title: [Somatostatin receptors in non-endocrine tumours].
abstract: The study of the antiproliferative action of somatostatin (ss) is important not only to understand the regulation of neuroendocrine tumours that express receptors (sst), but also non-endocrine tumours which express these receptors. We previously demonstrated the presence of sst2 in a wide panel of cell lines from human neuroblastoma. Although hypotheses have been put forward that treatment with ss or its analogs may be beneficial in oncological patients, this does not appear to be the case in neuroblastoma; patients with high sst2 levels (who are therefore sensitive to ss treatment) have per se a relatively positive outcome. Therefore, adjuvant treatment with ss is not necessary. Viceversa, patients with a poor prognosis are essentially characterized by a low expression of sst2 (and therefore are insensitive to a therapy with ss). In these patients adjuvant treatment with ss might be indicated, but would have little chance of success. Although the majority of neuroendocrine tumours expresses sst2, pancreas and prostate cancer express sst1 but not sst2, and are therefore insensitive to octreotide treatment which binds preferentially to sst2. Tumours like colorectal carcinoma and breast cancer also express sst2 in their more favourable forms. However, the concentration of sst2 in colorectal cancer is similar, if not lower than that in the surrounding normal tissue. Therefore, the probability of successful adjuvant therapy with ss is relatively low. In breast cancer, it is possible that sensitivity to estrogens may have a positive influence on the expression of sst2. This might justify clinical trials with ss in breast cancer.
authors.affiliation: Unità di Endocrinologia, Università degli Studi, Florence, Italy.
authors.forename: C
authors.initials: C
authors.lastname: Casini Raggi
authors.forename: P
authors.initials: P
authors.lastname: Pinzani
authors.forename: S
authors.initials: S
authors.lastname: Gelmini
authors.forename: C
authors.initials: C
authors.lastname: Tricarico
authors.forename: C
authors.initials: C
authors.lastname: Orlando
authors.forename: A
authors.initials: A
authors.lastname: Calabrò
authors.forename: D
authors.initials: D
authors.lastname: Renzi
authors.forename: F
authors.initials: F
authors.lastname: Cianchi
authors.forename: R
authors.initials: R
authors.lastname: Valanzano
authors.forename: V
authors.initials: V
authors.lastname: Distante
authors.forename: C
authors.initials: C
authors.lastname: Cortesini
authors.forename: F
authors.initials: F
authors.lastname: Tonelli
authors.forename: L
authors.initials: L
authors.lastname: Cataliotti
authors.forename: M
authors.initials: M
authors.lastname: Cameron Smith
authors.forename: L
authors.initials: L
authors.lastname: Messerini
authors.forename: S
authors.initials: S
authors.lastname: Bianchi
authors.forename: M
authors.initials: M
authors.lastname: Pazzagli
authors.forename: M
authors.initials: M
authors.lastname: Serio
authors.forename: M
authors.initials: M
authors.lastname: Maggi
mesh_terms: D000230:Adenocarcinoma / Q000188:drug therapy / Q000235:genetics / Q000378:metabolism; D018931:Antineoplastic Agents, Hormonal / Q000627:therapeutic use; D001943:Breast Neoplasms / Q000188:drug therapy / Q000378:metabolism; D015179:Colorectal Neoplasms / Q000188:drug therapy / Q000378:metabolism; D005260:Female; D006801:Humans; D008297:Male; D009363:Neoplasm Proteins / Q000096:biosynthesis / Q000235:genetics / Q000502:physiology*; D009369:Neoplasms / Q000188:drug therapy / Q000378:metabolism*; D009447:Neuroblastoma / Q000235:genetics / Q000378:metabolism; D015282:Octreotide / Q000627:therapeutic use; D017481:Receptors, Somatostatin / Q000096:biosynthesis / Q000235:genetics / Q000502:physiology*; D013004:Somatostatin / Q000502:physiology / Q000627:therapeutic use
chemical_list: D018931:Antineoplastic Agents, Hormonal; D009363:Neoplasm Proteins; D017481:Receptors, Somatostatin; D013004:Somatostatin; C093733:somatostatin receptor 2; D015282:Octreotide