Surgical Treatment of Endocrine Pancreatic Tumours

Åkerström, Göran; Hellman, Per; Hessman, Ola; Osmak, Liliana

doi:10.1159/000080744

Cited by 30 publications

(22 citation statements)

References 38 publications

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“…In both tumor types formal, oncological pancreatic resection with peripancreatic lymph node dissection is mandatory to attempt favorable survival (Akerstrom et al 2004). Slow tumor progression may necessitate repeated surgical interventions for lymph node and/or LM during the course of the disease (Madeira et al 1998).…”

Section: Glucagonomas and Vipomasmentioning

confidence: 99%

Neuroendocrine tumor disease: an evolving landscape

Frilling

Åkerström

Falconi

et al. 2012

Endocrine-Related Cancer

149

106

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Gastroenteropancreatic neuroendocrine neoplasms (GEP-NENs) represent a heterogenous group of tumors arising from a variety of neuroendocrine cell types. The incidence and prevalence of GEPNENs have markedly increased over the last three decades. Symptoms are often absent in early disease, or vague and nonspecific even in advanced disease. Delayed diagnosis is thus common. Chromogranin A is the most commonly used biomarker but has limitations as does the proliferative marker Ki-67%, which is often used for tumor grading and determination of therapy. The development of a multidimensional prognostic nomogram may be valuable in predicting tumor behavior and guiding therapy but requires validation. Identification of NENs that express somatostatin receptors (SSTR) allows for SSTR scintigraphy and positron emission tomography imaging using novel radiolabeled compounds. Complete surgical resection of limited disease or endoscopic ablation of small lesions localized in stomach or rectum can provide cure; however, the majority of GEP-NENs are metastatic (most frequently the liver and/or mesenteric lymph nodes) at diagnosis. Selected patients with metastatic disease may benefit from advanced surgical techniques including hepatic resection or liver transplantation. Somatostatin analogs are effective for symptomatic treatment and exhibit some degree of antiproliferative activity in small intestinal NENs. There is a place for streptozotocin, temozolomide, and capecitabine in the management of pancreatic NENs, while new agents targeting either mTOR (everolimus) or angiogenic (sunitinib) pathways have shown efficacy in these lesions.

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Section: Glucagonomas and Vipomasmentioning

confidence: 99%

Neuroendocrine tumor disease: an evolving landscape

Frilling

Åkerström

Falconi

et al. 2012

Endocrine-Related Cancer

149

106

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“…Functional tumors are associated with different clinical syndromes of hormone excess due to release of specific hormones (insulin, gastrin, glucagon, vasoactive intestinal peptide, somatostatin), whereas non-functional tumors are non-secreting or release hormones without clinical symptoms (often pancreatic polypeptide). In the absence of metastases or local invasiveness, there are currently no reliable histopathological or molecular genetic methods to classify PETs as malignant [1,2,3,4]. Loss of heterozygosity (LOH) analyses have displayed abnormalities on a number of chromosomal arms [5].…”

Section: Introductionmentioning

confidence: 99%

Cyclin-Dependent Kinase 4 (CDK4) Expression in Pancreatic Endocrine Tumors

Lindberg¹,

Hessman²,

Åkerström³

et al. 2007

Neuroendocrinology

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Background/Aims: Pancreatic endocrine tumors (PETs) occur sporadically, in association with the multiple endocrine neoplasia type 1 (MEN1) and the von Hippel-Lindau syndromes. CDK4 is central to the cell cycle control in pancreatic β cells, and we have assessed whether CDK4 expression is deregulated in 18 human sporadic or familial PETs. Methods: Real-time quantitative PCR, immunohistochemistry, DNA sequencing, and Western blot analysis were used. Results: CDK4 mRNA was expressed in all PETs within the range of the arbitrary control. CDK4 protein was absent in normal pancreatic islets but distinctly expressed in all PETs as determined by immunohistochemistry. CDK4 expression was confirmed by Western blot analysis. No significant differences of CDK4 expression were observed between the groups of benign and malignant PETs or between tumors with or without MEN1 gene mutations. CDK4 expression was not due to gene amplification, and no mutations were identified in coding exons and RNA splice sites. c-Myc is known to be overexpressed in PETs and directly augments CDK4 expression in other cell types. Analysis of consecutive tissue sections for CDK4 and c-Myc showed overlapping homo- or heterogeneous immunostaining in all 18 PETs. Conclusion: We conclude that CDK4 and c-Myc is generally expressed in benign and malignant PETs, and regardless of MEN1 mutational status. Targeting of CDK4 may present an alternative to traditional chemotherapy of PETs in the future.

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“…6 Surgical resection can lead to prolonged disease-free remission. [28][29][30] As for the liver metastases, control by metastasectomy, cryoablation, radiofrequency ablation, or chemoembolization has been reported. 19,22 Our patient was also treated with somatostatin analogue (SSA), a potent inhibitor of glucagon secretion preoperatively and she responded well in terms of weight gain, general well-being and resolution of paraneoplastic manifestation i.e., NME.…”

Section: Discussionmentioning

confidence: 99%

Glucagonoma Syndrome: A Case Report

Roslan

Yahaya

2016

JAFES

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A 58-year-old Malay female with underlying diabetes mellitus, presented with chronic skin lesions, associated with weight loss and anemia. There were erosive, scaling skin lesions over the extremities, gluteal region and perioral area. Skin biopsy histopathological examination revealed Necrolytic Migratory Erythema (NME). A CT scan of the abdomen revealed a pancreatic neck and body tumor with possible liver metastases. She was successfully treated with subcutaneous somatostatin and underwent distal pancreatectomy with wedge resection of liver nodule.

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Surgical Treatment of Endocrine Pancreatic Tumours

Cited by 30 publications

References 38 publications

Neuroendocrine tumor disease: an evolving landscape

Neuroendocrine tumor disease: an evolving landscape

Cyclin-Dependent Kinase 4 (CDK4) Expression in Pancreatic Endocrine Tumors

Glucagonoma Syndrome: A Case Report

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