title: Is lymphovascular invasion degree one of the important factors to predict neoadjuvant chemotherapy efficacy in breast cancer?
abstract: BACKGROUND
  Patients who achieve pathologic complete response (pCR) after neoadjuvant chemotherapy (NAC) have favorable disease-free survival rates. A few studies have suggested that lymphovascular invasion degree may play an important role in predicting pCR. This study aims to confirm the role of lymphatic invasion degree in predicting pCR in breast cancer patients after NAC.
  
  
  METHODS
  We retrospectively analyzed 120 patients treated with NAC and surgery. The following pathological features were evaluated on surgical specimens after NAC: histological grade, estrogen receptor (ER), progesterone receptor (PR), human epidermal growth factor receptor 2 (HER-2), lymphovascular invasion degree, intratumoral necrosis positivity, and axillary lymph node positivity.
  
  
  RESULTS
  pCR and marked response were achieved in 12% (14/120) and 35% (42/120), respectively, of 120 breast cancers in 120 women. Breast cancers with pCR or marked response were classified as chemosensitive. The remaining 64 breast cancers (53%) were classified as chemoresistant. Severe lymphovascular invasion (P = .003), large tumor size (P = .029), ER positivity (P = .001), and PR positivity (P = .006) were significantly associated with chemoresistant breast cancer. Invasive ductal carcinoma (P = .028) and HER-2 positivity (P < .0001) were significantly associated with chemosensitive breast cancer. On multivariate analysis, HER-2 positivity (P < .0001), invasive ductal carcinoma (P = .047), and marked/moderate lymphovascular invasion (P = .023) were the three factors that remained statistically significant in the model to predict histological therapeutic effect.
  
  
  CONCLUSIONS
  Lymphovascular invasion degree is one of the important factors to predict NAC efficacy for breast cancer.
authors.affiliation: Breast Imaging and Breast Intervention Section, Shizuoka Cancer Center Hospital, Naga-izumi, Shizuoka, 411-8777, Japan. t.uematsu@scchr.jp
authors.forename: Takayoshi
authors.initials: T
authors.lastname: Uematsu
authors.forename: Masako
authors.initials: M
authors.lastname: Kasami
authors.forename: Junichiro
authors.initials: J
authors.lastname: Watanabe
authors.forename: Kaoru
authors.initials: K
authors.lastname: Takahashi
authors.forename: Seiji
authors.initials: S
authors.lastname: Yamasaki
authors.forename: Kumiko
authors.initials: K
authors.lastname: Tanaka
authors.forename: Yukiko
authors.initials: Y
authors.lastname: Tadokoro
authors.forename: Akiko
authors.initials: A
authors.lastname: Ogiya
mesh_terms: D000328:Adult; D000368:Aged; D000970:Antineoplastic Agents / Q000627:therapeutic use*; D001943:Breast Neoplasms / Q000188:drug therapy* / Q000378:metabolism / Q000473:pathology / Q000601:surgery; D002277:Carcinoma / Q000188:drug therapy* / Q000378:metabolism / Q000473:pathology / Q000601:surgery; D017024:Chemotherapy, Adjuvant; D005260:Female; D006801:Humans; D008207:Lymphatic Metastasis; D008875:Middle Aged; D020360:Neoadjuvant Therapy; D060787:Neoplasm Grading; D009361:Neoplasm Invasiveness; D018719:Erb-b2 Receptor Tyrosine Kinases / Q000378:metabolism; D011960:Receptors, Estrogen / Q000378:metabolism; D011980:Receptors, Progesterone / Q000378:metabolism; D012189:Retrospective Studies; D016896:Treatment Outcome
chemical_list: D000970:Antineoplastic Agents; D018719:Erb-b2 Receptor Tyrosine Kinases; D011960:Receptors, Estrogen; D011980:Receptors, Progesterone; C508053:ERBB2 protein, human