Dear Editor,

Pheochromocytomas (PCCs) are rare catecholamine-secreting tumors arising from the chromaffin cells in the adrenal medulla. Closely related paragangliomas share developmental origin but arise extra-adrenally in the paraganglia that belongs to the sympathetic and parasympathetic ganglia. Most PCCs are sporadic; however, around 25–30% of them are associated with familial syndromes caused by germ line mutations of at least ten genes (Gimenez-Roqueplo et al. 2012). The low incidence of pheochromocytomas poses difficulties to the development of diagnostic or prognostic markers as well as effective therapies, and thus, the development of novel animal and cellular models for the study of the disease is needed. Sprouty (Spry) family of genes is composed of four members of feedback inhibitors of receptor tyrosine kinase signaling that specifically targets the MAPK pathway. As such, they have been proposed as tumor suppressors in several cancerous pathologies such as tumors of the prostate, thyroid, or liver (Masoumi-Moghaddam et al. 2014). Here, we present a novel mouse model of pheochromocytoma consisting of double-heterozygous mice for Pten and Sprouty1 (Spry1). These animals develop pheochromocytomas that appear at earlier onset and grow at a higher rate than those from Pten^+/− mice.

In a previous report, we have found that mice bearing a Spry1-null mutation in the context of Pten haploin­sufficiency developed thyroid hyperplasia at higher frequencies and earlier onset than Pten^+/− littermates (Macià et al. 2014). While examining thyroid glands from these animals, we noticed that Pten^+/−; Spry1^+/− mice also developed thyroid hyperplasia with a frequency comparable to that of Pten^+/−; Spry1−^/− mice at 3 months of age (M Vaquero, A Macià, C Anerillas, A Velasco, X Matias-Guiu, J Ribera and M Encinas, unpublished observations), indicating that deletion of a single Spry1 allele was enough to accelerate thyroid tumorigenesis in the context …