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Two single nucleotide substitutions detected in the SSTR2 promoter sequence at positions −83 and −57 from the major transcription initiation site were not associated with differences in clinical characteristics, hormonal profile, or responsiveness to SS ( Finally, the expression of a truncated variant of SSTR5 (SST5TMD4) that shows a preferential intracellular localization but is able to mediate signal transduction (46) has been found to correlate with a reduced ability of octreotide at normalizing hormone secretion in poorly responsive tumors in vivo (47) and with aggressive features, including SS-resistance and tumor invasiveness (48, 49)