Human Pathology
Volume 41, Issue 4 , Pages 477-484, April 2010

IMP3 expression is correlated with histologic grade of lung adenocarcinoma

  • Jennifer J. Findeis-Hosey, MD

      Affiliations

    • Department of Pathology and Laboratory Medicine, University of Rochester Medical Center, Rochester, NY 14642, USA
  • ,
  • Qi Yang, AAS

      Affiliations

    • Department of Pathology and Laboratory Medicine, University of Rochester Medical Center, Rochester, NY 14642, USA
  • ,
  • Betsy O. Spaulding, BS

      Affiliations

    • Dako North America, Carpinteria, CA 93013, USA
  • ,
  • Hanlin L. Wang, MD, PhD

      Affiliations

    • Department of Pathology and Laboratory Medicine, Cedars-Sinai Medical Center, Los Angeles, CA 90048, USA
  • ,
  • Haodong Xu, MD, PhD

      Affiliations

    • Department of Pathology and Laboratory Medicine, University of Rochester Medical Center, Rochester, NY 14642, USA
    • Corresponding Author InformationCorresponding author. Department of Pathology and Laboratory Medicine, Box 626, University of Rochester Medical Center, Elmwood 601, Rochester, NY 14642, USA.

Received 28 May 2009; received in revised form 30 September 2009; accepted 7 October 2009. published online 11 December 2009.

Summary 

Insulin-like growth factor II mRNA binding protein 3 is an oncofetal protein that is expressed in multiple malignancies. This study aimed to determine the correlation of insulin-like growth factor II mRNA binding protein 3 expression with histologic grade of lung adenocarcinoma. Eighty-nine cases, including 11 atypical adenomatous hyperplasias, 10 pure bronchioloalveolar carcinomas, 36 well-differentiated adenocarcinomas and 41 moderately or poorly differentiated adenocarcinomas, were immunohistochemically studied using a monoclonal antibody against insulin-like growth factor II mRNA binding protein 3. Twenty-nine (70.7%) of 41 moderately to poorly differentiated adenocarcinomas were positive for insulin-like growth factor II mRNA binding protein 3, with 26 (89.7%) tumors demonstrating either a strong staining or staining in greater than 30% of tumor cells. Four (40.0%) of 10 bronchioloalveolar carcinomas and 13 (36.1%) of 36 well-differentiated adenocarcinomas exhibited insulin-like growth factor II mRNA binding protein 3 positivity with a variable degree and percentage of tumor cells staining. When bronchioloalveolar carcinomas were present in a pure form or as a component of adenocarcinomas, positive insulin-like growth factor II mRNA binding protein 3 staining was always patchy, with less than 20% of tumor cells stained. Overall, the frequency of positive insulin-like growth factor II mRNA binding protein 3 staining was lower in bronchioloalveolar carcinomas and well-differentiated adenocarcinomas compared to moderately/poorly differentiated adenocarcinomas (P < .01). No insulin-like growth factor II mRNA binding protein 3 signal was detected in any case of atypical adenomatous hyperplasia. These findings show that insulin-like growth factor II mRNA binding protein 3 is strongly and diffusely expressed in a large proportion of moderately/poorly differentiated lung adenocarcinomas, in particular in the solid component of mixed subtype adenocarcinomas, less frequently expressed in well-differentiated adenocarcinomas and bronchioloalveolar carcinomas, and negative in atypical adenomatous hyperplasias. The higher frequency of expression in moderately/poorly differentiated adenocarcinomas suggests that insulin-like growth factor II mRNA binding protein 3 expression may be associated with an aggressive biological behavior.

Keywords: Lung, Atypical adenomatous hyperplasia, Bronchioloalveolar carcinoma, Adenocarcinoma, IMP3, KOC, RNA-binding protein, AAH, BAC

To access this article, please choose from the options below

Login to an existing account or Register a new account.

  • Purchase this article for 31.50 USD (You must login/register to purchase this article)

    Online access for 24 hours. The PDF version can be downloaded as your permanent record.

  • Subscribe to this title

    Get unlimited online access to this article and all other articles in this title 24/7 for one year.

  • Claim access now

    For current subscribers with Society Membership or Account Number.

  • Visit SciVerse ScienceDirect to see if you have access via your institution.
 

PII: S0046-8177(09)00369-4

doi:10.1016/j.humpath.2009.10.004

Human Pathology
Volume 41, Issue 4 , Pages 477-484, April 2010