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ABSTRACT
Typical and atypical carcinoids are neuroendocrine epithelial lung tumours which are difficult to distinguish. Confusion has been introduced by designating atypical carcinoids as well differentiated neuroendocrine carcinomas and including some tumours which are large cell neuroendocrine carcinomas.
We therefore investigated 32 typical and 23 atypical carcinoids of the lung, and 9 combined forms of atypical carcinoid and small cell carcinoma. The following parameters were each independently correlated in a multivariate analysis with 10-year survival data: nuclear and nucleolar polymorphism, mitotic counts, vascular invasion, lymph node metastasis, structural pattern, location of the tumours, immunohistochemistry, age and sex of the patients.
Typical carcinoids were characterized by an absence of vascular invasion and lymph node metastases, and a mean mitotic rate of 0.75/10 high power fields (HPFs), while atypical carcinoids were characterized by vascular invasion and/or metastases, a mean mitotic rate of 4.25/10 HPFs and nuclear pleomorphism. Combined forms of atypical carcinoid and small cell carcinoma were characterized by vascular invasion, metastases and a mean mitotic rate of 20.7/10 HPFs. Vascular invasion, lymph node metastases, mitotic counts and nuclear pleomorphism significantly correlated with 10-year survival data, whereas location, size and structural pattern of the tumour, age and sex did not correlate with survival. All tumours were positive for cytokeratins and at least two out of three general neuroendocrine markers. However, positive reactivity for different peptides, hormones, and neurotransmitters did not correlate with one of the structural subtypes of carcinoid or with patient survival.
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The prognostic significance of neuroendocrine differentiation in prostatic malignancy is controversial, but the results of recent studies with markers such as chromogranin A and neurone-specific enolase suggest that neuroendocrine differentiation, as reflected by increased tissue expression or blood concentrations of these neuroendocrine secretory products, is associated with a poor prognosis, tumour progression, and androgen independence. As all malignant neuroendocrine cells are devoid of androgen receptors and the expression of neuroendocrine cells is not suppressed by androgen ablation, clonal propagation of androgen receptor-negative neuroendocrine cells may have an important role in the development of androgen-independent prostatic carcinoma. This has significant implications for the treatment of prostate cancer, because several of the hormones that are secreted by neuroendocrine differentiated, malignant prostatic cells are potential candidates for use in drug treatment. A limited number of hormones have been tested in this context, in particular somatostatin, bombesin, and serotonin. As there is currently no successful treatment for differentiated prostate cancer, new therapeutic procedures and trials need to be developed to test drugs based on neuroendocrine hormones or their antagonists.
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Neuroendocrine tumours are a heterogeneous group including, for example, carcinoid, gastroenteropancreatic neuroendocrine tumours, pituitary tumours, medullary carcinoma of the thyroid and phaeochromocytomas. They have attracted much attention in recent years, both because they are relatively easy to palliate and because they have indicated the chronic effect of the particular hormone elevated. As neuroendocrine phenotypes became better understood, the definition of neuroendocrine cells changed and is now accepted as referring to cells with neurotransmitter, neuromodulator or neuropeptide hormone production, dense-core secretory granules, and the absence of axons and synapses. Neuroendocrine markers, particularly chromogranin A, are invaluable diagnostically. Study of several neuroendocrine tumours has revealed a genetic etiology, and techniques such as genetic screening have allowed risk stratification and prevention of morbidity in patients carrying the particular mutation. Pharmacological therapy for these often slow-growing tumours, e.g. with somatostatin analogues, has dramatically improved symptom control, and radiolabelled somatostatin analogues offer targeted therapy for metastatic or inoperable disease. In this review, the diagnosis and management of patients with carcinoid, gut neuroendocrine tumours, multiple endocrine neoplasia types 1 and 2, and isolated phaeochromocytoma are evaluated.
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Introduction As a basic component of oncogenesis, neuroendocrine tumour cells usually develop very potent autocrine/paracrine signalling pathways that play a crucial part in the dysregulation of cellular growth ( Hanahan & Weinberg
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others are more rapidly growing and invade surrounding areas. Very rarely, PAs do metastasize, and these adenomas are called pituitary carcinomas. Mode of treatment of PAs includes drug therapy, surgery and, in some cases, irradiation. In prolactin (PRL
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Abstract
Background: Salmon calcitonin (sCT) injection into rats has been reported to induce pituitary tumours. We have demonstrated the co-existence, in the rat-derived α-TSH cell line, of an sCT-like peptide, as well as a receptor for sCT.
Aim: This was to investigate the possible existence of sCT-like immunoreactivity (sCT-LI) in human neuroendocrine tumours.
Methods: A collection of human neuroendocrine tumours was tested, using a highly specific antibody for sCT. Immunostaining was abolished by preabsorption with sCT at concentrations higher than 1 μg/ml. However, as immunofluorescence was still obvious at the highest concentration (100 pg/ml) of hCT employed, any significant cross-reactivity was excluded.
Results: Of the human pituitary null cell tumours studied, positive staining was obtained in 2 out of 12, suggesting a similarity between the rat and human pituitary glands. None of the other pituitary tumours tested showed sCT-LI (these included 8 corticotroph tumours, 6 prolactinomas and 2 somatotroph tumours).
This work was extended to medullary thyroid carcinomas (MTCs) and a further group of neuroendocrine tumours, looking for the specificity of this sCT-LI among the various APUDomas.
All the tested MTCs (n=14) expressed sCT-LI, while none of the examined phaeochromocytomas (n=23), intestinal carcinoids (n=14), lung carcinoids (n=16), stomach carcinoids (n=2), rectal carcinoids (n=2), gastrinomas (n=4), insulinomas (n=12), oat cell carcinomas (n=7), carotid body tumours (n=9), VIPomas (n=3), or a glucagonoma (n=1) expressed sCT-LI. This indicates that this sCT-LI might be unique to MTC (and possibly the pituitary).
Conclusion: The possible existence of the most potent form of CT may provide an explanation for the vasomotor disturbances in MTC and may be a potential new tumour marker for MTC. Phylogenetically, the presence of a lower form of CT in mammalian tissues would give an insight into the conservation of the CT peptide family in evolution.
Endocrine-Related Cancer (1997) 4 191-195
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negative for PAX-8 ( Suzuki et al . 2018 ). It is worth noting that PAX-8 is positive for renal epithelial tumours such as renal cell carcinoma and neuroendocrine tumours ( Long et al . 2010 , El-Maqsoud et al . 2016 ). Thus, if malignant cells were
Member of the German Cancer Consortium (DKTK), Germany
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poorly differentiated NENs called neuroendocrine carcinomas (NECs) ( Capella et al. 1995 , Klöppel et al. 2017 a , Rindi et al. 2018 b ). In fact, the similarities between the site-specific NEN entities are so large that a concept has been
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( Fenton et al . 2001 ). Also, Cameselle-Teijeiro and coworkers presented a 42-year-old man with known FAP having a CMV-PTC associated with neuroendocrine carcinoma component. The patient died with lung and brain metastases ( Cameselle-Teijeiro et al
Department of Clinical Sciences, University of Bergen, Bergen, Norway
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Sir Peter MacCallum Department of Oncology, The University of Melbourne, Melbourne, Australia
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of their proliferation index (G1–G3), whereas neuroendocrine carcinoma (NEC) category is used for poorly differentiated neoplasms. The high-grade GEP NEN G3 group (Ki-67 >20%) is therefore now separated into two groups: NET G3 and NEC ( Table 1 ) and
