scholarly journals Liver metastases of pancreatic neuroendocrine tumor as an incidental finding in the explant of a patient with liver polycystic disease

2021 ◽  
Vol 44 (6) ◽  
pp. 528-530
Author(s):  
C Lara Romero ◽  
A Poyato González ◽  
S Rubiales Trujillano
Keyword(s):  
Liver Metastases ◽  
Neuroendocrine Tumor ◽  
Incidental Finding ◽  
Pancreatic Neuroendocrine Tumor ◽  
Polycystic Disease

scholarly journals The Impact of Repeating Endosonography with Confocal Endomicroscopy for the Diagnosis of Cystic Neuroendocrine Tumor

2019 ◽  
Vol 2019 ◽  
pp. 1-4
Author(s):  
Iqra Haq ◽  
Somashekar G. Krishna ◽  
Bhaveshkumar Patel ◽  
Thavam Thambi-Pillai ◽  
Chencheng Xie ◽  
...  
Keyword(s):  
Neuroendocrine Tumor ◽  
Neuroendocrine Tumors ◽  
Pancreatic Pseudocyst ◽  
Incidental Finding ◽  
Pancreatic Neuroendocrine Tumor ◽  
Needle Aspiration ◽  
Confocal Laser Endomicroscopy ◽  
Confocal Laser ◽  
The Impact

Cystic pancreatic neuroendocrine tumors represent around 13% of all neuroendocrine tumors (Hurtado-Pardo 2017). There has been an increase in the incidence of cases due to improvement in imaging modalities. This is a case of a 68-year-old male with the incidental finding of a pancreatic cyst on CT. Initial Endoscopic Ultrasound with Fine Needle Aspiration (EUS-FNA) showed sonographic and cytology features suggestive of a pancreatic pseudocyst. However the cyst persisted with no change in size after aspiration leading to a follow-up EUS- FNA, which was combined with needle based confocal laser endomicroscopy (nCLE). The nCLE features were consistent with a cystic pancreatic neuroendocrine tumor, which was later confirmed on histology after surgical resection.

scholarly journals Pancreatic neuroendocrine tumor accompanied with multiple liver metastases

2014 ◽  
Vol 6 (8) ◽  
pp. 596 ◽  
Author(s):  
Tomohide Hori ◽  
Kyoichi Takaori ◽  
Shinji Uemoto
Keyword(s):  
Liver Metastases ◽  
Neuroendocrine Tumor ◽  
Pancreatic Neuroendocrine Tumor ◽  
Multiple Liver Metastases

Growth factor signaling in pancreatic neuroendocrine tumor metastases.

2019 ◽  
Vol 37 (4_suppl) ◽  
pp. 256-256
Author(s):  
Brenna Rheinheimer ◽  
Ronald Heimark ◽  
Tun Jie
Keyword(s):  
Liver Metastases ◽  
Neuroendocrine Tumor ◽  
Signaling Pathways ◽  
Surgical Resection ◽  
Metastatic Disease ◽  
Genetic Variants ◽  
Genomic Analysis ◽  
Pancreatic Neuroendocrine Tumor ◽  
Proliferation Index ◽  
Who Grade

256 Background: Pancreatic neuroendocrine tumors (PanNETs) are among one of the fastest growing cancer diagnoses, yet clinical management for patients with metastatic disease is largely empirically based. Currently, surgical resection remains the only curative option; however, surgical resection of metastatic disease may not be feasible. Preliminary genomic analysis of primary PanNETs revealed a complex mutational landscape with four common oncogenic events; but, critical activation pathways of metastatic lesions have yet to be elucidated. Therefore, pan-genomic analysis of metastatic PanNETs is necessary to understand which genes/pathways are deregulated in PanNET metastases for potential therapeutic exploitation. Methods: We initiated a preliminary genomic sequencing study to evaluate mutations in a set of matched primary and metastatic PanNETs to determine genetic variants involved in metastasis to the liver. De-identified FFPE tumor samples were analyzed from patients who underwent surgical resection without receiving preoperative therapy. DNA was isolated and whole exome sequencing was performed using the Nextera Rapid Capture Exome Kit by Illumina on an Illumina HiSeq 2000/2500. The following criteria were used to define genetic variants: bidirectional, non-synonymous, clean mapping in IGV, ≥ 15X coverage, and an alternate allele frequency of 0.3 ≤ x ≤ 0.7. Results: All metastatic PanNETs were classified as WHO grade G2/G3 based on their KI-67 proliferation index. Each primary PanNET contained an average of 102 genetic variants while liver metastases showed an average of 124 genetic variants. MUFFINN and string analysis revealed that primary PanNETs contained enrichment for mutations involved in the PI3K/Akt and Ras signaling pathways while liver metastases showed enrichment for mutations involved in the MAPK and ErbB signaling pathways. Additionally, two-thirds of liver metastases contained somatic mutations in FGFR3. Conclusions: We have discovered novel pathways that have the potential to regulate pancreatic neuroendocrine tumor metastasis along with an innovative signaling pathway that may sustain metastatic growth and survival as well as exploitation for therapeutic potential.

Clinical Analysis and Comprehensive Treatment of Nonfunctional Pancreatic Neuroendocrine Tumor With Liver Metastases

Pancreas ◽  
2015 ◽  
Vol 44 (6) ◽  
pp. 995-996 ◽  
Author(s):  
Xuefeng Xu ◽  
Xu Han ◽  
Lingxiao Liu ◽  
Yuan Ji ◽  
Jianang Li ◽  
...  
Keyword(s):  
Liver Metastases ◽  
Neuroendocrine Tumor ◽  
Pancreatic Neuroendocrine Tumor ◽  
Clinical Analysis ◽  
Comprehensive Treatment

Successful Management of Multiple Liver Metastases From Pancreatic Neuroendocrine Tumor by Hepatic Arterial Administration of Cisplatin Powder

Pancreas ◽  
2007 ◽  
Vol 35 (3) ◽  
pp. 288-290 ◽  
Author(s):  
Hisato Igarashi ◽  
Tetsuhide Ito ◽  
Masahiro Yoshinaga ◽  
Makoto Kodama ◽  
Hiroshi Hayashi ◽  
...  
Keyword(s):  
Liver Metastases ◽  
Neuroendocrine Tumor ◽  
Pancreatic Neuroendocrine Tumor ◽  
Successful Management ◽  
Multiple Liver Metastases ◽  
Cisplatin Powder

scholarly journals Prolonged survival in a patient with multiple liver metastases from a pancreatic neuroendocrine tumor treated with Peptide Receptor Radiotherapy (PRRT)

Suizo ◽  
2020 ◽  
Vol 35 (1) ◽  
pp. 97-103
Author(s):  
Noritoshi KOBAYASHI ◽  
Takeshi SHIMAMURA ◽  
Yuuma TAKEDA ◽  
Naoki OHKUBO ◽  
Motohiko TOKUHISA ◽  
...  
Keyword(s):  
Liver Metastases ◽  
Neuroendocrine Tumor ◽  
Pancreatic Neuroendocrine Tumor ◽  
Prolonged Survival ◽  
Peptide Receptor ◽  
Multiple Liver Metastases

scholarly journals Peptide receptor radionuclide therapy controls inappropriate calcitriol secretion in a pancreatic neuro-endocrine tumor: a case report

2020 ◽  
Vol 20 (1) ◽  
Author(s):  
Maarten Haemels ◽  
Thierry Delaunoit ◽  
Koen Van Laere ◽  
Eric Van Cutsem ◽  
Chris Verslype ◽  
...  
Keyword(s):  
Liver Metastases ◽  
Neuroendocrine Tumor ◽  
Neuroendocrine Tumors ◽  
Serum Calcium ◽  
Radionuclide Therapy ◽  
Active Form ◽  
Peptide Receptor Radionuclide Therapy ◽  
Pancreatic Neuroendocrine Tumor ◽  
Neuroendocrine Neoplasm ◽  
Peptide Receptor

Abstract Background Hypercalcemia of malignancy is not uncommon in patients with advanced stage cancer. In rare cases the cause of the hypercalcemia is excessive production of calcitriol, the active form of vitamin D. Although inappropriate tumoral secretion of calcitriol is typically associated with lymphomas and some ovarian germ cell tumors, we present a case of calcitriol overproduction-induced hypercalcemia due to a pancreatic neuroendocrine tumor. The high expression of somatostatin receptors on this neuroendocrine neoplasm opened up the opportunity to treat the patient with radiolabelled somatostatin analogs, which successfully controlled the refractory hypercalcaemia and calcitriol levels. This case documents a rare finding of refractory hypercalcaemia of underlying malignancy due to a calcitriol-producing pancreatic neuroendocrine tumor, responding to peptide receptor radionuclide therapy (PRRT). Case presentation A 57 years-old patient presented with back pain, general discomfort, polydipsia, polyuria, fatigue and recent weight loss of 10 kg. Clinical examination was normal and there was no relevant medical history. Biochemical evaluation showed hypercalcemia with markedly increased calcitriol levels. CT-thorax-abdomen and ultrasound guided biopsy revealed a pancreatic neuroendocrine tumor with multifocal liver metastases, suggesting that excessive overproduction of calcitriol by this neuroendocrine tumor was the cause of the refractory hypercalcemia. The patient was eligible for PRRT. Four cycles of 177Lu-DOTATATE PRRT resulted in a morphological response and a normalization of serum calcium levels, confirming the hypothesis of a calcitriol producing pancreatic neuroendocrine tumor. Progression of liver metastases warranted further therapy and temozolomide-capecitabine was started with morphological and biochemical (serum calcium, calcitriol) stabilization. Conclusion Although up to 30–40% of gastroenteropancreatic neuroendocrine tumors are known to be functional (i.e. producing symptoms associated with the predominant hormone/peptide secreted), calcitriol secreting pancreatic neuroendocrine tumors are very rare. However, treatment with PRRT resulted in normalization of calcium and calcitriol levels, strongly supporting the hypothesis of a calcitriol-producing pancreatic neuroendocrine tumor.

Resection of the primary pancreatic neuroendocrine tumor in patients with unresectable liver metastases: Possible indications for a multimodal approach

Surgery ◽  
2014 ◽  
Vol 155 (4) ◽  
pp. 607-614 ◽  
Author(s):  
Emilio Bertani ◽  
Nicola Fazio ◽  
Edoardo Botteri ◽  
Antonio Chiappa ◽  
Massimo Falconi ◽  
...  
Keyword(s):  
Liver Metastases ◽  
Neuroendocrine Tumor ◽  
Pancreatic Neuroendocrine Tumor ◽  
Multimodal Approach ◽  
Unresectable Liver Metastases
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