Molecular Biology Reports

, Volume 39, Issue 5, pp 5387–5391 | Cite as

No evidence for PML-RARa bcr1 fusion gene in colorectal cancer

  • Marta Herreros-Villanueva


Colorectal cancer is the third most prevalent cancer and a leading cause of cancer death. Metastatic colorectal cancer patients are treated with anti-EGFR monoclonal antibodies in combination with chemotherapy; however, the efficiency is only 10-20% of such patients. An increasing amount of data has demonstrated that response to anti-EGFR therapies is confined to patients with KRAS and BRAF wild type tumors but still some of these patients are non responders to this treatment. The presence of oncogenic deregulation of different members of EGFR downstream signaling or crosstalk molecules could predict the lack of response in these patients. In this study, 40 wild type KRAS and BRAF colorectal tumors were analyzed to elucidate whether PML-RARa bcr1 fusion gene may play a role in colorectal carcinogenesis. Specifically we want to determine if this fusion could be responsible for the inability to respond to anti-EGFR monoclonal antibodies. Here, for the first time it is reported, that PML-RARa bcr1 fusion is not responsible for colorectal tumor development and also, this translocation is not predicting the lack of efficacy of anti-EGFR therapies in wild type KRAS and BRAF colorectal cancer patients. These results also suggest that PML-RARa is unlikely to be a promising target for adjuvant therapy in colorectal cancer patients.


PML-RARa bcr1 EGFR KRAS BRAF Colorectal cancer 



V-raf murine sarcoma viral oncogene homolog B1


Human homolog of the Kirsten rat sarcoma-2 virus oncogene


Epidermal grown factor


Metastatic colorectal cancer


Promyelocytic leukemia (PML) gene and retinoic acid receptor-alpha (RARa) fusion gene



Thanks to Sabrice Guerrier for his technical help. This work was supported by Junta de Castilla y León.

Conflict of interest

The author declares that she has no competing interests.

Supplementary material

11033_2011_1337_MOESM1_ESM.doc (500 kb)
Supplementary material 1 (DOC 500 kb)


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Copyright information

© Springer Science+Business Media B.V. 2011

Authors and Affiliations

  1. 1.Unidad de InvestigaciónHospital General YagüeBurgosSpain

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