Limitations of Chromogranin A in Clinical Practice Abstract #498

Introduction: Chromogranin-A (CgA) is the most accurate marker for the histological diagnosis of neuroendocrine tumors (NETs). However diagnostic usefulness of circulating CgA is controversial as several conditions, both neoplastic and non-neoplastic, may induce false positive increases of this marker.
Aim(s): To assess the diagnostic value of serum CgA as screening test for NETs.
Materials and methods: Serum blood samples were obtained from 42 subjects affected with NETs, 120 subjects affected with NONET and 100 healthy subjects with benign nodular goitre (NG) at the time of diagnosis. Determination of CgA was performed by means of IRMA. Kolmogorov-Smirnov test was used to analyze the distribution of CgA levels. Kruskall-Wallis test was used to compare different groups. ROC analysis was performed in order to identify a cut-off value that could discriminate NET patients either from NONET or NG subjects.
Conference: 9th Annual ENETS Conference (2012)
Category: Clinical
Presenting Author: Dr Vincenzo Marotta

To read results and conclusion, please login ...

Further abstracts you may be interested in

#11 Plasma chromogranin - A response to octreotide test: Prognostic value for clinical outcome in endocrine digestive tumors
Introduction: Gastroenteropancreatic neuroendocrine tumors (GEP-NETs) expressing somatostatin receptors may be treated with somatostatin analogues (SSAs). Selection criteria are a positive Octreoscan® or a >50% hormone level decrease after octreotide s.c. injection (octreotide test) (OT). Plasma chromogranin A (CgA) is the best general GEP-NET marker, but data on CgA response to OT are scant.
Conference: 7th Annual ENETS Conference (2010)
Category: Clinical
Presenting Author: MD, PhD Sara Massironi
#12 Chromogranin A as a predictor of progression, regression or stable disease in ileo-cecal (midgut) carcinoid tumors
Introduction: A general characteristic for NETs is their expression of certain proteins, such as chromogranin A (CgA), which is released from the dense core vesicles of NE cells, occasionally together with cell specific hormones, such as gastrin and serotonin. Plasma CgA seems to be closely related to tumor burden of intestinal carcinoid tumors in humans.
Conference: 7th Annual ENETS Conference (2010)
Category: Clinical
Presenting Author: Kenneth Jensen
#16 Endoglin as indicator of metastatic neuroendocrine tumors of the pancreas
Introduction: Neuroendocrine tumors of the pancreas are rare, highly vascularized tumors. Endoglin, a Transforming Growth Factor-β co-receptor, is a marker for angiogenic endothelial cells. Angiogenesis is required for tumor progression and the development of metastases. Recently, endoglin expression was found to be a prognostic marker in pancreatic carcinomas. However, the role of endoglin in neuroendocrine pancreatic tumors has so far not been studied.
Conference: 7th Annual ENETS Conference (2010)
Category: Basic
Presenting Author: Patricia Kuiper
#18 Long-acting release octreotide induce complete response in type 1 gastric carcinoid tumors
Introduction: Gastric endocrine tumors (GET) are increasingly recognized due to expanding indications of upper gastrointestinal endoscopy. Often silent and benign, GET may also be aggressive when sporadic and may sometimes mimic the course of gastric adenocarcinoma. Current incidence of GETs is estimated at around 8% of digestive endocrine tumors. Yearly age-adjusted incidence is around 0.2 per population of 100,000. Gastric carcinoids (ECLomas) develop from gastric enterochromaffin-like cells (ECL cells) in response to chronically elevated gastrin. Type 1 tumors (ECLomas in the course of atrophic gastritis) may occur in conditions of achlorhydria secondary to auto-immune atrophic fundic gastritis. It occurs mostly in women and they are non-functioning tumors, typically found during upper GI endoscopy performed for dyspepsia. ECLomas present frequently as multiple polyps, usually < 1 cm in diameter in the gastric fundus. Type 1 tumors are almost exclusively benign lesions with little risk of deep invasion of the gastric parietal wall. The neoplastic ECL cells become progressively dedifferentiated with an increasing number of Ki-67 immunoreactive (IR) cell nuclei. In addition, there is a substantial decrease in argynophil and IR NE cells that can be visualized by conventional methods. ECLomas secondary to hypergastrinemia should be closely followed for signs of clinical and histopathological tumor progression. Such ECLomas deserve early, active, radical surgical treatment.
Traditionally, gastric carcinoid type 1 (GCA1s) are endoscopically or surgically removed, depending on the number, appearance and size of the tumors. Antrectomy, with surgical excision of the majority of the G cells, is thought to facilitate regression of these tumors by removing the source of excessive gastrin secretion; however, the long-term benefits of antrectomy still remain uncertain. Although proton pump inhibitors are effective in reducing hypergastrinemia-induced gastric acid hypersecretion in GCA2, they do not affect ECL-cell hyperplasia, and therefore their role in GCA1 is limited. Moreover, in selected cases, significant reduction of hypergastrinemia does not prevent development of ECL carcinoid, suggesting that, in addition to hypergastrinemia, other pathogenic or genetic factors may be involved. Treatment with somatostatin analogues (SSA) might impede ECL-cell hyperplasia by suppressing gastrin secretion and/or by a direct anti-proliferative effect on ECL cells. Treatment with SSAs in GCA1 leads to a substantial tumor load reduction, with a concomitant decrease of serum gastrin levels. Published data indicate an important anti-proliferative effect of SSA on ECL cells, providing clinical benefit and obviating, at least temporarily, the need for invasive therapies for GCA1. Morphometric studies demonstrated that, while antrectomy specifically decreased the volume of ECL cells versus the total volume of endocrine cells, octreotide reduces the overall endocrine cell volume. Although the number of treated patients is small, it has been suggested that SSA may exert important anti-proliferative effects either directly, by inhibiting ECL-cells proliferation, or indirectly through suppression of gastrin hypersecretion.
Conference: 7th Annual ENETS Conference (2010)
Category: Clinical
Presenting Author: MD Ricardo Caponero
#20 Paraneoplastic antigen Ma2 (PNMA2) auto-antibodies as biomarkers for early small intestine neuroendocrine tumors detection
Introduction: Small intestine neuroendocrine tumors (NETs) comprise well-differentiated NET (benign carcinoid), well-differentiated neuroendocrine carcinoma (malignant carcinoid) and poorly differentiated neuroendocrine carcinoma (NEC). The majority of NET patients have developed liver metastases at the time of diagnosis and surgery is then seldom curative. Novel predictive, diagnostic and prognostic markers are thus needed to improve our capabilities to diagnose and cure these tumors. We have previously identified six novel marker genes for neuroendocrine tumor cells by using Affymetrix microarrays and advanced bioinformatics. One of this markers, the paraneoplastic antigen Ma2 (PNMA2), which is normally expressed only in nervous tissue, can in the process of carcinogenesis be detected in tumors located outside the nervous system. The finding that Ma2 is expressed in small intestine neuroendocrine primary tumors and their metastases made it interesting to screen whether antibodies against Ma2 are present in the serum of NET patients.
Conference: 7th Annual ENETS Conference (2010)
Category: Basic
Presenting Author: PhD Valeria Giandomenico
Authors: Cui T, Elgue G, Li S C, Hurtig M, ...
Close
Notice

WARNING – FRAUDULENT WEBSITES

ENETS is aware that its members have been confronted with fake websites, which seem to relate to our congress but have not been commissioned or authorised by us. The websites offer fraudulent hotel reservation services. We therefore strongly recommend that you please only use the official enetsconference.org website when booking your tickets and accommodation. Please be vigilant when it comes to providing your credit card details. 

If you have any questions, please do not hesitate to contact us at info@enets.org.