Display Settings:

Format

Send to:

Choose Destination
See comment in PubMed Commons below
Eur J Cancer. 2006 Nov;42(17):2954-60. Epub 2006 Aug 28.

Predictive value of HER-2 and Topoisomerase IIalpha in response to primary doxorubicin in breast cancer.

Author information

  • 1Servicio de Oncologia Medica, Institut Catala d'Oncologia, Duran I Reynals, Hospitalet de Llobregat, Barcelona, Spain. edurne.arriola@icr.ac.uk

Abstract

AIM:

To study the predictive role of HER-2 and Topoisomerase IIalpha (TOP2A) in response to primary doxorubicin.

METHODS:

Two hundred and thirty-two patients with operable breast cancer were treated with doxorubicin prior to surgery. ER, PgR, grade, Ki-67 and HER-2 status were prospectively assessed. HER-2 overexpression was evaluated with immunohistochemistry; positive cases were then studied for gene copy number of HER-2, TOP2A and chromosome 17 centromere by chromogenic in situ hybridisation. Clinical response was assessed by mammography. Pathological response was evaluated as the percentage of tumour replaced by changes due to chemotherapy.

RESULTS:

HER-2 amplification was associated with clinical response (p=0.04). ER and PgR negativity, high Ki-67 and HER-2 amplification significantly correlated to pathological response (p<0.05). Tumours with coamplification of HER-2 and TOP2A showed a higher percentage of pathological changes (p=0.6). However, in the multivariate analysis for complete pathological response, ER negativity and high Ki-67 index were the only parameters that maintained statistical significance.

CONCLUSION:

HER2 and Topoisomerase IIalpha amplification failed to show an association with pathological response to doxorubicin, whereas ER negativity and a high proliferation rate were predictive of complete pathological response to this regime.

PMID:
16935488
[PubMed - indexed for MEDLINE]
PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for Elsevier Science
    Loading ...
    Write to the Help Desk