We recently reported the presence of a truncated form (h-CTR2) of the
human calcitonin receptor (CTR) in TT cells, a cell line derived from
medullary thyroid carcinoma (MTC). This form (h-CTR2), characterized b
y the absence of 16 amino acids in the first intracellular domain, was
also detected in two cases of MTC. In the present study we determined
the expression of CTR mRNA in a larger sample, representative of the
different clinical forms of MTC, and in normal thyroid. h-CTR2 was exp
ressed in all MTC specimens (both sporadic and familial) and in the no
rmal thyroid samples. The expression of the receptor mRNA was higher i
n MTC compared with normal thyroid. Moreover, CT and CTR mRNA levels w
ere modified significantly during proliferation. This result suggests
that CT may be involved in proliferation of MTC via autocrine/paracrin
e regulation. Calcitonin secretion by MTC may play a role in the devel
opment and spread of these tumors.