[502] Study of the Transferrin Receptor Expression in Melanocytic Lesions: Diagnosis and Prognosis Evaluation

Solene Houlle, Philippe Courville, Jean-Christophe Sabourin. Rouen University Hospital, Rouen, France

Background: Melanoma is a malignant tumor with poor prognosis and is associated with a very high mortality rate. Treatment is limited and not very efficient even though new targeted therapies (anti-BRAF) are promising. The identification of molecules acting on cell growth could be another way to counteract tumor aggressivity. Highly dividing cells overexpress the transferrin receptor (TfR or CD71) as they require large amount of iron for DNA replication. Recent studies have also shown that cancer cells overexpress this receptor (TfR). The aims of our study were to analyze CD71 expression on benign and malignant melanocytic lesions in order to determine its diagnosis and prognosis value.
Design: CD71 immunohistochemistry was performed on 68 melanocytic lesions diagnosed at Rouen University Hospital between 2008 and 2011. The lesions included 30 benign melanocytic lesions (compound nevus, congenital nevus, blue nevus, Reed nevus, Spitz nevus and dysplastic nevus), 28 malignant melanocytic lesions (in situ, SSM, nodular, acral lentiginous, desmoplastic and spitzoid melanoma) and 10 melanoma metastases.
Results: Benign lesions disclosed no CD71 immunostaining, whereas 46.4% of melanomas were CD71+ with 50% for SSM, 60% for acral lentiginous melanomas and 83% for nodular melanomas. There was a 100% specificity for malignant lesions. CD71 staining seemed to be correlated to Breslow>2mm (p=0.0271). 90% of metastases were CD71+.
Conclusions: Our results show that this marker could be useful in the diagnosis of melanoma with 100% specificity. Its expression also seems to be associated with bad prognosis tumors and therefore could be used as a target to develop new drugs to improve patient treatment, especially in metastatic cases.
Category: Dermatopathology

Wednesday, March 21, 2012 1:00 PM

Poster Session VI # 117, Wednesday Afternoon


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