Peter Jordan

Research Focus

My group is interested in signalling pathways that promote colorectal tumorigenesis and we study (i) the alternative splice variant Rac1b overexpressed in tumours, (ii) the effect of activated b-catenin/TCF signalling on splicing, (iii) the effect on splicing of exonic missense mutations diagnosed by our department in colorectal tumour suppressor genes, and (iv) the role of a novel cell-cycle regulating protein that co-immunoprecipitates with cdc5L and Prp19.


  1. Matos, P., Oliveira, C., Velho, S., Gonçalves, V., da Costa, L.T., Moyer, M.P., Seruca, R. and Jordan, P. (2008). B-RafV600E cooperates with alternative spliced Rac1b to sustain colorectal cancer cell survival. Gastroenterology 135, 899-906.
  2. Vieira, L., Sousa, A.C., Matos, P., Marques, B., Alaiz, H., Ribeiro, M.J., Braga, P., da Silva, M.G., Jordan, P. (2006). Three-way translocation involves MLL, MLLT3, and a novel cell cycle control gene, FLJ10374, in the pathogenesis of acute myeloid leukemia with t(9;11;19)(p22;q23;p13.3). Genes Chromosomes Cancer 45, 455-469.
  3. Matos, P., Collard, J. and Jordan, P. (2003). Tumor-related alternative- spliced Rac1b is not regulated by Rho-GDI and exhibits selective downstream signaling. Journal of Biological Chemistry 278, 50442-50448.
  4. Clarke, L.A., Veiga, I., Isidro, G., Jordan, P., Silva Ramos, J., Castedo, S. and Boavida, M.G. (2000). Pathological exon skipping in an HNPCC proband with hMLH1 splice acceptor site mutation. Genes Chromosomes Cancer 29, 367-370.

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