;35(1):112-28 - PubMed
  21. Chest. 2001 Jun;119(6):1647-51 - PubMed
  22. Eur Respir Rev. 2014 Mar 1;23(131):79-91 - PubMed
  23. Curr Cancer Drug Targets. 2014;14(2):167-80 - PubMed
  24. Eur J Cardiothorac Surg. 2007 Feb;31(2):186-91 - PubMed
  25. J Clin Oncol. 2012 Jun 10;30(17):2070-8 - PubMed
  26. Oncologist. 2010;15(5):436-46 - PubMed
  27. Curr Cancer Drug Targets. 2014;14(1):59-69 - PubMed
  28. Histopathology. 2010 Feb;56(3):356-63 - PubMed
  29. Cell Death Differ. 2008 Mar;15(3):504-14 - PubMed
  30. Lancet. 2011 May 28;377(9780):1846-54 - PubMed
  31. J Thorac Cardiovasc Surg. 2002 Aug;124(2):285-92 - PubMed
  32. J Exp Clin Cancer Res. 2013 Nov 25;32:97 - PubMed
  33. Ther Deliv. 2013 Oct;4(10):1221-3 - PubMed
  34. Chest. 2004 May;125(5 Suppl):158S-62S - PubMed
  35. Clin Cancer Res. 2010 Jun 1;16(11):3028-34 - PubMed
  36. Drug Des Devel Ther. 2013 Jul 18;7:571-83 - PubMed
  37. Gene Ther. 2014 Feb;21(2):158-67 - PubMed
  38. Chest. 2001 Apr;119(4):1143-50 - PubMed
  39. Histochem J. 1991 Nov-Dec;23(11-12):541-7 - PubMed
  40. Am J Surg Pathol. 1998 Aug;22(8):934-44 - PubMed
  41. N Engl J Med. 1971 Nov 18;285(21):1182-6 - PubMed
  42. Cancer. 2005 Mar 15;103(6):1154-64 - PubMed
  43. Biomaterials. 2014 Mar;35(9):2905-14 - PubMed
  44. J Clin Oncol. 2011 Mar 10;29(8):1059-66 - PubMed
  45. Carcinogenesis. 2014 Jul;35(7):1556-63 - PubMed
  46. FASEB J. 2014 Mar;28(3):1412-21 - PubMed
  47. Immunome Res. 2013 Aug 12;9(62):16535 - PubMed

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