gms | German Medical Science

60. Jahrestagung der Deutschen Gesellschaft für Neurochirurgie (DGNC)
Joint Meeting mit den Benelux-Ländern und Bulgarien

Deutsche Gesellschaft für Neurochirurgie (DGNC) e. V.

24. - 27.05.2009, Münster

Does molecularcytogenetic testing allow to predict which colorectal carcinomas metastasize to the brain?

Meeting Abstract

  • A. Gutenberg - Neurochirurgische Klinik, Universitätsklinikum Göttingen
  • J. Gerdes - Pathologie, Universitätsklinikum Göttingen
  • C. Enders - Pathologie, Universitätsklinikum Göttingen
  • W. Brück - Neuropathologie, Universitätsklinikum Göttingen
  • L. Füzesi - Pathologie, Universitätsklinikum Göttingen
  • V. Rohde - Neurochirurgische Klinik, Universitätsklinikum Göttingen

Deutsche Gesellschaft für Neurochirurgie. 60. Jahrestagung der Deutschen Gesellschaft für Neurochirurgie (DGNC), Joint Meeting mit den Benelux-Ländern und Bulgarien. Münster, 24.-27.05.2009. Düsseldorf: German Medical Science GMS Publishing House; 2009. DocP08-11

DOI: 10.3205/09dgnc339, URN: urn:nbn:de:0183-09dgnc3390

Veröffentlicht: 20. Mai 2009

© 2009 Gutenberg et al.
Dieser Artikel ist ein Open Access-Artikel und steht unter den Creative Commons Lizenzbedingungen (http://creativecommons.org/licenses/by-nc-nd/3.0/deed.de). Er darf vervielfältigt, verbreitet und öffentlich zugänglich gemacht werden, vorausgesetzt dass Autor und Quelle genannt werden.


Gliederung

Text

Objective: Information about structural chromosomal changes in brain metastases of colorectal carcinoma (CRC) is very limited. There are two main questions for the clinician: 1-Do chromosomal changes in the primary tumor allow to predict whether the tumor will metastasize; 2-Do genomic imbalances exist which are characteristic for the site where metastases will develop. The aim of this study was to investigate genomic imbalance differences between primary CRC and their cerebral as well as pulmonary metastases to identify chromosomal regions that may contain candidate genes important for the development of brain metastases in the course of CRC.

Methods: We studied two groups of patients: 32 patients with CRC who developed brain metastases (n=38), and 54 patients with CRC who did not develop brain metastases, but showed lung metastases (n=62) during the course of their disease. Primary CRC as well as their related metastases were analyzed by comparative genomic hybridization (CGH).

Results: Both groups of primary CRC were compatible showing no significant chromosomal differences. Brain metastases revealed significantly higher numbers of copy number changes (14.0 on average) than lung metastases (6.6 on average). Brain metastases showed more chromosomal losses at 3q and 18p as well as gains at 7p, 7q, 8q, 12p, 13q, 20p, and 20q in comparison to their primary CRC and to lung metastases. Additionally, loss of 3p and 9p as well as gain on chromosome 12 was more selectively found in brain metastases.

Conclusions: The present study provides the largest collection of cytogenetically analyzed primary CRC and their brain and lung metastases. Selective losses at 3 and 9q as well as gain at 12 seem to be characteristic of brain metastases in CRC, whereas all other genomic differences between primary and metastatic CRC were rather quantitative than qualitative. Our results support the idea that CRC with selected chromosomal aberrations metastasize to the brain. Unfortunately, this propensity is only partially detectable at the time of initial diagnosis of the CRC.