Publications by authors named "Jean-Pierre Kains"

Purpose: Genomic Grade Index (GGI) is a 97-gene signature that improves histologic grade (HG) classification in invasive breast carcinoma. In this prospective study we sought to evaluate the feasibility of performing GGI in routine clinical practice and its impact on treatment recommendations.

Methods: Patients with pT1pT2 or operable pT3, N0-3 invasive breast carcinoma were recruited from 8 centers in Belgium.

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Article Synopsis
  • Validated biomarkers predicting response or resistance to anthracyclines in breast cancer are currently missing, leading to the development of the A-Score in the TOP trial to identify patients who may not benefit from this treatment.
  • The TOP trial involved 149 patients with ER-negative tumors treated with epirubicin, and found that TOP2A amplification was significantly associated with better treatment response, resulting in a pathologic complete response (pCR) in 14% of evaluable patients.
  • The A-Score, which combines TOP2A and other gene signatures, showed a high negative predictive value, suggesting it could be a valuable tool for determining patient response to anthracycline therapy, pending further validation.
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This randomized phase-II trial investigated the efficacy and tolerability of weekly docetaxel or paclitaxel in metastatic breast cancer (MBC) patients considered unfit for a 3-weekly therapy. The primary study endpoint was antitumor activity, the second endpoint was tolerability, time to progression (TTP) and overall survival (OS). In intent-to-treat analysis, we observed for paclitaxel and docetaxel respectively partial response (PR) in 48% versus 38%, stable disease (SD) in 24% versus 16%, PD in 15% versus 30%.

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Aim: Trastuzumab (T), a humanised monoclonal antibody against HER-2, is active in HER-2-positive MBC patients. However, nearly 60% of the patients do not benefit from T, stressing the need for additional predictive markers. The following markers could be implicated in response to T: (1) the magnitude of Her-2 gene amplification; (2) the co-expression of the other HER family receptors, possibly responsible for HER-2 trans-activation; (3) the activated status of HER-2; (4) the activated status of downstream effectors as mitogen-activated protein kinases (MAPKs), p38 and p27.

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