Primary chemotherapy in breast invasive carcinoma: predictive value of the immunohistochemical detection of hormonal receptors, p53, c-erbB-2, MiB1, pS2 and GST pi.
Primary chemotherapy in operable breast invasive carcinoma enables tumour reduction and conservative surgery. In order to search for one or more biological factors capable of predicting tumour behaviour under primary chemotherapy, and subsequent patient survival, an immunohistochemical study was performed with specific antibodies to p53, c-erbB-2 (Her-2/neu), Mib1 (antiKi-67), pS2, GST pi, oestrogen receptors (ERs) and progesterone receptors (PRs). Core biopsies, obtained before primary chemotherapy, were available from a series of 128 breast invasive carcinomas treated between January 1985 and April 1989, with a median follow-up of 93.3 months. Univariate statistical analysis showed that negative ER detection by immunohistochemistry (IHC) was highly correlated with chemosensitivity (P = 0.001). A high percentage of Mib1-positive tumour cells (> 40%), as well as initial tumour size less than 4 cm, were also correlated with tumour responsiveness to chemotherapy (P = 0.009 and P = 0.03). By multivariate analysis IHC-ER, Mib1 and initial tumour size were independent predictors, the last parameter being the most important. Concerning subsequent patient survival, c-erbB-2 overexpression, as detected by IHC, was significant with respect to overall survival (OS) (P = 0.0006), disease-free interval (DFI) (P = 0.03) and metastasis-free interval (MFI) (P = 0.008) by univariate analysis. Furthermore, c-erbB-2 was the major independent prognostic factor for OS and MFI by multivariate analysis.
MacGrogan
G
G
Institut Bergonié, Comprehensive Cancer Center, Bordeaux, France.
Mauriac
L
L
Durand
M
M
Bonichon
F
F
Trojani
M
M
de Mascarel
I
I
Coindre
J M
JM
D000328:Adult; D000368:Aged; D000912:Antibodies, Neoplasm / Q000032:analysis; D000971:Antineoplastic Combined Chemotherapy Protocols / Q000627:therapeutic use*; D014408:Biomarkers, Tumor / Q000032:analysis*; D001943:Breast Neoplasms / Q000737:chemistry* / Q000188:drug therapy*; D015251:Epirubicin / Q000008:administration & dosage; D005260:Female; D005982:Glutathione Transferase / Q000032:analysis; D006801:Humans; D007150:Immunohistochemistry; D008727:Methotrexate / Q000008:administration & dosage; D008875:Middle Aged; D016685:Mitomycin / Q000008:administration & dosage; D009363:Neoplasm Proteins / Q000032:analysis*; D011379:Prognosis; D011506:Proteins; D018719:Erb-b2 Receptor Tyrosine Kinases / Q000032:analysis; D011960:Receptors, Estrogen / Q000032:analysis; D011980:Receptors, Progesterone / Q000032:analysis; D013852:Thiotepa / Q000008:administration & dosage; D000071163:Trefoil Factor-1; D016159:Tumor Suppressor Protein p53 / Q000032:analysis; D025521:Tumor Suppressor Proteins; D014750:Vincristine / Q000008:administration & dosage; D014751:Vindesine / Q000008:administration & dosage
D000912:Antibodies, Neoplasm; D014408:Biomarkers, Tumor; D015251:Epirubicin; D005982:Glutathione Transferase; D008727:Methotrexate; D016685:Mitomycin; D009363:Neoplasm Proteins; D011506:Proteins; D018719:Erb-b2 Receptor Tyrosine Kinases; D011960:Receptors, Estrogen; D011980:Receptors, Progesterone; D013852:Thiotepa; D000071163:Trefoil Factor-1; D016159:Tumor Suppressor Protein p53; D025521:Tumor Suppressor Proteins; D014750:Vincristine; D014751:Vindesine; C051838:TFF1 protein, human