title: Low nuclear grade but not cell proliferation predictive of pathological complete response to docetaxel in human breast cancers.
abstract: OBJECTIVE
  Predictive factors for response to docetaxel in human breast cancers have yet to be identified. The aim of the present study was to investigate the relationship of various clinicopathological and biological parameters with pathological response to docetaxel in the neoadjuvant setting.
  
  
  METHODS
  The study population comprised 78 patients with primary breast cancers who were treated with docetaxel [60 mg/m(2); four (median) cycles, range 3-6; q3w] as neoadjuvant therapy and subsequently treated with mastectomy or breast conserving surgery. Tumor samples obtained before chemotherapy were subjected to histological examination and immunohistochemistry of HER-2 and Ki-67.
  
  
  RESULTS
  The pathological complete response (pCR) rate was significantly (P=0.04) higher for tumors with low nuclear grade (NG-I or -II) (21%) than for tumors with high NG (NG-III) (5%). The pCR rate (20%) of small (<or=5 cm) tumors was marginally significantly (P=0.05) higher than that of large (>5 cm) tumors (5%). Combined analysis of NG and tumor size showed that low-NG small tumors have a higher response rate (30%) than high-NG small tumors (11%; P=0.13), low-NG large tumors (11%; P=0.15), and high-NG large tumors (0%; P=0.009). No statistically significant association was observed between pCR rate and menopausal status, lymph node status, ER, PR, HER-2, or Ki-67.
  
  
  CONCLUSIONS
  Low nuclear grade, but not cell proliferation determined by Ki-67, is associated with a good pathological response to docetaxel. Combination of low nuclear grade and small tumor size may be useful for the selection of breast tumors with a high pCR rate (30%).
authors.affiliation: Department of Breast and Endocrine Surgery, Osaka University Graduate School of Medicine, 2-2 Yamadaoka, Suita, Osaka 565-0871, Japan.
authors.forename: Yasuo
authors.initials: Y
authors.lastname: Miyoshi
authors.forename: Masafumi
authors.initials: M
authors.lastname: Kurosumi
authors.forename: Junichi
authors.initials: J
authors.lastname: Kurebayashi
authors.forename: Nariaki
authors.initials: N
authors.lastname: Matsuura
authors.forename: Masato
authors.initials: M
authors.lastname: Takahashi
authors.forename: Eriko
authors.initials: E
authors.lastname: Tokunaga
authors.forename: Chiyomi
authors.initials: C
authors.lastname: Egawa
authors.forename: Norikazu
authors.initials: N
authors.lastname: Masuda
authors.forename: Seung Jin
authors.initials: SJ
authors.lastname: Kim
authors.forename: Masatsugu
authors.initials: M
authors.lastname: Okishiro
authors.forename: Tetsu
authors.initials: T
authors.lastname: Yanagisawa
authors.forename: Satsuki
authors.initials: S
authors.lastname: Ueda
authors.forename: Tetsuya
authors.initials: T
authors.lastname: Taguchi
authors.forename: Yasuhiro
authors.initials: Y
authors.lastname: Tamaki
authors.forename: Shinzaburo
authors.initials: S
authors.lastname: Noguchi
mesh_terms: D000970:Antineoplastic Agents / Q000494:pharmacology*; D001943:Breast Neoplasms / Q000188:drug therapy* / Q000473:pathology* / Q000601:surgery; D002467:Cell Nucleus / Q000473:pathology*; D049109:Cell Proliferation; D003131:Combined Modality Therapy; D000077143:Docetaxel; D005260:Female; D006801:Humans; D007150:Immunohistochemistry; D019394:Ki-67 Antigen / Q000378:metabolism; D008408:Mastectomy; D020360:Neoadjuvant Therapy; D018719:Erb-b2 Receptor Tyrosine Kinases / Q000096:biosynthesis; D043823:Taxoids / Q000494:pharmacology*
chemical_list: D000970:Antineoplastic Agents; D000077143:Docetaxel; D019394:Ki-67 Antigen; D018719:Erb-b2 Receptor Tyrosine Kinases; D043823:Taxoids