Irregularity in the nuclear shape, with extensive folds and invaginations of the nuclear membrane (NM), remain the basic diagnostic feature of papillary thyroid carcinoma (PTC). The biological reasons for these irregularities are obscure, but evidence has been presented that they might be linked to RET÷PTC gene translocation. In the present study, we have investigated the hypothesis that the NM irregularities in PTC might be linked to alterations in the expression of lamin B receptor (LBR), a component of the inner NM responsible for the distribution of Lamin B and associated chromatin. Fisher AH et al. already reported on the lack of LBR in PTC, a finding in contrast with the observation that a reduced expression of LBR because of gene mutation is responsible for the lack of nuclear segmentation of granulocytes in Pelger-Huët anomaly. In the present study, we confirmed the lack of immunohistochemical staining for LBR in PTC nuclei, in contrast to a positive staining in intestinal epithelium and stromal cells. However, Western blot and RT-PCR analysis demonstrated a strongly positive reaction in PTC extracts, thus proving an expression of LBR higher in PTC cases and cells than in follicular carcinoma cells. In conclusion, our data suggest that LBR is heavily expressed in PTC cells, but an abnormal folding of the protein might explain its lack of immunohistochemical reactivity and be associated with the anomalous folding of the NM.