Serum chromogranin A levels for the diagnosis and follow-up of well-differentiated non-functioning neuroendocrine tumors

Tumor Biology ◽  
2015 ◽  
Vol 37 (3) ◽  
pp. 2863-2869 ◽  
Author(s):  
Yuejuan Cheng ◽  
Zhao Sun ◽  
Chunmei Bai ◽  
Xiaoyan Yan ◽  
Ran Qin ◽  
...  
Keyword(s):  
Neuroendocrine Tumors ◽  
Chromogranin A ◽  
Well Differentiated

Somatostatin receptor scintigraphy and chromogranin A assay in staging and follow-up of patients with well-differentiated neuroendocrine tumors

2011 ◽  
Vol 32 (8) ◽  
pp. 731-737 ◽  
Author(s):  
Marcel P.M. Stokkel ◽  
Daphne D. Rietbergen ◽  
Catharina M. Korse ◽  
Babs G. Taal
Keyword(s):  
Neuroendocrine Tumors ◽  
Chromogranin A ◽  
Somatostatin Receptor ◽  
Somatostatin Receptor Scintigraphy ◽  
Receptor Scintigraphy ◽  
Well Differentiated

Chromogranin a Measurement in Neuroendocrine Tumors

1998 ◽  
Vol 13 (1) ◽  
pp. 3-9 ◽  
Author(s):  
L. Ferrari ◽  
E. Seregni ◽  
A. Martinetti ◽  
B Van Graafeiland ◽  
S. Nerini-Molteni ◽  
...  
Keyword(s):  
Tumor Marker ◽  
Neuroendocrine Tumors ◽  
Chromogranin A ◽  
High Sensitivity ◽  
Biologically Active ◽  
Proliferative Index ◽  
Favorable Prognosis ◽  
Blood Marker ◽  
Active Substances

Neuroendocrine tumors (NETs) are rare neoplasms characterized by a low proliferative index and, in some cases, a favorable prognosis. These tumors often overproduce and release biologically active substances that are responsible for severe syndromes. Tumor marker measurement provides the clinician with useful information for the management of NET patients. The substances released by overproducing tumors are currently used as biomarkers, but there is a need for sensitive markers also for the “biochemically silent” NETs. The most effective and reliable blood marker available today is chromogranin A (CgA). Because of its high sensitivity and specificity, this glycoprotein can be used for the diagnosis, prognosis and follow-up of NETs. Furthermore, CgA measurement can be used for monitoring those tumors not overproducing or releasing any hormones or biological amines. This paper is a synthetic review on the value of CgA in NET management and reports our experiences with CgA measurement in NET patients.

scholarly journals FAS and Subsequent Therapies in Pancreatic Neuroendocrine Tumors

2021 ◽  
Author(s):  
Jane E. Rogers ◽  
Michael Lam ◽  
Daniel M. Halperin ◽  
Cecile G. Dagohoy ◽  
James C. Yao ◽  
...  
Keyword(s):  
Neuroendocrine Tumors ◽  
Cox Regression ◽  
Progression Free Survival ◽  
Pancreatic Neuroendocrine Tumors ◽  
Free Survival ◽  
Prior Therapy ◽  
Well Differentiated ◽  
Grade 3 ◽  
Line Of Therapy

We evaluated outcomes of treatment with 5-fluorouracil (5-FU), doxorubicin, and streptozocin (FAS) in well-differentiated pancreatic neuroendocrine tumors (PanNETs) and its impact on subsequent therapy (everolimus or temozolomide). Advanced PanNET patients treated at our center from 1992 to 2013 were retrospectively reviewed. Patients received bolus 5-FU (400 mg/m2), streptozocin (400 mg/m2) (both IV, days 1-5) and doxorubicin (40 mg/m2 IV, day 1) every 28 days. Overall response rate (ORR) was assessed using RECIST version 1.1. Of 243 eligible patients, 220 were evaluable for ORR, progression-free survival (PFS), and toxicity. Most (90%) had metastatic, nonfunctional PanNETs; 14% had prior therapy. ORR to FAS was 41% (95% confidence interval [CI]: 36-48%). Median follow-up was 61 months. Median PFS was 20 (95% CI: 15-23) months; median overall survival (OS) was 63 (95% CI: 60-71) months. Cox regression analyses suggested improvement with first-line vs subsequent lines of FAS therapy. Main adverse events ≥ grade 3 were neutropenia (10%) and nausea/vomiting (5.5%). Dose reductions were required in 32% of patients. Post-FAS everolimus (n=108; 68% second line) had a median PFS of 10 (95% CI: 8-14) months. Post-FAS temozolomide (n=60; 53% > fourth line) had an ORR of 13% and median PFS of 5.2 (95% CI: 4-12) months. In this largest reported cohort of PanNETs treated with chemotherapy, FAS demonstrated activity without significant safety concerns. FAS did not appear to affect subsequent PFS with everolimus; this sequence is being evaluated prospectively. Responses were noted with subsequent temozolomide-based regimens although PFS was possibly limited by line of therapy.

Chromogranin a Measurement in Metastatic Well-Differentiated Gastroenteropancreatic Neuroendocrine Carcinoma: Screening for False Positives and a Prospective Follow-Up Study

2011 ◽  
Vol 26 (2) ◽  
pp. 94-101 ◽  
Author(s):  
Delphine Vezzosi ◽  
Thomas Walter ◽  
Agnès Laplanche ◽  
Jean Luc Raoul ◽  
Clarisse Dromain ◽  
...  
Keyword(s):  
False Positive ◽  
Chromogranin A ◽  
Morphological Changes ◽  
Surrogate Marker ◽  
False Positive Result ◽  
Gastroenteropancreatic Neuroendocrine Tumors ◽  
Follow Up Study ◽  
Well Differentiated ◽  
Positive Results

Background Multiple causes of false-positive chromogranin A (CgA) measurement have been reported that may affect its impact as a surrogate marker of RECIST progression in well-differentiated gastroenteropancreatic neuroendocrine tumors (WDGEPNET). Aims 1) To evaluate the frequency of false-positive CgA results. 2) To prospectively compare CgA variations with RECIST morphological changes in patients without known causes of false-positive CgA measurements. Methods First, the conditions responsible for potentially false-positive CgA measurements were screened in 184 consecutive patients with metastatic WDGEPNET. Secondly, a variation in CgA at a 6-month interval was compared to RECIST results at 6 months in 46 patients. Results Among 184 patients, elevated CgA was found in 130 cases (71%) including 99 patients with at least one cause of a false-positive result. Impaired kidney function as well as medication with proton pump inhibitors were found to be the 2 major causes of false-positive results. The sensitivity and specificity of CgA measurements compared with morphological tumor changes according to the RECIST criteria were 71% and 50%, respectively, at 6 months. Conclusion Routine screening for the causes of false-positive CgA measurements is mandatory in WDGEPNET patients. Our study does not validate the use of CgA as a surrogate marker of tumor progression.

scholarly journals Chromogranin A: From Laboratory to Clinical Aspects of Patients with Neuroendocrine Tumors

2018 ◽  
Vol 2018 ◽  
pp. 1-12 ◽  
Author(s):  
Paola Di Giacinto ◽  
Francesca Rota ◽  
Laura Rizza ◽  
Davide Campana ◽  
Andrea Isidori ◽  
...  
Keyword(s):  
Neuroendocrine Tumors ◽  
Phase Ii ◽  
Chromogranin A ◽  
Carcinoid Syndrome ◽  
Phase Ii Trial ◽  
Randomized Study ◽  
Clinical Aspects ◽  
Clinical Activity ◽  
Octreotide Lar ◽  
Well Differentiated

Background. Neuroendocrine tumors (NETs) are characterized by having behavior and prognosis that depend upon tumor histology, primary site, staging, and proliferative index. The symptoms associated with carcinoid syndrome and vasoactive intestinal peptide tumors are treated with octreotide acetate. The PROMID trial assesses the effect of octreotide LAR on the tumor growth in patients with well-differentiated metastatic midgut NETs. The CLARINET trial evaluates the effects of lanreotide in patients with nonfunctional, well-, or moderately differentiated metastatic enteropancreatic NETs. Everolimus has been approved for the treatment of advanced pancreatic NETs (pNETs) based on positive PFS effects, obtained in the treated group. Sunitinib is approved for the treatment of patients with progressive gastrointestinal stromal tumor or intolerance to imatinib, because a randomized study demonstrated that it improves PFS and overall survival in patients with advanced well-differentiated pNETs. In a phase II trial, pasireotide shows efficacy and tolerability in the treatment of patients with advanced NETs, whose symptoms of carcinoid syndrome were resistant to octreotide LAR. An open-label, phase II trial assesses the clinical activity of long-acting repeatable pasireotide in treatment-naive patients with metastatic grade 1 or 2 NETs. Even if the growth of the neoplasm was significantly inhibited, it is still unclear whether its antiproliferative action is greater than that of octreotide and lanreotide. Because new therapeutic options are needed to counter the natural behavior of neuroendocrine tumors, it would also be useful to have a biochemical marker that can be addressed better in the management of these patients. Chromogranin A is currently the most useful biomarker to establish diagnosis and has some utility in predicting disease recurrence, outcome, and efficacy of therapy.

scholarly journals Baseline plasma chromogranin A levels in patients with well-differentiated neuroendocrine tumors of the pancreas: A potential predictor of postoperative recurrence

Pancreatology ◽  
2017 ◽  
Vol 17 (2) ◽  
pp. 291-294 ◽  
Author(s):  
Yoshihide Nanno ◽  
Hirochika Toyama ◽  
Ippei Matsumoto ◽  
Kyoko Otani ◽  
Sadaki Asari ◽  
...  
Keyword(s):  
Neuroendocrine Tumors ◽  
Chromogranin A ◽  
Postoperative Recurrence ◽  
Potential Predictor ◽  
Well Differentiated

Serum chromogranin A in the diagnosis and follow-up of neuroendocrine tumors of the gastroenteropancreatic tract

1992 ◽  
Vol 16 (4) ◽  
pp. 697-701 ◽  
Author(s):  
Guido Schürmann ◽  
Ulrich Raeth ◽  
Bertram Wiedenmann ◽  
Heinz Buhr ◽  
Christian Herfarth
Keyword(s):  
Neuroendocrine Tumors ◽  
Chromogranin A

scholarly journals SUN-929 An Unusual Presentation of Insulinomas-Profound Hypophosphatemia

2020 ◽  
Vol 4 (Supplement_1) ◽  
Author(s):  
William West ◽  
Gabriel Ikponmosa Uwaifo
Keyword(s):  
Neuroendocrine Tumors ◽  
Early Morning ◽  
Needle Aspiration ◽  
The Body ◽  
Serum Phosphorus ◽  
Men 1 ◽  
Dietary Phosphorus ◽  
Multiple Imaging ◽  
Well Differentiated

Abstract BACKGROUND: Insulin induces intracellular shift of phosphorus, causing hypophosphatemia. This is mild, transient and quiescent in normal persons. Persistent hyperinsulinemia in patients with depleted phosphorus stores can cause profound symptomatic hypophosphatemia. Clinical Case: A 36yr old man with MEN 1 presented in follow-up. His original manifestation of MEN 1 was familial primary hyperparathyroidism (pHPT) for which he had parathyroidectomy in 2009. At one of his endocrine clinic visits, he was noted to have asymptomatic hypophosphatemia with serum phosphorus of 2.4 (2.7–4.5 mg/dL) and mildly elevated PTH of 89 (9–77 pg/mL). This was presumed to be due to mild persistent/recurrent pHPT, and he was advised to increase dietary phosphorus intake. About a year later, he presented to the emergency room (ER) with palpitations and marked asthenia. Serum phosphorus was 1.0. He was treated with intravenous phosphorus and discharged on oral phosphorus replacement with advice to increase his dietary phosphate intake. Despite this, he continued to have recurrent spells of dizziness, weakness, palpitations, and marked hypophosphatemia several requiring repeat ER visits. His degree of mild pHPT remained stable and imaging studies to identify a possible cause for tumor induced osteomalacia with phosphate wasting was unrevealing. He volunteered at a follow up visit that he had a long history of low blood sugar spells (confirmed by fingerstick) that he had learnt to manage with frequent carbohydrate rich snacks. This prompted the consideration of a possible insulinoma as the cause for his persistent hypophosphatemia. Despite significant hypoglycemia on an abbreviated supervised fast, an OGTT and mixed meal test showed profound severe insulin mediated hypoglycemia. CGMS also showed multiple extended early morning severe hypoglycemic spells <50mg/dl over a 2 wk period. Multiple imaging tests were negative but a Gallium Dotatate scan revealed multiple areas of uptake in his pancreas. Endoscopic ultrasound of the pancreas demonstrated multiple masses in the pancreas: one 7 x 5 cm mass in the body and one 4 x 4 cm mass near the neck of the pancreas. Fine needle aspiration biopsy revealed well-differentiated neuroendocrine tumors. He had distal pancreatectomy and tumor enucleation of 5 tumors identified on intraoperative sonography. Histopathology confirmed multiple neuroendocrine tumors, with immunostaining for insulin. He has had no further episodes of hypophosphatemia since despite being off oral phosphate supplements. Conclusion: Profound hypophosphatemia can be the dominant presentation of persistent hyperinsulinemia seen in patients with insulinoma. Insulinomas and other causes of persistent hyperinsulinemia need to be considered in the differential diagnosis of persistent/recurrent hypophosphatemia.

scholarly journals Neuroendocrine Tumors — Laboratory Diagnosis

2010 ◽  
Vol 29 (4) ◽  
pp. 254-264 ◽  
Author(s):  
Anna Tzontcheva
Keyword(s):  
Gastrointestinal Tract ◽  
Tumor Markers ◽  
Neuroendocrine Tumors ◽  
Chromogranin A ◽  
Endocrine Cells ◽  
Neuron Specific Enolase ◽  
Laboratory Diagnosis ◽  
Pancreatic Tumors ◽  
Endocrine Pancreatic Tumors ◽  
Well Differentiated

Neuroendocrine Tumors — Laboratory DiagnosisNeuroendocrine tumors (NETs) are a heterogeneous group of neoplasms originating from endocrine cells, which are characterized by the presence of secretory granules as well as the ability to produce biogenic amines and polypeptide hormones. These tumors originate from endocrine glands such as the adrenal medulla, the pituitary, and the parathyroids, as well as endocrine islets within the thyroid or the pancreas, and dispersed endocrine cells in the respiratory and gastrointestinal tract. The clinical behavior of NETs is extremely variable; they may be functioning or not functioning, ranging from very slow-growing tumors (well-differentiated NETs), which are the majority, to highly aggressive and very malignant tumors (poorly differentiated NETs). Classically, NETs of the gastrointestinal tract are classified into 2 main groups: (1) carcinoids and (2) endocrine pancreatic tumors (EPTs). Most neuroendocrine tumors produce and secrete a multitude of peptide hormones and amines. Some of these substances cause a specific clinical syndrome: carcinoid, Zollinger-Ellison, hyperglycemic, glucagonoma and WDHA syndrome. Specific markers for these syndromes are basal and/or stimulated levels of urinary 5-HIAA, serum or plasma gastrin, insulin, glucagon and vasoactive intestinal polypeptide, respectively. Some carcinoid tumors and about one third of endocrine pancreatic tumors do not present any clinical symptoms and are called ‘nonfunctioning’ tumors. Therefore, general tumor markers such as chromogranin A, pancreatic polypeptide, serum neuron-specific enolase and subunits of glycoprotein hormones have been used for screening purposes in patients without distinct clinical hormone-related symptoms. Among these general tumor markers chromogranin A, although its precise function is not yet established, has been shown to be a very sensitive and specific serum marker for various types of neuroendocrine tumors. This is because it may also be elevated in many cases of less well-differentiated tumors of neuroendocrine origin that do not secrete known hormones. At the moment, chromogranin A is considered the best general neuroendocrine serum or plasma marker available both for diagnosis and therapeutic evaluation, and is increased in 50-100% of patients with various neuroendocrine tumors. Chromogranin A serum or plasma levels reflect tumor load, and it may be an independent marker of prognosis in patients with midgut carcinoids.

scholarly journals Endoscopic mucosal resection: still a reliable therapeutic option for gastrointestinal neuroendocrine tumors

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Gholam Reza Sivandzadeh ◽  
Fardad Ejtehadi ◽  
Shima Shoaee ◽  
Ladan Aminlari ◽  
Ramin Niknam ◽  
...  
Keyword(s):  
Endoscopic Mucosal Resection ◽  
Neuroendocrine Tumors ◽  
Therapeutic Option ◽  
Disease Recurrence ◽  
Therapeutic Modalities ◽  
Mucosal Resection ◽  
Well Differentiated ◽  
Pathology Reports ◽  
Age Range

Abstract Background Neuroendocrine tumors (NETs), as a rare and heterogeneous category of solid tumors, feature various morphologies and behaviors. In recent years, the incidence of NETs has continued to increase. Endoscopic mucosal resection (EMR) is one of the therapeutic modalities for the treatment of gastric and rectal NETs. Methods We evaluated patients with well-differentiated NETs of the stomach, duodenum, or rectum between 2011 and 2018. In this study, all cases with tumors confined to the mucosal or submucosal layers and smaller than 20 mm were resected using the EMR technique. We used EUS, CT scan, or MRI to exclude patients with advanced disease. All patients were actively monitored for recurrence according to the recommended protocols. Results A total of 36 patients with NETs entered the study; 17 (47.2%) were female and the remaining 19 (52.8%) were male, with a total age range of 20–74 years (mean: 52.47 ± 13.47 years). Among the tumors, 31 cases (86.1%) were G1 and the remaining 5 (13.9%) were G2. Based on the pathology reports, 22 tumors (61.1%) were smaller than 1 cm, while the remaining 14 (38.9%) were between 1–2 cm. Twenty-two patients (61.1%) had a margin of specimen involved with the tumor. No recurrence was observed during the mean follow-up time of 63.5 ± 19.8 months (range: 39–103 months). All 36 cases survived during the study period. Conclusion Conventional EMR procedure provides low chance of R0 (complete resection) achievement in gastrointestinal NETs smaller than 20 mm and limited to the mucosa or sub mucosa. However, it could be an option if patients are closely followed. Postoperative marginal involvement is not a reliable predictor of disease recurrence, which may be explained by the deleterious effect of heat coagulation and cauterization applied during tumor removal.

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