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Pancreatic Neoplasms: HELP
Articles by Wigdan Al-Sukhni
Based on 4 articles published since 2010
(Why 4 articles?)

Between 2010 and 2020, Wigdan Al-Sukhni wrote the following 4 articles about Pancreatic Neoplasms.
+ Citations + Abstracts
1 Article Exome sequencing identifies nonsegregating nonsense ATM and PALB2 variants in familial pancreatic cancer. 2013

Grant, Robert C / Al-Sukhni, Wigdan / Borgida, Ayelet E / Holter, Spring / Kanji, Zaheer S / McPherson, Treasa / Whelan, Emily / Serra, Stefano / Trinh, Quang M / Peltekova, Vanya / Stein, Lincoln D / McPherson, John D / Gallinger, Steven. ·Samuel Lunenfeld Research Institute, Mount Sinai Hospital, Toronto, M5G 1X5, Canada. ·Hum Genomics · Pubmed #23561644.

ABSTRACT: We sequenced 11 germline exomes from five families with familial pancreatic cancer (FPC). One proband had a germline nonsense variant in ATM with somatic loss of the variant allele. Another proband had a nonsense variant in PALB2 with somatic loss of the variant allele. Both variants were absent in a relative with FPC. These findings question the causal mechanisms of ATM and PALB2 in these families and highlight challenges in identifying the causes of familial cancer syndromes using exome sequencing.

2 Article Identification of germline genomic copy number variation in familial pancreatic cancer. 2012

Al-Sukhni, Wigdan / Joe, Sarah / Lionel, Anath C / Zwingerman, Nora / Zogopoulos, George / Marshall, Christian R / Borgida, Ayelet / Holter, Spring / Gropper, Aaron / Moore, Sara / Bondy, Melissa / Klein, Alison P / Petersen, Gloria M / Rabe, Kari G / Schwartz, Ann G / Syngal, Sapna / Scherer, Stephen W / Gallinger, Steven. ·Samuel Lunenfeld Research Institute, Mount Sinai Hospital, Toronto, ON, Canada. wigdan.al.sukhni@utoronto.ca ·Hum Genet · Pubmed #22665139.

ABSTRACT: Adenocarcinoma of the pancreas is a significant cause of cancer mortality, and up to 10 % of cases appear to be familial. Heritable genomic copy number variants (CNVs) can modulate gene expression and predispose to disease. Here, we identify candidate predisposition genes for familial pancreatic cancer (FPC) by analyzing germline losses or gains present in one or more high-risk patients and absent in a large control group. A total of 120 FPC cases and 1,194 controls were genotyped on the Affymetrix 500K array, and 36 cases and 2,357 controls were genotyped on the Affymetrix 6.0 array. Detection of CNVs was performed by multiple computational algorithms and partially validated by quantitative PCR. We found no significant difference in the germline CNV profiles of cases and controls. A total of 93 non-redundant FPC-specific CNVs (53 losses and 40 gains) were identified in 50 cases, each CNV present in a single individual. FPC-specific CNVs overlapped the coding region of 88 RefSeq genes. Several of these genes have been reported to be differentially expressed and/or affected by copy number alterations in pancreatic adenocarcinoma. Further investigation in high-risk subjects may elucidate the role of one or more of these genes in genetic predisposition to pancreatic cancer.

3 Article Screening for pancreatic cancer in a high-risk cohort: an eight-year experience. 2012

Al-Sukhni, Wigdan / Borgida, Ayelet / Rothenmund, Heidi / Holter, Spring / Semotiuk, Kara / Grant, Robert / Wilson, Stephanie / Moore, Malcolm / Narod, Steven / Jhaveri, Kartik / Haider, Masoom A / Gallinger, Steven. ·Hepatobiliary/Pancreatic Surgical Oncology Program, Division of General Surgery, Department of Surgery, University Health Network, University of Toronto, Toronto, Canada. ·J Gastrointest Surg · Pubmed #22127781.

ABSTRACT: BACKGROUND: Pancreatic adenocarcinoma is the fourth leading cause of cancer death. METHODS: A prospective cohort study was undertaken between 2003 and 2011 at a tertiary care centre in Toronto, Canada. Two hundred and sixty-two subjects were enrolled based on an elevated estimated lifetime risk for pancreatic cancer due to known genetic mutations and/or cancer family history. Subjects underwent annual magnetic resonance imaging, followed by additional investigations if abnormal findings were detected. Evidence of malignancy or suspicious macroscopic abnormalities prompted referral for surgical intervention. RESULTS: Average length of follow-up was 4.2 years, during which 84/262 (32%) subjects demonstrated pancreatic abnormalities. Three participants developed pancreatic adenocarcinoma (one 1.5-cm tumor was resected but recurred, while the other two subjects developed metastatic cancer), and a fourth participant developed a pancreatic neuroendocrine tumor that was resected. Fifteen subjects had radiologic evidence of branch-duct intraductal papillary mucinous neoplasms, of which two underwent surgical resection. Sixty-five subjects had simple pancreatic cysts that have remained stable. CONCLUSION: Magnetic resonance imaging can detect small pancreatic tumors and cystic lesions, but further improvement in sensitivity is needed. An understanding of the natural history of pre-invasive lesions in members of high-risk families is necessary for developing a more effective screening program.

4 Article Management of pancreatic adenocarcinoma in Ontario, Canada: a population-based study using novel case ascertainment. 2011

Borgida, Ayelet Eppel / Ashamalla, Shady / Al-Sukhni, Wigdan / Rothenmund, Heidi / Urbach, David / Moore, Malcolm / Cotterchio, Michelle / Gallinger, Steven. ·Mount Sinai Hospital, Joseph and Wolf Lebovic Health Complex, 69 Murray Street, Toronto, Ontario. aborgida@mtsinai.on.ca ·Can J Surg · Pubmed #21251433.

ABSTRACT: BACKGROUND: Pancreatic adenocarcinoma (PA) is largely incurable, although recent progress has been made in the safety of surgery for PA and in adjuvant and palliative chemotherapy. The purpose of this study was to describe the management of PA in Ontario, Canada. METHODS: The Pathology Information Management System (PIMS), which uses electronic pathology reporting (E-path), was used to rapidly identify and recruit patients based on a pathologic diagnosis of PA between 2003 and 2006. Patients were mailed questionnaires for additional data. RESULTS: The patient participation rate was 26% (351 of 1325). Nonresponders were more likely to be older than 70 years (43% v. 28%, p < 0.001) and to have received treatment in nonacademic centres (53% v. 34%, p < 0.001). Fifty-four percent of responders underwent a potentially curative operation, and most (77%) were 70 years or younger (p = 0.03). Completed resections were documented in 83% of patients who underwent exploratory surgery with curative intent; 17% of patients had unresectable and/or metastatic disease at laparotomy. Of the completed resections, 24% were performed in nonacademic centres with a 32% positive margin rate; 76% were performed in academic centres with a 29% positive margin rate (p = 0.84). Resections with curative intent were less frequently aborted in academic centres (10% v. 33%, p < 0.001). Of the patients who responded to our questionnaire, 43% received chemotherapy and 7% participated in clinical trials. CONCLUSION: Despite using PIMS and E-path, the response rate for this study was low (< 30%). Nonresponders were older and more commonly treated in nonacademic centres. Patients undergoing surgery in academic centres had higher resection rates. The rate of adjuvant and palliative chemotherapy was stage-dependent and low.