Her2 Status in Small Intestinal Adenocarcinoma
OTM Chan, Z Chen, DC Phan, E Himmelfarb, HL Wang. Cedars-Sinai Medical Center, Los Angeles, CA; Northwestern University Feinberg School of Medicine, Chicago, IL
Background: The amplification of Her2, a type I receptor tyrosine kinase, has been described in breast, gastric, colorectal, biliary tract, lung, and head and neck cancers. This finding has important clinical significance, as the overexpression of this protein may enable these tumors to be susceptible to targeted monoclonal antibody therapy. Our study investigates the incidence of Her2 overexpression in primary small intestinal adenocarcinoma to assess the potential role for antibody therapy.
Design: The study involved 50 primary small intestinal adenocarcinoma resection specimens. Immunohistochemistry was performed on formalin-fixed, paraffin-embedded sections using anti-human Her2 protein. All slides were interpreted based on the DAKO HercepTest scoring guidelines, as follows: 0, no staining is observed or membrane staining is observed in less than 10% of the tumor cells; 1+, a faint/barely perceptible membrane staining is detected in more than 10% of the tumor cells; 2+, a weak to moderate complete membrane staining is observed in more than 10% of the tumor cells; 3+, a strong complete membrane staining is observed in more than 10% of the tumor cells. Protein overexpression was considered to have 3+ staining. For FISH, probes to Her2 and the chromosome 17 centromere were utilized. At least 100 cells were counted from all tumor areas. More than a mean number of four fluorescence signals per two signals of the chromosome 17 centromere were considered amplified. Specimens were considered negative when less than 10% of tumor cells showed amplification of HER-2.
Results: 88% (44/50) of the specimens had no observable immunohistochemical staining (score of 0). The remaining 12% (6/50) demonstrated 1+ staining. No Her2 amplification was detected by FISH in any of the specimens.
Conclusions: Primary small intestinal adenocarcinoma did not exhibit Her2 amplification in our sample. Therefore, monoclonal antibody therapy may not have therapeutic effect on these tumors.
Tuesday, March 23, 2010 1:00 PM
Poster Session IV # 69, Tuesday Afternoon