Changing biological behaviour of NETs during the evolution of the disease: progress on progression

Author:

Alexandraki Krystallenia I1,Spyroglou Ariadni12,Kykalos Stylianos3,Daskalakis Kosmas45,Kyriakopoulos Georgios6,Sotiropoulos Georgios C2,Kaltsas Gregory A5,Grossman Ashley B789

Affiliation:

1. 1Second Department of Surgery, Aretaieion Hospital, National and Kapodistrian University of Athens, Athens, Greece

2. 2Clinic for Endocrinology, Diabetology and Clinical Nutrition, University Hospital Zurich, Zurich, Switzerland

3. 3Second Department of Propaedeutic Surgery, Laiko Hospital, National and Kapodistrian University of Athens, Medical School, Athens, Greece

4. 4Department of Surgery, Faculty of Medicine and Health, Örebro University, Örebro, Sweden

5. 5Endocrine Unit, First Department of Propaedeutic Medicine, Laiko University Hospital, Medical School, National and Kapodistrian University of Athens, Athens, Greece

6. 6Department of Pathology, Evaggelismos Hospital, Athens, Greece

7. 7Oxford Centre for Diabetes, Endocrinology and Metabolism, Churchill Hospital, University of Oxford, Oxford, UK

8. 8NET Unit, Royal Free Hospital, London, UK

9. 9Barts and the London School of Medicine, London, UK

Abstract

Following improvements in the management and outcome of neuroendocrine neoplasms (NENs) in recent years, we see a subset, particularly of pancreatic NENs, which become more aggressive during the course of the disease. This is reflected by an increase in the Ki-67 labelling index, as a marker of proliferation, which may lead to an occasion of increase in grading, but generally does not appear to be correlated with histologically confirmed dedifferentiation. A systematic review of the literature was performed in PubMed, Cochrane Library, and Embase until May 2020 to identify cases that have behaved in such a manner. We screened 244 articles: only seven studies included cases in their cohort, or in a subset of the cohort studied, with a proven increase in the Ki-67 during follow-up through additional biopsy. In addition to these studies, we have also tried to identify possible pathophysiological mechanisms implicated in advanced NENs, although currently no studies appear to have addressed the mechanisms implicated in the switch to a more aggressive biological phenotype over the course of the disease. Such progression of the disease course may demand a change in the management. Summarising the overall evidence, we suggest that future studies should concentrate on changes in the molecular pathways during disease progression with sequential biopsies in order to shed light on the mechanisms that render a neoplasm more aggressive than its initial phenotype or genotype.

Publisher

Bioscientifica

Subject

Cancer Research,Endocrinology,Oncology,Endocrinology, Diabetes and Metabolism

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