title: Pretreatment haemoglobin levels significantly predict the tumour response to primary chemotherapy in human breast cancer.
abstract: The purpose of this study was to evaluate whether tumour response to primary chemotherapy in human breast cancer is influenced by baseline haemoglobin (Hb) status. A total of 157 patients with T2-4, N0-1 M0 breast cancer were treated with chemotherapy consisting of either the CMF regimen + tamoxifen (the first 76 cases) or the single-agent epirubicin (the subsequent 81) before definitive surgery. In total, 144 patients were fully assessable. Ki67, p53, bcl-2, c-erbB2, steroid hormone receptor, and microvessel density were evaluated immunohistochemically in tumour specimens obtained before chemotherapy and at surgery. Tumour shrinkage >50% occurred in 72.1% of patients. Responding patients had higher baseline Hb levels and red blood cell counts than nonresponders (P<0.01 and <0.003, respectively). The distribution of disease response according to increasing cutoffs of baseline Hb status showed that from 12.5 mg l(-1) onwards, patients with Hb levels above the cutoff obtained a greater response rate than those with lower Hb values. The difference attained the statistical significance at 12.5 (76.1 vs 59.5%, P<0.05) and 13.0 g/dl(-1) (81.0 vs 57.6%, P<0.002) cutoffs, respectively. The predictive role of Hb levels was maintained in multivariate analysis after adjustment for clinical and biological characteristics and treatment regimen. Patients with baseline Hb levels </=13 g dl(-1) showed a lower treatment-induced reduction in Ki67 expression (P<0.04) and a higher Ki67 expression at postoperative evaluation (P<0.02) than their counterparts. In conclusion, low Hb levels may negatively influence the response rate of chemotherapy in breast cancer patients. Inhibition of antiproliferative activity could be a possible mechanism.
authors.affiliation: Breast Unit, Azienda Ospedaliera Istituti Ospitalieri, Cremona, Italy.
authors.forename: A
authors.initials: A
authors.lastname: Bottini
authors.forename: A
authors.initials: A
authors.lastname: Berruti
authors.forename: M P
authors.initials: MP
authors.lastname: Brizzi
authors.forename: A
authors.initials: A
authors.lastname: Bersiga
authors.forename: D
authors.initials: D
authors.lastname: Generali
authors.forename: G
authors.initials: G
authors.lastname: Allevi
authors.forename: S
authors.initials: S
authors.lastname: Aguggini
authors.forename: G
authors.initials: G
authors.lastname: Bolsi
authors.forename: S
authors.initials: S
authors.lastname: Bonardi
authors.forename: G
authors.initials: G
authors.lastname: Bertoli
authors.forename: P
authors.initials: P
authors.lastname: Alquati
authors.forename: L
authors.initials: L
authors.lastname: Dogliotti
mesh_terms: D015703:Antigens, CD / Q000378:metabolism; D000971:Antineoplastic Combined Chemotherapy Protocols / Q000627:therapeutic use; D014408:Biomarkers, Tumor / Q000032:analysis*; D001943:Breast Neoplasms / Q000097:blood / Q000188:drug therapy* / Q000601:surgery; D003520:Cyclophosphamide / Q000627:therapeutic use; D015251:Epirubicin / Q000627:therapeutic use; D004906:Erythrocyte Count; D005260:Female; D005472:Fluorouracil / Q000627:therapeutic use; D006454:Hemoglobins / Q000032:analysis*; D006801:Humans; D007124:Immunoenzyme Techniques; D019394:Ki-67 Antigen / Q000032:analysis; D008727:Methotrexate / Q000627:therapeutic use; D011960:Receptors, Estrogen / Q000032:analysis; D011980:Receptors, Progesterone / Q000032:analysis; D013629:Tamoxifen / Q000627:therapeutic use; D016896:Treatment Outcome; D016159:Tumor Suppressor Protein p53 / Q000032:analysis
chemical_list: D015703:Antigens, CD; D014408:Biomarkers, Tumor; D006454:Hemoglobins; D019394:Ki-67 Antigen; D011960:Receptors, Estrogen; D011980:Receptors, Progesterone; D016159:Tumor Suppressor Protein p53; D013629:Tamoxifen; D015251:Epirubicin; D003520:Cyclophosphamide; D005472:Fluorouracil; D008727:Methotrexate