Association between c-myc amplification and pathological complete response to neoadjuvant chemotherapy in breast cancer

Autor: Kazuki Kishi, Yasuto Naoi, Seung Jin Kim, Atsushi Shimomura, Yasuhiro Tamaki, Shinzaburo Noguchi, Yousuke Baba, Takahiro Nakayama, Kenzo Shimazu, Hiroyuki Yasojima
Rok vydání: 2011
Předmět:
Oncology
Cancer Research
Receptor
ErbB-2
medicine.medical_treatment
Biopsy
chemistry.chemical_compound
Antineoplastic Combined Chemotherapy Protocols
Odds Ratio
Poly-ADP-Ribose Binding Proteins
In Situ Hybridization
Fluorescence
Oligonucleotide Array Sequence Analysis
Middle Aged
Immunohistochemistry
Neoadjuvant Therapy
DNA-Binding Proteins
Gene Expression Regulation
Neoplastic
Treatment Outcome
Paclitaxel
Receptors
Estrogen
Chemotherapy
Adjuvant
Lymphatic Metastasis
Female
Fluorouracil
Ultrasonography
Mammary
Receptors
Progesterone
Epirubicin
medicine.drug
Adult
medicine.medical_specialty
Cyclophosphamide
Breast Neoplasms
Proto-Oncogene Proteins c-myc
Breast cancer
Antigens
Neoplasm
Predictive Value of Tests
Internal medicine
Progesterone receptor
medicine
Biomarkers
Tumor
Humans
Aged
Neoplasm Staging
Retrospective Studies
Chemotherapy
Analysis of Variance
business.industry
Gene Expression Profiling
Gene Amplification
Cancer
medicine.disease
DNA Topoisomerases
Type II
Ki-67 Antigen
chemistry
business
Zdroj: European journal of cancer (Oxford, England : 1990). 47(12)
ISSN: 1879-0852
Popis: Background The aim of this study was to investigate whether c-myc amplification in human breast cancer is associated with response to neoadjuvant chemotherapy comprising paclitaxel followed by 5-FU/epirubicin/cyclophosphamide (P-FEC). Methods Tumour tissue samples were obtained before neoadjuvant chemotherapy (P-FEC) from 100 primary breast cancer patients (stage II/III). C-myc and HER2 amplification were examined by FISH, and oestrogen receptor (ER), progesterone receptor (PR), Ki67, and topoisomerase 2α (TOP2A) expression were examined immunohistochemically. Pathological complete response (pCR) was defined by a complete loss of tumour cells in the breast without any lymph node metastasis. Results C-myc amplification was observed in 40% (40/100) of breast tumours, and was significantly associated with ER-negative tumours (23/40 for ER(–) versus 17/60 for ER(+), P = 0.004), high histological grade tumours (11/18 for grade 3 versus 29/82 for grades 1 + 2, P = 0.043) and TOP2A-positive tumours (28/51 for TOP2A(+) versus 12/49 for TOP2A(–), P = 0.002). pCR rate was 20% for total patients (10.0% for ER(+) and 35.0% for ER(–)). Further, breast tumours with c-myc amplification (c-myc(+)) showed a significantly (P = 0.041) higher pCR rate (12/40) than those without such amplification (c-myc(–)) (8/60). This association between pCR and c-myc amplification was observed in ER-positive tumours (4/17 for c-myc(+) versus 2/43 for c-myc(–), P = 0.048) but not in ER-negative tumours (8/23 for c-myc(+) versus 6/17 for c-myc(–), P = 0.973). Conclusion Our results suggest that c-myc amplification is significantly associated with a high pCR rate to P-FEC in breast tumours, especially in ER-positive tumours.
Databáze: OpenAIRE
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