Laminin receptor in lymph node negative breast carcinoma

Mehrdad Nadji, Mehdi Nassiri, Manuel Fresno, Edward Terzian, Azorides R. Morales

Research output: Contribution to journalArticlepeer-review

25 Scopus citations


BACKGROUND. Expression of 67 kD laminin binding protein, 67LR, is reported to be associated with invasive and metastatic phenotypes in several types of human malignancies. In mammary carcinomas, however, the biologic role of 67LR has been less clear. The authors explored the potential biologic significance of expression of 67LR in 148 patients with axillary lymph node negative breast carcinoma. METHODS. Formalin fixed, paraffin embedded histologic sections were immunohistochemically evaluated for 67LR using monoclonal antibody MLuC5. The staining results were correlated with morphologic data as well as with estrogen receptor content and p53 product accumulation. RESULTS. There were statistically significant correlations between positivity for 67LR and lower histologic grade (P = 0.003), lower nuclear grade (P = 0.002), positivity for estrogen receptor (P = 0.003), and lack of p53 abnormality (P < 0.001). Expression of 67LR had no independent effect on the disease free or overall survival of lymph node negative patients with breast carcinoma. Nevertheless, in the subgroup of 67LR positive patients, positivity for estrogen receptor was associated with significantly longer overall survival (P = 0.008). CONCLUSIONS. The data from this study suggest that tissue expression of 67LR, as detected by antibody MLuC5, is associated with better differentiated, less aggressive forms of axillary lymph node negative breast carcinoma.

Original languageEnglish (US)
Pages (from-to)432-436
Number of pages5
Issue number2
StatePublished - 1999


  • 67LR
  • Breast carcinoma
  • Immunohistochemistry
  • Laminin receptor

ASJC Scopus subject areas

  • Cancer Research
  • Oncology


Dive into the research topics of 'Laminin receptor in lymph node negative breast carcinoma'. Together they form a unique fingerprint.

Cite this