PubMed · 4327680
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1971-08-26. Glucagon.. https://pubmed.ncbi.nlm.nih.gov/4327680/
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The hypothalamic satiety peptide CART (cocaine and amphetamine regulated transcript) is expressed at high levels in anorectic rat glucagonomas but not in hypoglycemic insulinomas. However, a non-anorectic metastasis derived from the glucagonoma retained high CART expression levels and produced circulating CART levels comparable to that of the anorectic tumors. Moreover, distinct glucagonoma lines derived by stable HES-1 transfection of the insulinoma caused severe anorexia but retained low circulating levels of CART comparable to that of insulinoma bearing or control rats. Islet tumor associated anorexia and circulating CART levels are thus not correlated, and in line with this peripheral administration of CART (5-50 mg/kg) produced no effect on feeding behavior. In the rat two alternatively spliced forms of CART mRNA exist and quantitative PCR revealed expression of both forms in the hypothalamus, in the different islet tumors, and in the islets of Langerhans. Immunocytochemistry as well as in situ hybridization localized CART expression to the somatostatin producing islet D cell. A potential endocrine/paracrine role of islet CART remains to be clarified.
Although adrenal tumors detected during pregnancy are extraordinarily rare, the pathophysiologic repercussions of untreated adrenal neoplasms are enormous to both mother and fetus. From our computer-based registry of pregnant patients from 1975 through 1996 (n = 30,246), four cases of adrenal neoplasms associated with pregnancy were identified (0.013%), analyzed, and compared with the current medical literature. Four women ages 36, 29, 22, and 21 years had adrenal neoplasms diagnosed with pregnancy. Patient 1 had an unsuspected pheochromocytoma identified at autopsy. At 27 weeks into her pregnancy the patient suffered a myocardial infarction, and both she and the fetus died. Patient 2 was incidentally found to have adrenal and pancreatic neoplasms on screening abdominal computed tomography for von Hippel-Lindau disease. The study identified a pregnancy. She elected to terminate the pregnancy and underwent resection of both tumors. She died 3 years later of metastatic islet cell cancer. Both of these patients had previously delivered healthy babies, but both pregnancies were complicated by hypertension. Patient 3 had a functional adrenal tumor identified initially by urinary aldosterone studies because of symptoms of severe hypertension, and patient 4 had an adrenal mass diagnosed via ultrasonography at 30 weeks' gestation because of concerns for right-sided pyelonephritis. These two women underwent careful monitoring throughout the remainder of their pregnancies with eventual delivery of healthy babies. Both women later underwent successful operative resection of benign adrenal adenomas. Adrenal neoplasms discovered during pregnancy are rare. The onus, however, is on physicians to consider this diagnosis in pregnant women with hypertension, headaches, or other manifestations of adrenal disorders. Surgical management of identified adrenal lesions is thereafter straightforward. Missing the diagnosis has grave implications for these young women and their fetuses.
Endocrine pancreatic tumors (EPT) and neuroendocrine tumors (NET) occur sporadically and rarely in association with multiple endocrine neoplasia type 1 (MEN1). We analyzed the frequency of allelic deletions and mutations of the recently identified MEN1 gene in 53 sporadic tumors including 30 EPT and 23 NET (carcinoids) of different locations and types. Allelic deletion of the MEN1 locus was identified in 18/49 (36.7%) tumors (13/30, 43.3% in EPT and 5/19, 26.3% in NET) and mutations of the MEN1 gene were present in 8/52 (15.3%) tumors (4/30 (13.3%) EPT and 4/22 (18.1%) NET). The somatic mutations were clustered in the 5' region of the coding sequence and most frequently encompassed missense mutations. All tumors with mutations exhibited a loss of the other allele and a wild-type sequence of the MEN1 gene in nontumorous DNA. In one additional patient with a NET of the lung and no clinical signs or history of MEN1, a 5178-9G-->A splice donor site mutation in intron 4 was identified in both the tumor and blood DNA, indicating the presence of a thus far unknown MEN1 syndrome. In most tumor groups the frequency of allelic deletions at 11q13 was 2 to 3 times higher than the frequency of identified MEN1 gene mutations. Some tumor types, including rare forms of EPT and NET of the duodenum and small intestine, exhibited mutations more frequently than other types. Furthermore, somatic mutations were not restricted to foregut tumors but were also detectable in a midgut tumor (15.2% versus 16.6%). Our data indicate that somatic MEN1 gene mutations contribute to a subset of sporadic EPT and NET, including midgut tumors. Because the frequency of mutations varies significantly among the investigated tumor subgroups and allelic deletions are 2 to 3 times more frequently observed, factors other than MEN1 gene inactivation, including other tumor-suppressor genes on 11q13, may also be involved in the tumorigenesis of these neoplasms.