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Limited data suggest that prostatic adenocarcinoma containing neuroendocrine cells are more resistant to hormonal treatment. Similarly patients with colorectal adenocarcinoma containing numerous neuroendocrine cells seem to have a worse prognosis [13]. On the other hand, patients with pancreatic adenocarcinoma or non-small cell cancer whose cancer contains many neuroendocrine cells, seem to have a better prognosis [41]. In addition, there are some other pitfalls in the interpretation of CgA levels.

J Clin Endocrinol Metab 1999;84:775–780. 20 Buscail L, Saint-Laurent N, Chastre E, Vaillant JC, Gespach C, Capella G, Kalthoff H, Lluis F, Vaysse N, Susini C: Loss of sst2 somatostatin receptor gene expression in human pancreatic and colorectal cancer. Cancer Res 1996;56: 1823–1827. 32 21 Patel YC: Molecular pharmacology of somatostatin receptor subtypes. J Endocrinol Invest 1997;20:348–367. 22 Zheng H, Bailey A, Jiang MH, Honda K, Chen HY, Trumbauer ME, Van der Ploeg LH, Schaeffer JM, Leng G, Smith RG: Somatostatin receptor subtype 2 knockout mice are refractory to growth hormone-negative feedback on arcuate neurons.

Published results and circulating levels of CgA from different centers may vary depending on what assay they have been using. The plasma levels of CgA are elevated in various peptide-producing neuroendocrine tumors and the highest levels are noted in patients with metastatic carcinoid tumors, particularly midgut carcinoids [3]. In malignant EPT plasma CgA varies from slightly elevated to extreme levels. Plasma CgB is usually a better marker for benign insulin-producing tumors than CgA. In an earlier study, involving 44 patients with malignant carcinoid tumors, 17 patients with sporadic EPT and 11 patients with EPT as part of multiple endocrine neoplasia type 1 (MEN1), plasma level of CgA was increased in 99%, whereas CgB was increased in 88% and CgC in 6% and pancreastatin in 46% of the patients, illustrating that it is definitely superior to measure CgA compared to pancreastatin [13].

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