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Pancreatic Neoplasms: HELP
Articles by Sylvia L. Asa
Based on 7 articles published since 2010
(Why 7 articles?)
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Between 2010 and 2020, Sylvia L. Asa wrote the following 7 articles about Pancreatic Neoplasms.
 
+ Citations + Abstracts
1 Review Treatment Options for Pancreatic Neuroendocrine Tumors. 2019

Akirov, Amit / Larouche, Vincent / Alshehri, Sameerah / Asa, Sylvia L / Ezzat, Shereen. ·Institute of Endocrinology, Beilinson Hospital, Petach Tikva 49100, Israel. amit.akirov@gmail.com. · Sackler School of Medicine, Tel Aviv University, Tel Aviv 69978, Israel. amit.akirov@gmail.com. · Department of Endocrine Oncology, Princess Margaret Cancer Centre, Toronto, ON M5G 1Z5, Canada. amit.akirov@gmail.com. · Department of Endocrine Oncology, Princess Margaret Cancer Centre, Toronto, ON M5G 1Z5, Canada. vincent.larouche@uhn.ca. · Department of Medicine, Division of Endocrinology and Metabolism, Jewish General Hospital, McGill University, Montreal, QC H3T 1E2, Canada. vincent.larouche@uhn.ca. · Department of Endocrine Oncology, Princess Margaret Cancer Centre, Toronto, ON M5G 1Z5, Canada. sameerah.alsherhri@uhn.ca. · Department of Pathology, University Health Network, University of Toronto, Toronto, ON M5S 1A1, Canada. pathlady01@gmail.com. · Department of Endocrine Oncology, Princess Margaret Cancer Centre, Toronto, ON M5G 1Z5, Canada. Shereen.Ezzat@sinaihealthsystem.ca. ·Cancers (Basel) · Pubmed #31207914.

ABSTRACT: The management of pancreatic neuroendocrine tumors (PanNETs) involves classification into non-functional or functional PanNET, and as localized or metastatic PanNET. In addition, while most PanNETs are sporadic, these endocrine neoplasms can also be manifestations of genetic syndromes. All these factors may assist in forming a risk stratification system permitting a tailored management approach. Most PanNETs are classified as non-functional because they are not associated with clinical sequelae of hormone excess. They are characterized by non-specific symptoms, such as abdominal pain or weight loss, resulting from mass effect related to the pancreatic tumor or secondary to distant metastases. Accurate staging of the disease is essential for determining the appropriate approach to therapy. As cure is only potentially possible with surgical resection of the tumor, it is recommended to remove all localized and limited metastatic disease. However, many patients present with metastatic and/or advanced local disease. In such instances, the goal of therapy is to control tumor growth and/or decrease tumor burden, lengthen survival, and palliate local symptoms and those of hormone excess. This typically requires a multimodal approach, including surgery, liver-directed treatment, and systemic medical therapy.

2 Review Pancreatic endocrine tumors. 2011

Asa, Sylvia L. ·Department of Pathology and Ontario Cancer Institute, University Health Network, University of Toronto, Toronto, ON, Canada. sylvia.asa@uhn.on.ca ·Mod Pathol · Pubmed #21455203.

ABSTRACT: The endocrine cells of the pancreas and their related cells throughout the gastrointestinal tract give rise to a variety of tumors that pose a diagnostic challenge. There has been progress in understanding their histogenesis, morphology, immunohistochemistry, molecular biology and classifications. This review will focus on nomenclature/terminology, classification, the role of immunohistochemistry, molecular advances, including genetic predisposition, and potential therapeutic targets to define the role of pathology in the application of prognostic and predictive markers for this disease.

3 Article Pancreatic Neuroendocrine Tumor Producing Insulin and Vasopressin. 2018

Alshaikh, Omalkhaire M / Yoon, Ju-Yoon / Chan, Bryan A / Krzyzanowska, Monika K / Butany, Jagdish / Asa, Sylvia L / Ezzat, Shereen. ·Department of Internal Medicine, Al Imam Mohammad Ibn Saud Islamic University (IMSIU), Riyadh, Saudi Arabia. · Department of Medicine, Princess Margaret Cancer Centre, University Health Network, 610 University Avenue, Room 7-327, Toronto, ON, M5G 2M9, Canada. · Department of Pathology, University Health Network, University of Toronto, Toronto, ON, Canada. · Department of Medicine, Princess Margaret Cancer Centre, University Health Network, 610 University Avenue, Room 7-327, Toronto, ON, M5G 2M9, Canada. shereen.ezzat@utoronto.ca. ·Endocr Pathol · Pubmed #28718084.

ABSTRACT: The objective of the study is to report a rare case of pancreatic neuroendocrine tumor (pNET) producing insulin and vasopressin. We describe the clinical presentation and management of a metastatic pNET with refractory hypoglycemia and progressive severe hyponatremia. A 52-year-old patient had abdominal pain leading to the diagnosis of a tumor that was initially presumed to be splenic in origin. Investigations ultimately identified a pancreatic mass that on biopsy proved to be a pNET. Eventually, he developed extensive liver metastases, and with tumor progression, he manifested hypoglycemia and severe hyponatremia. He was managed with multiple therapies including somatostatin analogue, peptide-receptor-radionuclide-therapy (PRRT), diazoxide, and everolimus; none of these therapeutic modalities was successful in controlling functional and structural progression of the tumor. Ultimately, the pNET proved fatal and autopsy confirmed widely metastatic disease that stained strongly and diffusely for vasopressin, a feature not seen in the previous liver biopsy. This case illustrates the challenges of diagnosis and management of aggressive insulin-producing pNETs and highlights the potential concomitant ectopic production of vasopressin leading to refractory hyponatremia.

4 Article Pancreatic Struma with Papillary Thyroid Carcinoma: a Diagnostic Dilemma. 2017

Liu, Jerry / Marcaccio, Michael J / Young, J E M / Aziz, Tariq / Wat, Josephine / Asa, Sylvia L. ·Department of Pathobiology and Laboratory Medicine, University of Toronto, Toronto, ON, Canada. · Department of Pathology, University Health Network, 200 Elizabeth Street, 11th floor, Toronto, ON, M5G 2S3, Canada. · Department of Surgery, Hamilton Health Sciences Center, Juravinski Hospital and McMaster University, Hamilton, ON, Canada. · Department of Pathology, Hamilton Health Sciences Center, Juravinski Hospital and McMaster University, Hamilton, ON, Canada. · Department of Radiology, Hamilton Health Sciences Center, Juravinski Hospital and McMaster University, Hamilton, ON, Canada. · Department of Pathobiology and Laboratory Medicine, University of Toronto, Toronto, ON, Canada. sylvia.asa@uhn.ca. · Department of Pathology, University Health Network, 200 Elizabeth Street, 11th floor, Toronto, ON, M5G 2S3, Canada. sylvia.asa@uhn.ca. ·Endocr Pathol · Pubmed #28078619.

ABSTRACT: -- No abstract --

5 Article Hormone profiling, WHO 2010 grading, and AJCC/UICC staging in pancreatic neuroendocrine tumor behavior. 2013

Morin, Emilie / Cheng, Sonia / Mete, Ozgur / Serra, Stefano / Araujo, Paula B / Temple, Sara / Cleary, Sean / Gallinger, Steven / Greig, Paul D / McGilvray, Ian / Wei, Alice / Asa, Sylvia L / Ezzat, Shereen. ·Department of Medicine, Princess Margaret Cancer Centre, University Health Network, Toronto, Ontario, Canada. ·Cancer Med · Pubmed #24403235.

ABSTRACT: Pancreatic neuroendocrine tumors (pNETs) are the second most common pancreatic neoplasms, exhibiting a complex spectrum of clinical behaviors. To examine the clinico-pathological characteristics associated with long-term prognosis we reviewed 119 patients with pNETs treated in a tertiary referral center using the WHO 2010 grading and the American Joint Committee on Cancer/International Union Against Cancer (AJCC/UICC) staging systems, with a median follow-up of 38 months. Tumor size, immunohistochemistry (IHC) profiling and patient characteristics-determining stage were analyzed. Primary clinical outcomes were disease progression or death. The mean age at presentation was 52 years; 55% were female patients, 11% were associated with MEN1 (multiple endocrine neoplasia 1) or VHL (Von Hippel-Lindau); mean tumor diameter was 3.3 cm (standard deviation, SD) (2.92). The clinical presentation was incidental in 39% with endocrine hypersecretion syndromes in only 24% of cases. Nevertheless, endocrine hormone tissue immunoreactivity was identified in 67 (56.3%) cases. According to WHO 2010 grading, 50 (42%), 38 (31.9%), and 3 (2.5%) of tumors were low grade (G1), intermediate grade (G2), and high grade (G3), respectively. Disease progression occurred more frequently in higher WHO grades (G1: 6%, G2: 10.5%, G3: 67%, P = 0.026) and in more advanced AJCC stages (I: 2%, IV: 63%, P = 0.033). Shorter progression free survival (PFS) was noted in higher grades (G3 vs. G2; 21 vs. 144 months; P = 0.015) and in more advanced AJCC stages (stage I: 218 months, IV: 24 months, P < 0.001). Liver involvement (20 vs. 173 months, P < 0.001) or histologically positive lymph nodes (33 vs. 208 months, P < 0.001) were independently associated with shorter PFS. Conversely, tissue endocrine hormone immunoreactivity, independent of circulating levels was significantly associated with less aggressive disease. Age, gender, number of primary tumors, and heredity were not significantly associated with prognosis. Although the AJCC staging and WHO 2010 grading systems are useful in predicting disease progression, tissue endocrine hormone profiling provides additional information of potentially important prognostic value.

6 Article Inhibin-expressing clear cell neuroendocrine tumor of the ampulla: an unusual presentation of von Hippel-Lindau disease. 2013

Gucer, Hasan / Szentgyorgyi, Eva / Ezzat, Shereen / Asa, Sylvia L / Mete, Ozgur. ·Department of Pathology, University Health Network, 200 Elizabeth Street, 11th floor, Toronto, Ontario,, M5G 2C4, Canada. ·Virchows Arch · Pubmed #23913169.

ABSTRACT: von Hippel-Lindau (VHL) disease is a hereditary autosomal dominant disorder associated with deletions or mutations in the VHL tumor suppressor gene. Characteristically, up to 60 % of neuroendocrine tumors (NETs) associated with VHL disease display a spectrum of clear cell morphology including multivacuolated lipid-rich cell change. Unlike neurofibromatosis type 1 and multiple endocrine neoplasia type 1 syndromes, ampullary NETs have not been described in association with VHL disease. In this report, we discuss the features of an incidental ampullary clear cell NET occurring in a patient with pancreatic VHL disease including multiple pancreatic NETs. The ampullary lesion consisted of epithelial cells resembling lipoblasts or signet ring cells. In our case, all NETs showing clear cell change were positive for inhibin. While the underlying mechanism of this finding is largely unknown, it is of note that positivity for inhibin has not been observed in clear cell NETs associated with multiple endocrine neoplasia type 1 syndrome. Our case proves that NETs can develop in the ampullary region in patients with VHL; clear cell change can occur in these lesions and can mimic signet ring cell carcinoma. This issue is of clinical significance especially in small biopsy samples; thus, positivity for keratin alone should not be taken as evidence of an adenocarcinoma. Moreover, demonstration of inhibin expression in a NET with clear cell change along with other clinical stigmata should alert the diagnostician to the possibility of VHL disease. However, further larger series examining inhibin expression in both syndrome-related and sporadic clear cell NETs are needed to confirm our findings.

7 Article The FGFR4-G388R single-nucleotide polymorphism alters pancreatic neuroendocrine tumor progression and response to mTOR inhibition therapy. 2012

Serra, Stefano / Zheng, Lei / Hassan, Manal / Phan, Alexandria T / Woodhouse, Linda J / Yao, James C / Ezzat, Shereen / Asa, Sylvia L. ·Departments of Pathology, Campbell Family Institute for Cancer Research, University Health Network, Toronto, Ontario, Canada. ·Cancer Res · Pubmed #22986737.

ABSTRACT: Pancreatic neuroendocrine tumors (pNET), also known as islet cell tumors, exhibit a wide range of biologic behaviors ranging from long dormancy to rapid progression. Currently, there are few molecular biomarkers that can be used to predict recurrence/metastasis or response to therapy. This study examined the predictive and prognostic value of a single nucleotide polymorphism substituting an arginine (R) for glycine (G) in codon 388 of the FGFR4 transmembrane domain. We established the FGFR4 genotype of 71 patients with pNETs and correlated genotype with biologic behavior. We created an in vivo model of pNET with BON1 cells and transfected them with either FGFR4-G388 or FGFR4-R388 to determine the mechanism of action and to examine response to the mTOR inhibitor everolimus. We then validated the predictive results of experimental studies in a group of patients treated with everolimus. FGFR4-R388 is associated with more aggressive clinical behavior in patients with pNETs with a statistically significant higher risk of advanced tumor stage and liver metastasis. Using an orthotopic mouse xenograft model, we show that FGFR4-R388 promotes tumor progression by increasing intraperitoneal spread and metastatic growth within the liver. Unlike FGFR4-G388, FGFR4-R388 BON1 tumors exhibited diminished responsiveness to everolimus. Concordantly, there was a statistically significant reduction in response to everolimus in patients with FGFR4-R388. Our findings highlight the importance of the FGFR4 allele in pNET progression and identify a predictive marker of potential therapeutic importance in this disease.