Molecular Profiling of Inflammatory Breast Cancer

  • Ivan Bièche
    1Laboratoire d’Oncogénétique - INSERM E0017, Centre René Huguenin, St-Cloud;
  • Sengül Tozlu
    1Laboratoire d’Oncogénétique - INSERM E0017, Centre René Huguenin, St-Cloud;
  • Marc Espie
    3Service d’Oncologie Médicale, Hôpital Saint-Louis, Paris;
  • Michel Marty
    4Direction de la Recherche Thérapeutique, Institut Gustave Roussy, Villejuif, France
  • Rosette Lidereau
    1Laboratoire d’Oncogénétique - INSERM E0017, Centre René Huguenin, St-Cloud;
  • Florence Lerebours
    1Laboratoire d’Oncogénétique - INSERM E0017, Centre René Huguenin, St-Cloud;

書誌事項

公開日
2004-10-15
DOI
  • 10.1158/1078-0432.ccr-04-0306
公開者
American Association for Cancer Research (AACR)

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説明

<jats:title>Abstract</jats:title> <jats:p>Purpose: Inflammatory breast cancer (IBC) is a rare but particularly aggressive form of primary breast cancer. The molecular mechanisms responsible for IBC are largely unknown.</jats:p> <jats:p>Experimental Design: To obtain further insight into the molecular pathogenesis of IBC, we used real-time quantitative reverse transcription (RT)-PCR to quantify the mRNA expression of 538 selected genes in IBC relative to non-IBC.</jats:p> <jats:p>Results: Twenty-seven (5.0%) of the 538 genes were significantly up-regulated in IBC compared with non-IBC. None were down-regulated. The 27 up-regulated genes mainly encoded transcription factors (JUN, EGR1, JUNB, FOS, FOSB, MYCN, and SNAIL1), growth factors (VEGF, DTR/HB-EGF, IGFBP7, IL6, ANGPT2, EREG, CCL3/MIP1A, and CCL5/RANTES) and growth factor receptors (TBXA2R, TNFRSF10A/TRAILR1, and ROBO2). We also identified a gene expression profile, based on MYCN, EREG, and SHH, which discriminated subgroups of IBC patients with good, intermediate, and poor outcome.</jats:p> <jats:p>Conclusion: Our study has identified a limited number of signaling pathways that require inappropriate activation for IBC development. Some of the up-regulated genes identified here could offer useful diagnostic or prognostic markers and could form the basis of novel therapeutic strategies.</jats:p>

収録刊行物

  • Clinical Cancer Research

    Clinical Cancer Research 10 (20), 6789-6795, 2004-10-15

    American Association for Cancer Research (AACR)

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