Ki-67 is a Better Prognostic Marker than Mitotic Count in Neuroendocrine Tumors Abstract #251

Introduction: The recent classification system proposed by ENETS assigns grade by Ki-67 index +/- mitotic count. It has been adopted into routine practice but there is limited data on the relationship between them.
Aim(s): To explore the prognostic value of grading according to Ki-67 and mitotic count in gastroenteropancreatic (GEP) neuroendocrine tumors (NETs).
Materials and methods: Two-hundred and eighty-five NET patients (144 midgut, 141 pancreatic) had their cases reviewed. Ki-67 index and mitotic count were evaluated by an experienced pathologist with expertise in NETs and grade assigned using both indices. Progression-free survival(PFS) and overall survival (OS) from diagnosis were estimated and multivariate analysis performed with Cox regression.
Conference: 8th Annual ENETS Conference (2011)
Category: Clinical
Presenting Author: Dr Mohid S Khan

To read results and conclusion, please login ...

Further abstracts you may be interested in

#9 Case Management of Metastatic carcinoid of the Foregut,Midgut and Hindgut:the relevance of Ki-67 prognostication
Introduction: The predictive value of tumor grade in the prognosis of carcinoid is insufficient and somehow misleading. The grade and differentiation in carcinoid tumors must be seen in conjunction with the Ki-67 index. The Ki-67 protein is a cellular marker for proliferation, present during all active phases of the cell cycle (G1, S, G2 and mitosis) and absent from resting cells (G0). It is therefore an excellent marker to determine the growth fraction of a given cell population. The Ki-67 labelling index is often correlated with the clinical course of carcinoid.
Conference: 7th Annual ENETS Conference (2010)
Category: Basic
Presenting Author: Dr Marianne J Kohler
#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, ...
#28 Prognostic Clinicopathologic Factors in Longitudinally Followed Patients with Metastatic Small Bowel Carcinoid
Introduction: Neuroendocrine tumors demonstrate heterogeneous behavior based upon site of origin and specific histology. Even after controlling for anatomic location, disease stage and histologic grade, registry studies show persistent diversity of outcome in patients with midgut carcinoid.
Conference: 7th Annual ENETS Conference (2010)
Category: Clinical
Presenting Author: Mr. Thomas Curran
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.