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Pancreatic Neoplasms: HELP
Articles by David J. Gross
Based on 7 articles published since 2008
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Between 2008 and 2019, D. Gross wrote the following 7 articles about Pancreatic Neoplasms.
 
+ Citations + Abstracts
1 Guideline ENETS Consensus Guidelines Update for the Management of Distant Metastatic Disease of Intestinal, Pancreatic, Bronchial Neuroendocrine Neoplasms (NEN) and NEN of Unknown Primary Site. 2016

Pavel, M / O'Toole, D / Costa, F / Capdevila, J / Gross, D / Kianmanesh, R / Krenning, E / Knigge, U / Salazar, R / Pape, U-F / Öberg, K / Anonymous6880853. ·Charite Virchow Klinikum, Berlin, Germany. ·Neuroendocrinology · Pubmed #26731013.

ABSTRACT: -- No abstract --

2 Guideline ENETS Consensus Guidelines for the Standards of Care in Neuroendocrine Tumors: biochemical markers. 2009

O'Toole, Dermot / Grossman, Ashley / Gross, David / Delle Fave, Gianfranco / Barkmanova, Jaroslava / O'Connor, Juan / Pape, Ulrich-Frank / Plöckinger, Ursula / Anonymous990637 / Anonymous1000637. ·Department of Gastroentereology and Clinical Medicine, St. James's Hospital and Trinity College, Dublin 8, Ireland. otooled1@tcd.ie ·Neuroendocrinology · Pubmed #19713711.

ABSTRACT: -- No abstract --

3 Review Update in the Therapy of Advanced Neuroendocrine Tumors. 2017

Uri, Inbal / Avniel-Polak, Shani / Gross, David J / Grozinsky-Glasberg, Simona. ·Neuroendocrine Tumor Unit, Endocrinology and Metabolism Department, Division of Medicine, Hadassah-Hebrew University Medical Center, P.O.B. 12000, 91120, Jerusalem, Israel. · Neuroendocrine Tumor Unit, Endocrinology and Metabolism Department, Division of Medicine, Hadassah-Hebrew University Medical Center, P.O.B. 12000, 91120, Jerusalem, Israel. simonag@hadassah.org.il. ·Curr Treat Options Oncol · Pubmed #29143892.

ABSTRACT: OPINION STATEMENT: Neuroendocrine tumors (NETs) are rare neoplasms, with an estimated annual incidence of ~ 6.9/100,000. NETs arise throughout the body from cells of the diffuse endocrine system. More than half originate from endocrine cells of the gastrointestinal tract and the pancreas, thus being referred to as gastroenteropancreatic NETs (GEP-NETs). The only treatment that offers a cure is surgery; however, most patients are diagnosed with metastatic disease, and curative surgery is usually not an option. These patients can be offered long-term systemic treatment, for both symptomatic relief and tumor growth suppression. Evidence-based treatment options include somatostatin analogs, everolimus (a mTOR inhibitor), sunitinib (a tyrosine kinase inhibitor), and peptide receptor radionuclide therapy, alone or combined with cytoreductive procedures (surgery or liver-directed procedures). Other treatment options being investigated are immunotherapy and epigenetic assessment that may lead to more personalized interventions. We believe that each patient should be thoroughly evaluated and their case discussed by a multidisciplinary team that is up-to-date with all treatment modalities including ongoing clinical trials, before selecting the proper treatment option.

4 Article Clinical features of pancreatic neuroendocrine tumors. 2015

Grozinsky-Glasberg, Simona / Mazeh, Haggi / Gross, David J. ·Neuroendocrine Tumor Unit, Endocrinology and Metabolism Service, Department of Medicine, Hadassah-Hebrew University Medical Center, P.O.B. 12000, Jerusalem, 91120, Israel. simonag@hadassah.org.il. · Department of Surgery, Hadassah-Hebrew University Medical Center, Jerusalem, Israel. · Neuroendocrine Tumor Unit, Endocrinology and Metabolism Service, Department of Medicine, Hadassah-Hebrew University Medical Center, P.O.B. 12000, Jerusalem, 91120, Israel. ·J Hepatobiliary Pancreat Sci · Pubmed #25689919.

ABSTRACT: Pancreatic neuroendocrine tumors (PNETs), also known as islet cell tumors, are rare neoplasms that arise in the endocrine tissues of the pancreas. Most of pancreatic NETs (50-75%) are nonfunctioning (not associated with a hormonal clinical syndrome); however, in up to one third they can secrete a variety of peptide hormones, including insulin, gastrin, glucagon, vasoactive intestinal peptide, somatostatin etc., resulting in rare but unique clinical syndromes. In this article, the clinical features of the different types of PNETs will be reviewed. Other aspects of the management of these tumors (surgery, treatment of advanced disease, tumor localization) are not dealt with here, as they are covered by other papers in this volume.

5 Article Ga-68 DOTA-NOC uptake in the pancreas: pathological and physiological patterns. 2012

Krausz, Yodphat / Rubinstein, Rina / Appelbaum, Liat / Mishani, Eyal / Orevi, Marina / Fraenkel, Merav / Tshori, Sagi / Glaser, Benjamin / Bocher, Moshe / Salmon, Asher / Chisin, Roland / Gross, David J / Freedman, Nanette. ·Departments of Medical Biophysics and Nuclear Medicine, Hadassah-Hebrew University Medical Center, Jerusalem, Israel. yodphat@hadassah.org.il ·Clin Nucl Med · Pubmed #22157030.

ABSTRACT: OBJECTIVE: Gallium-68 (Ga-68) DOTA-1-NaI3-octreotide (DOTA-NOC) positron emission tomography (PET)/computed tomography (CT) is increasingly used for neuroendocrine tumors (NETs), often found primarily in the pancreas. However, physiologic uptake of DOTA-NOC has been described in the uncinate process of the pancreas. We studied DOTA-NOC uptake in this organ. MATERIALS AND METHODS: Ninety-six patients underwent 103 DOTA-NOC scans, with pathology-proven pancreatic NET (n = 40) and nonpancreatic NET or biochemical suspicion of NET (n = 63). RESULTS: DOTA-NOC uptake was detected in 35 documented pancreatic tumor sites (SUV: 5.5-165; mean: 25.7 ± 28.8; median: 17.8). Among 63 cases without previous known pathology, uptake was suspicious for tumor in 24 sites (SUV: 4.7-35; mean 16.3 ± 8.0; median: 14.1), and in 38 sites, it was judged as physiological, generally lower relative to adjacent structures (SUV: 2.2-12.6; mean: 6.6 ± 2.2; median: 6.2). In 24 scans with suspected tumor and in 37 of 38 scans with physiological uptake, diagnostic computed tomography or magnetic resonance imaging or endoscopic ultrasonography failed to detect tumor. CONCLUSIONS: Pancreatic DOTA-NOC uptake must be interpreted with caution, and further studies are required.

6 Article Glucagonoma and the glucagonoma syndrome - cumulative experience with an elusive endocrine tumour. 2011

Eldor, Roy / Glaser, Benjamin / Fraenkel, Merav / Doviner, Victoria / Salmon, Asher / Gross, David J. ·Endocrinology & Metabolism Service, Department of Medicine, Hadassah-Hebrew University Medical Center, Jerusalem, Israel. eldorroy@yahoo.com ·Clin Endocrinol (Oxf) · Pubmed #21470282.

ABSTRACT: OBJECTIVE: Glucagonoma is a pancreatic neuroendocrine tumour that arises from alpha cells in the pancreas and is often accompanied by a characteristic clinical syndrome. DESIGN: In this report, we present the cumulative experience and clinical characteristics of six patients diagnosed with glucagonoma and the glucagonoma syndrome and treated at our centre during the past 25 years. RESULTS: Although the course of the disease was variable, some features were similar. The median age at diagnosis was 53·5 years; the median time from onset of symptoms to diagnosis was 39 months. Presenting symptoms were as follows: weight loss 5/6 (83%), necrotizing migratory erythema (NME) 5/6 (83%), diabetes mellitus 4/6 (66%) and diarrhoea, weakness and thrombosis 2/6 (33%). Plasma glucagon was elevated in all patients upon diagnosis (range 200-10,000 pm; N < 50). Skin biopsy was diagnostic only in 1/6 specimens obtained, even after revision. Metastatic disease developed in all patients; 4/6 initially presented with hepatic metastasis. All patient symptoms responded to somatostatin analogue therapy. In 4/6, the NME responded to amino acid solutions. Other modes of therapy were as follows: surgery in 3/6 patients, peptide receptor radioligand therapy with (90) Y-DOTATOC (PRRT) in 3/6 patients (two responses) and chemotherapy in three patients (two responded). Four out of six patients died of the disease, and median survival time was 6·25 years (range 2-11) from diagnosis and 8 years (range 8-16) from initial symptoms. Five-year survival was 66%. CONCLUSION: Our data indicate that somatostatin analogues and an aggressive surgical approach offer symptom relief and tumour control. Among other available treatment modalities, PRRT seems to hold the most promise.

7 Article Peptide receptor radioligand therapy is an effective treatment for the long-term stabilization of malignant gastrinomas. 2011

Grozinsky-Glasberg, Simona / Barak, Dganit / Fraenkel, Merav / Walter, Martin A / Müeller-Brand, Jan / Eckstein, Joseph / Applebaum, Liat / Shimon, Ilan / Gross, David J. ·Institute of Endocrinology, Beilinson Hospital, Rabin Medical Center, Tel Aviv, Israel. simonag@clalit.org.il ·Cancer · Pubmed #21425137.

ABSTRACT: BACKGROUND: Gastrinomas, a rare group of neuroendocrine tumors, are responsible for severe peptic disease and diarrhea. Although symptomatic control may be achieved with proton-pump inhibitors (PPIs) and somatostatin analogues (SSAs), data are limited regarding the possible antitumor effect of the peptide receptor radioligand therapy (PRRT) with radiolabeled SSAs in gastrinoma patients. The goal of this study was to assess the effect of PRRT on symptoms, gastrin secretion, and tumor load in patients with progressive malignant gastrinomas. METHODS: We retrospectively studied 11 patients with metastatic gastrinomas followed for a mean period of 6 years. All patients were symptomatically treated with PPIs, and 9 of 11 patients received monthly injections of SSAs; all patients had an Eastern Cooperative Oncology Group score of 0-1, and received PRRT ((90) Yttrium- or (177) Lutetium-DOTATOC) for progressive disease. Serum gastrin measurements and radiological assessment (using the Response Evaluation Criteria in Solid Tumors criteria) were performed before and every 3-6 months following PRRT. RESULTS: PRRT induced symptomatic improvement in all patients. The mean serum gastrin decreased significantly from 4831 mI/L to 932.6 mI/L (normal, 40-108 mI/L; P < .001). Periodic radiological surveillance showed complete response in 1 (9%) patient, partial tumor response in 5/11 (45%) patients, and tumor stabilization in 5/11 (45%) patients. In 7/11 (64%) patients, the antitumor effect of PRRT persisted after a median period of 14 months. Four of 11 (36%) patients died due to tumor progression (median time to progression, 11 months); in this group, the mean survival time after the last PRRT was 14 ± 6.9 months. CONCLUSIONS: PRRT seems to be a promising tool for the management of patients with inoperable or progressive metastatic gastrinomas.