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At least 19 recordsLinked to original sources
PubMed1980

Ectopic hormone syndromes.

Ectopic hormone production is not always associated with endocrine manifestations and if extensive studies of tumour hormones are made it is found that asymptomatic hormone production is often concomitant with neoplasms. The nature of tumour hormones seems essentially indistinguishable from that of native hormones, although there exists in some cases an abundance of precursor or hormone fragments and unbalanced biosynthesis of subunits. Production of multiple hormones by a tumour is not uncommon. These facts may suggest abnormal gene expression as the basic mechanism responsible for ectopic hormone production. During the process of cellular differentiation, most of the genes are inactivated. Neoplastic transformation may activate repressed genes, thus producing hormones that are not produced by differentiated cells (derepression hypothesis). This hypothesis, however, makes it difficult to explain the higher incidence of ACTH-LPH-producing tumours among APUD tumours. Some investigators have postulated that only APUD tumours elaborate ACTH-LPH or other APUD hormones (neuro-endocrine cell hypothesis). However, there have been reported some definite non-APUD tumours which elaborate ACTH-LPH. These facts can be explained by the stepwise, irreversible repression hypothesis of cellular differentiation. In APUD cells, the gene for ACTH-LPH coding may be repressed at the terminal stage of differentiation and may, therefore, be very easily derepressed by neoplastic transformation. On the other hand, the ACTH-LPH gene may be repressed at a relatively early stage in non-APUD cells and be difficult to reactivate even after neoplastic transformation. Further studies on ectopic hormone producing tumours may clarify the mechanism of ectopic hormone production and yield new insights into the fundamental process of malignant change.

Adrenocorticotropic Hormone↗
PubMed1986

[Ectopic hormone production].

Ectopic hormone production by tumors is one particular form of paraneoplasia. Syndromes caused by inappropriate ectopic secretion of hormones or biologically active molecules with hormone-like effects may help to detect the presence of a tumor or its localization, and in monitoring the efficiency of therapy. Ectopic hormone production is difficult to demonstrate unequivocally. The pathogenesis remains unknown but may be elucidated in the near future by research into the pathogenesis of tumors at the molecular level. The tumors most frequently associated with ectopic hormone production are bronchogenic and pancreatic carcinomas, carcinoids, and thymomas.

Humans↗
PubMedDate not supplied

Ectopic hormone production by malignant tumors.

Malignant tumours of nonendocrine tissues may produce ectopic hormones. The most likely mechanism is depression of genes which code for hormones. Ectopic hormones are invariably peptides, and each is identical to some peptide product of an endocrine gland. However, the majority of ectopic hormones occur as biologically inactive precursors or subunits and therefore remain occult unless they are specifically sought. When appropriate assays are made for such inactive forms, it is found that ectopic production of hormone-like peptides occurs frequently. Clinical syndromes result only in the relatively rare patients in whom a biologically active form is synthesized in large quantities. Laboratory research in this area improves our understanding of genetic control mechanisms in neoplasia. Ectopic hormones may be of limited use in diagnosis of cancer, especially when multiple markers are measured simultaneously.

Chorionic Gonadotropin↗
PubMed1980

Ectopic hormones--biochemical aspects.

Biochemical evidence suggests that ectopic hormone production is much more common than suspected clinically. The majority of lung carcinomas of oat cell or carcinoid type appear to synthesise ACTH and related peptides, calcitonin and less frequently, chorionic gonadotrophin and vasopressin. The primary amino acid sequences of ectopic hormones closely resemble their normal counterparts but ectopic hormone producing tumours contain greater proportions of high molecular weight, subunit and fragment forms than the normal gland of origin. Assays for ectopic hormones are clinically useful in diagnosis, tumour localisation, and monitoring patients with ectopic hormonal syndromes. Currently the clinical value of hormone assays in the routine management of common forms of malignancy in the absence of overt ectopic hormonal syndromes is unproven. However, better characterisation of hormonal forms relatively specific for neoplasia together with improved assay specificity and sensitivity may enhance the clinical value of ectopic hormones as tumour markers, particularly in malignancies which are commonly associated with ectopic hormone production (e.g. lung cancer).

Adrenocorticotropic Hormone↗
PubMed1981

Ectopic hormone production by endocrine tumors: localization of hormones at the cellular level by immunocytochemistry.

Clinical and laboratory data, histologic, electron microscopic and immunocytochemical findings of the tumors of eight patients suffering from Cushing's syndrome and of one patient with hypercalcemia are described. The unlabeled antibody enzyme method was used for the detection of insulin, glucagon, somatostatin, pancreatic polypeptide, corticotropin, beta-lipotropin, calcitonin, parathyroid hormone, and gastrin. Ectopic Cushing's syndrome was caused by pancreatic endocrine tumors, medullary thyroid carcinoma, a bronchial, a gastric and a thymic carcinoid, and a carcinoid of the mediastinum. Hypercalcemia in one patient was related to a pancreatic endocrine tumor. After surgery the clinical symptoms disappeared in two patients, but persisted or relapsed in five patients. ACTH-immunoreactivity could be demonstrated in six of eight tumors; calcitonin-immunoreactivity was found in the tumor of the patient suffering from hypercalcemia. ACTH-immunoreactivity could be localized to secretory granules by immunoelectron microscopy, and the presence of ACTH and beta-LPH in the same tumor cells could be shown in one pancreatic tumor. A combination of production of orthotopic and ectopic hormones was found in one, and secretion of two ectopic hormones was detected in another pancreatic endocrine tumor.

Adrenocorticotropic Hormone↗
PubMed2004

[Etiology of ectopic hormone producing tumors].

Inappropriate secretion of peptide hormones and other associated proteins by tumors is the most common cause of paraneoplastic syndromes. Sensitive assay techniques have permitted detection of polypeptide hormone secretion by tumors even in the absence of clinically overt syndromes. Moreover, it has been demonstrated that most or all nonendocrine tissues produce small amounts of a variety of peptide hormones and hormone precursors. Nevertheless, the term ectopic hormone syndromes occurring with nonendocrine neoplasms is well established and widely used. We summarize etiology of 'classic' ectopic hormone producing tumors to help establish the diagnosis of paraneoplastic humoral syndromes.

ACTH Syndrome, Ectopic↗
PubMed1988

Ectopic hormone production.

Current understanding of the phenomenon of ectopic hormone production is largely based on a histopathological and immunocytochemical analysis of peptide hormone secreting tumours arising in non-endocrine tissues. Recent advances in the study of gene regulation show that the tissue-specific expression of genes is a highly sophisticated process and is unlikely to be disturbed by a spontaneous event such as point mutation in DNA. Study of several genes for frequently found ectopic hormones, i.e. prop-opiomelanocortin, vasopressin/neurophysin II, gastrin-releasing peptide, parathyroid hormone-related peptide, calcitonin gene-related peptide and beta-chorionic gonadotropin, suggests they are transcribed as they would be in their natural cell of origin. It is argued therefore that these data are compatible with the concept that the tumour cell of origin was capable of expressing these peptides, if only in a minor or transient manner. In one example, the ectopic ACTH syndrome, it is also necessary to explain the non-suppression of this gene's expression by elevated levels of glucocorticoids. Recent work suggests that this may result from physically present, but biologically inactive glucocorticoid receptors, a phenomenon that has occasionally been noted in hormonally inactive tumour tissue and cell lines.

Calcitonin↗
PubMed1982

The frequency and clinical biology of the ectopic hormone syndromes of small cell carcinoma.

Eighty-four patients with small cell carcinoma of the lung were reviewed with respect to the frequency and biologic behavior of patients with a demonstrated ectopic hormone syndrome. This subgroup of 12 patients (14%) was compared with regard to stage of disease, distribution of metastases, response rate, and survival to those patients not demonstrating a clinical syndrome. Stage, distribution, and response rates are comparable in the two groups but differences were observed with regard to sites of metastases and survival. The ectopic hormone syndrome patients had an increased likelihood of liver metastasis and CNS metastasis. The frequency of CNS metastasis in patients without the ectopic hormone syndrome was 11/72 (15%) of which four of the 11 were present at initial presentation. In contrast, 5/12 (42%) of the patients with ectopic hormone syndromes developed CNS metastasis, and all five had clinically demonstrated SIADH. Survival was consistently inferior in those patients with the ectopic hormone syndrome.

ACTH Syndrome, Ectopic↗
PubMed1984

Ectopic hormones as tumor markers.

Certain cancers are able to synthesize, store, and secrete peptide hormones. In some cases the hormones possess sufficient biologic activity to produce identifiable paraneoplastic syndromes. Occasionally the measurement of one or more of these hormones in the plasma or serum is clinically useful for monitoring tumor activity.

Adrenocorticotropic Hormone↗