We thank Ben-Shlomo and Melmed for their comments concerning the role of adrenocorticotropin hormone (ACTH) and thyrotropin secreting hormone (TSH) receptors in pituitary cancer. We may owe some clarification, as we did not intend to implicate the ACTH and TSH receptors as causing pituitary cancer through a mechanism that acts on endogenous pituitary gland receptors. Indeed, we have not stated this in the text of the review, nor does table 1 specify this. Pituitary tumours are characterized by the hyper-secretion of TSH and ACTH, resulting in systemic complications in the target organs of these hormones, the thyroid and adrenal glands. Given this information, we included these receptors in the pituitary section of table 1 on the basis that a characteristic of this cancer is the over-production of ACTH and TSH, which bind to their cognate G-protein-coupled receptors (GPCRs) in their target organs. This is well reviewed in the provided reference1 (reference 147 in the article). Our earlier version(s) of the text were more descriptive of this topic, but space limitations did not permit an in-depth treatment of this particular subject in the final version. Thus, table 1 was left with the receptors listed, and a reference to a review on the topic.

Table 1 GPCRs in cancer
Full size table

On the other hand, we agree on the role of TSH receptors and their mutations in thyroid tumours, which we believe was well described in the text (Page 87, first column, second paragraph) and in table 1, in agreement with Ben-Shlomo's and Melmed's comments. We did not describe these mutations in the context of pituitary tumours. Neither we nor the text of the review is at odds with the statements of Ben-Shlomo and Melmed, and we feel that a clarification is most practical.

Table 1 has been modified to reflect this point and is shown below.

We would like to thank Ben-Shlomo and Melmed for bringing this to our attention.