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Pancreatic Neoplasms: HELP
Articles by Spring Holter
Based on 11 articles published since 2009
(Why 11 articles?)
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Between 2009 and 2019, S. Holter wrote the following 11 articles about Pancreatic Neoplasms.
 
+ Citations + Abstracts
1 Article Candidate DNA repair susceptibility genes identified by exome sequencing in high-risk pancreatic cancer. 2016

Smith, Alyssa L / Alirezaie, Najmeh / Connor, Ashton / Chan-Seng-Yue, Michelle / Grant, Robert / Selander, Iris / Bascuñana, Claire / Borgida, Ayelet / Hall, Anita / Whelan, Thomas / Holter, Spring / McPherson, Treasa / Cleary, Sean / Petersen, Gloria M / Omeroglu, Atilla / Saloustros, Emmanouil / McPherson, John / Stein, Lincoln D / Foulkes, William D / Majewski, Jacek / Gallinger, Steven / Zogopoulos, George. ·Research Institute of the McGill University Health Centre, 1001 Décarie Boulevard, Montreal, QC, Canada H4A 3J1; Goodman Cancer Research Centre, McGill University, 1160 Pine Avenue West, Montreal, QC, Canada H3A 1A3. · McGill University and Genome Quebec Innovation Centre, 740 Dr. Penfield Avenue, Montreal, QC, Canada H3A 0G1. · Lunenfeld-Tanenbaum Research Institute, Mount Sinai Hospital, 600 University Avenue, Toronto, ON, Canada M5G 1X5; MaRS Centre, Ontario Institute for Cancer Research, 661 University Avenue, Toronto, ON, Canada M5G 0A3. · MaRS Centre, Ontario Institute for Cancer Research, 661 University Avenue, Toronto, ON, Canada M5G 0A3. · Lunenfeld-Tanenbaum Research Institute, Mount Sinai Hospital, 600 University Avenue, Toronto, ON, Canada M5G 1X5. · Lunenfeld-Tanenbaum Research Institute, Mount Sinai Hospital, 600 University Avenue, Toronto, ON, Canada M5G 1X5; Zane Cohen Centre for Digestive Diseases, Mount Sinai Hospital, 60 Murray Street, Toronto, ON, Canada M5T 3H7. · Department of Health Sciences Research, Mayo Clinic College of Medicine, 200 First Street SW, Rochester, MN 55905, USA. · Department of Pathology, McGill University Health Centre, 1001 Décarie Boulevard, Montreal, QC, Canada H4A 3J1. · Department of Medical Oncology, Hereditary Cancer Clinic, University Hospital of Heraklion, Voutes, Heraklion 71110, Greece. · Program in Cancer Genetics, Departments of Oncology and Human Genetics, Sir Mortimer B. Davis-Jewish General Hospital, McGill University, 3755 Côte-Ste-Catherine Road, Montreal, QC, Canada H3T 1E2. · Lunenfeld-Tanenbaum Research Institute, Mount Sinai Hospital, 600 University Avenue, Toronto, ON, Canada M5G 1X5; MaRS Centre, Ontario Institute for Cancer Research, 661 University Avenue, Toronto, ON, Canada M5G 0A3; Zane Cohen Centre for Digestive Diseases, Mount Sinai Hospital, 60 Murray Street, Toronto, ON, Canada M5T 3H7. Electronic address: steven.gallinger@uhn.ca. · Research Institute of the McGill University Health Centre, 1001 Décarie Boulevard, Montreal, QC, Canada H4A 3J1; Goodman Cancer Research Centre, McGill University, 1160 Pine Avenue West, Montreal, QC, Canada H3A 1A3; Program in Cancer Genetics, Departments of Oncology and Human Genetics, Sir Mortimer B. Davis-Jewish General Hospital, McGill University, 3755 Côte-Ste-Catherine Road, Montreal, QC, Canada H3T 1E2. Electronic address: george.zogopoulos@mcgill.ca. ·Cancer Lett · Pubmed #26546047.

ABSTRACT: The genetic basis underlying the majority of hereditary pancreatic adenocarcinoma (PC) is unknown. Since DNA repair genes are widely implicated in gastrointestinal malignancies, including PC, we hypothesized that there are novel DNA repair PC susceptibility genes. As germline DNA repair gene mutations may lead to PC subtypes with selective therapeutic responses, we also hypothesized that there is an overall survival (OS) difference in mutation carriers versus non-carriers. We therefore interrogated the germline exomes of 109 high-risk PC cases for rare protein-truncating variants (PTVs) in 513 putative DNA repair genes. We identified PTVs in 41 novel genes among 36 kindred. Additional genetic evidence for causality was obtained for 17 genes, with FAN1, NEK1 and RHNO1 emerging as the strongest candidates. An OS difference was observed for carriers versus non-carriers of PTVs with early stage (≤IIB) disease. This adverse survival trend in carriers with early stage disease was also observed in an independent series of 130 PC cases. We identified candidate DNA repair PC susceptibility genes and suggest that carriers of a germline PTV in a DNA repair gene with early stage disease have worse survival.

2 Article BRCA1 and BRCA2 mutations sensitize to chemotherapy in patient-derived pancreatic cancer xenografts. 2015

Lohse, I / Borgida, A / Cao, P / Cheung, M / Pintilie, M / Bianco, T / Holter, S / Ibrahimov, E / Kumareswaran, R / Bristow, R G / Tsao, M-S / Gallinger, S / Hedley, D W. ·Ontario Cancer Institute and Campbell Family Cancer Research Institute, Princess Margaret Cancer Centre, University Health Network, Toronto, Ontario, Canada M5G 2M9. · Mount Sinai Hospital, Joseph and Wolf Lebovic Health Complex, Toronto, Ontario, Canada M5G 2M9. · 1] Mount Sinai Hospital, Joseph and Wolf Lebovic Health Complex, Toronto, Ontario, Canada M5G 2M9 [2] Translational Research Initiative in Pancreas Cancer, Ontario Institute for Cancer Research, Toronto, Ontario, Canada M5G 2M9. · 1] Ontario Cancer Institute and Campbell Family Cancer Research Institute, Princess Margaret Cancer Centre, University Health Network, Toronto, Ontario, Canada M5G 2M9 [2] Mount Sinai Hospital, Joseph and Wolf Lebovic Health Complex, Toronto, Ontario, Canada M5G 2M9. · 1] Ontario Cancer Institute and Campbell Family Cancer Research Institute, Princess Margaret Cancer Centre, University Health Network, Toronto, Ontario, Canada M5G 2M9 [2] Department of Pathology, University Health Network, Toronto, Ontario, Canada M5G 2M9 [3] Department of Laboratory Medicine and Pathobiology, University of Toronto, Toronto, Ontario, Canada M5G 2M9. · 1] Ontario Cancer Institute and Campbell Family Cancer Research Institute, Princess Margaret Cancer Centre, University Health Network, Toronto, Ontario, Canada M5G 2M9 [2] Translational Research Initiative in Pancreas Cancer, Ontario Institute for Cancer Research, Toronto, Ontario, Canada M5G 2M9 [3] Department of Medical Oncology and Haematology, Princess Margaret Cancer Centre, Toronto, Ontario, Canada M5G 2M9. ·Br J Cancer · Pubmed #26180923.

ABSTRACT: BACKGROUND: Germline mutations of the BRCA tumour suppressors have been associated with increased risk of pancreatic cancer. Clinical evidence suggests that these patients may be more sensitive to treatment with cisplatin. As the frequency of germline BRCA mutations is low, definitive experimental data to support the clinical observations are still missing. METHODS: We tested gemcitabine and cisplatin sensitivity of four BRCA1 and BRCA2 mutant and three BRCA1 and BRCA2 wild-type (WT) patient-derived pancreatic cancer xenografts. RESULTS: We observed treatment sensitivity to gemcitabine and cisplatin in the BRCA WT and mutant models. The BRCA1 and BRCA2 mutant xenografts were significantly more sensitive to cisplatin although these models also showed sensitivity to gemcitabine. The BRCA1 and BRCA2 WT models showed sensitivity to gemcitabine but not cisplatin. Treatment sensitivity in the xenograft models closely resembled treatment response in the corresponding patients. DISCUSSION: We have characterised a panel of xenografts derived from pancreatic cancer patients carrying germline BRCA mutations, and shown that their genetic features resemble the patient donor. Our results support further clinical testing of treatment regimens combining gemcitabine and platinum drugs in this patient population, as well as preclinical research aiming to identify mechanisms of cisplatin resistance in BRCA mutant pancreatic cancers.

3 Article Germline BRCA Mutations in a Large Clinic-Based Cohort of Patients With Pancreatic Adenocarcinoma. 2015

Holter, Spring / Borgida, Ayelet / Dodd, Anna / Grant, Robert / Semotiuk, Kara / Hedley, David / Dhani, Neesha / Narod, Steven / Akbari, Mohammad / Moore, Malcolm / Gallinger, Steven. ·Spring Holter, Ayelet Borgida, Robert Grant, Kara Semotiuk, and Steven Gallinger, Lunenfeld-Tanenbaum Research Institute, Mount Sinai Hospital · Anna Dodd, David Hedley, Neesha Dhani, Malcolm Moore, and Steven Gallinger, McCain Pancreatic Cancer Centre, University Health Network · and Steven Narod and Mohammad Akbari, Women's College Research Institute, Toronto, Ontario, Canada. ·J Clin Oncol · Pubmed #25940717.

ABSTRACT: PURPOSE: The main purpose of this study was to determine the prevalence of pathogenic BRCA1 and BRCA2 mutations in a consecutively ascertained clinic-based cohort of patients with pancreatic ductal adenocarcinoma and describe the clinical and family history characteristics. PATIENTS AND METHODS: Unselected, consecutive, incident patients with pancreatic ductal adenocarcinoma were recruited at a single cancer center over a 2-year period. Participants provided blood for DNA analysis and cancer family history, and cancer treatment records were reviewed. DNA from all patients was analyzed by Sanger sequencing and multiplex ligation-dependent probe amplification for germline variants in BRCA1 and BRCA2. RESULTS: Three hundred six patients were eligible for analysis. Pathogenic germline BRCA mutations were identified in 14 patients (4.6%; 95% CI, 2.2% to 6.9%), including 11 patients with a BRCA2 mutation and three patients with a BRCA1 mutation. Having a cancer family history that met genetic testing criteria of the National Comprehensive Cancer Network or the Ontario Ministry of Health and Long-Term Care or self-reporting as Ashkenazi Jewish was significantly associated with BRCA mutation carrier status (P=.02, P<.001, and P=.05, respectively). However, the majority of the BRCA mutation-positive patients did not actually meet these genetic testing criteria. CONCLUSION: Pathogenic BRCA mutations were identified in 4.6% of a large cohort of clinic-based patients. Considering the implications for family members of BRCA carriers, and possibly tailored chemotherapeutic treatment of patients, our finding has implications for broader BRCA genetic testing for patients with pancreatic ductal adenocarcinoma.

4 Article Prevalence of germline mutations in cancer predisposition genes in patients with pancreatic cancer. 2015

Grant, Robert C / Selander, Iris / Connor, Ashton A / Selvarajah, Shamini / Borgida, Ayelet / Briollais, Laurent / Petersen, Gloria M / Lerner-Ellis, Jordan / Holter, Spring / Gallinger, Steven. ·Ontario Institute for Cancer Research, Canada; Department of Medicine, University of Toronto, Canada. · Lunenfeld-Tanenbaum Research Institute, Mount Sinai Hospital, Canada. · Division of General Surgery, Department of Surgery, University Health Network, University of Toronto, Canada. · Laboratory Medicine and Pathobiology, University of Toronto, Canada. · Department of Health Sciences Research, Mayo Clinic, Rochester, Minnesota. · Ontario Institute for Cancer Research, Canada; Laboratory Medicine and Pathobiology, University of Toronto, Canada; Pathology and Laboratory Medicine, Mount Sinai Hospital, Canada. · Ontario Institute for Cancer Research, Canada; Lunenfeld-Tanenbaum Research Institute, Mount Sinai Hospital, Canada; Division of General Surgery, Department of Surgery, University Health Network, University of Toronto, Canada. Electronic address: steven.gallinger@uhn.on.ca. ·Gastroenterology · Pubmed #25479140.

ABSTRACT: BACKGROUND & AIMS: We investigated the prevalence of germline mutations in APC, ATM, BRCA1, BRCA2, CDKN2A, MLH1, MSH2, MSH6, PALB2, PMS2, PRSS1, STK11, and TP53 in patients with pancreatic cancer. METHODS: The Ontario Pancreas Cancer Study enrolls consenting participants with pancreatic cancer from a province-wide electronic pathology database; 708 probands were enrolled from April 2003 through August 2012. To improve the precision of BRCA2 prevalence estimates, 290 probands were selected from 3 strata, based on family history of breast and/or ovarian cancer, pancreatic cancer, or neither. Germline DNA was analyzed by next-generation sequencing using a custom multiple-gene panel. Mutation prevalence estimates were calculated from the sample for the entire cohort. RESULTS: Eleven pathogenic mutations were identified: 3 in ATM, 1 in BRCA1, 2 in BRCA2, 1 in MLH1, 2 in MSH2, 1 in MSH6, and 1 in TP53. The prevalence of mutations in all 13 genes was 3.8% (95% confidence interval, 2.1%-5.6%). Carrier status was associated significantly with breast cancer in the proband or first-degree relative (P < .01), and with colorectal cancer in the proband or first-degree relative (P < .01), but not family history of pancreatic cancer, age at diagnosis, or stage at diagnosis. Of patients with a personal or family history of breast and colorectal cancer, 10.7% (95% confidence interval, 4.4%-17.0%) and 11.1% (95% confidence interval, 3.0%-19.1%) carried pathogenic mutations, respectively. CONCLUSIONS: A small but clinically important proportion of pancreatic cancer is associated with mutations in known predisposition genes. The heterogeneity of mutations identified in this study shows the value of using a multiple-gene panel in pancreatic cancer.

5 Article Overall survival and clinical characteristics of pancreatic cancer in BRCA mutation carriers. 2014

Golan, T / Kanji, Z S / Epelbaum, R / Devaud, N / Dagan, E / Holter, S / Aderka, D / Paluch-Shimon, S / Kaufman, B / Gershoni-Baruch, R / Hedley, D / Moore, M J / Friedman, E / Gallinger, S. ·1] The Oncology Institute the Chaim Sheba Medical Center, Tel Hashomer, Israel [2] The Sackler School of Medicine, Tel Aviv University, Tel Aviv, Israel. · 1] Department of Surgery, University Health Network, Toronto, ON, Canada [2] Samuel Lunenfeld Research Institute of Mount Sinai Hospital, Toronto, ON, Canada. · 1] Department of Oncology, Rambam Health Care Campus, University of Haifa, Haifa, Israel [2] Technion, Faculty of Medicine, Haifa, Israel. · 1] Faculty of Social Welfare and Health Sciences, University of Haifa, Haifa, Israel [2] Institute of Human Genetics, Rambam Health Care Campus, University of Haifa, Haifa, Israel. · 1] Technion, Faculty of Medicine, Haifa, Israel [2] Institute of Human Genetics, Rambam Health Care Campus, University of Haifa, Haifa, Israel. · Department of Surgery, University Health Network, Toronto, ON, Canada. · 1] The Sackler School of Medicine, Tel Aviv University, Tel Aviv, Israel [2] The Susanne Levy Gertner Oncogenetics Unit Chaim Sheba Medical Center, Tel Hashomer, Israel. ·Br J Cancer · Pubmed #25072261.

ABSTRACT: BACKGROUND: The BRCA1/2 proteins are involved in regulation of cellular proliferation by DNA damage repair via homologous recombination. Therefore, BRCA1/2 mutation carriers with pancreatic cancer may have distinct biologic outcomes. METHODS: Patients with BRCA1/2-associated pancreatic ductal adenocarcinoma (PDAC) diagnosed between January 1994 and December 2012 were identified from databases at three participating institutions. Clinical data were collected. Disease-free survival and overall survival (OS) were analysed. RESULTS: Overall, 71 patients with PDAC and BRCA1 (n=21), BRCA2 (n=49) or both (n=1) mutations were identified. Mean age at diagnosis was 60.3 years (range 33-83), 81.7% (n=58) had any family history of malignancy; 30% (n=21) underwent primary resection. Out of 71 participants, 12 received experimental therapy; one patient had missing data, these 13 cases were excluded from OS analysis. Median OS for 58 patients was 14 months (95% CI 10-23 months). Median OS for patients with stage 1/2 disease has not been reached with 52% still alive at 60 months. Median OS for stage 3/4 was 12 months (95% CI 6-15). Superior OS was observed for patients with stage 3/4 treated with platinum vs those treated with non-platinum chemotherapies (22 vs 9 months; P=0.039). CONCLUSION: Superior OS was observed for advanced-disease BRCA-associated PDAC with platinum exposure.

6 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.

7 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.

8 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.

9 Article Moderators of cancer-related distress and worry after a pancreatic cancer genetic counseling and screening intervention. 2012

Hart, Stacey L / Torbit, Lindsey A / Crangle, Cassandra J / Esplen, Mary Jane / Holter, Spring / Semotiuk, Kara / Borgida, Ayelet / Ardiles, Paola / Rothenmund, Heidi / Gallinger, Steve. ·Ryerson University, Psychology, Toronto, Ontario, Canada. stacey.hart@psych.ryerson.ca ·Psychooncology · Pubmed #21774034.

ABSTRACT: OBJECTIVES: Although the hereditary breast and ovarian cancer literature has demonstrated short-term gains in psychological adjustment following genetic counseling, there has been limited research examining long-term outcomes and moderators. Moreover, there has been minimal research into the psychological effects of this intervention in populations at high risk for pancreatic cancer. This study examines the long-term effects of pancreatic cancer screening and genetic counseling on cancer-related distress and cancer worry in a high-risk population at 1-year follow-up. Additionally, this study explores potential moderators of the effectiveness of this intervention. METHODS: One hundred twenty-nine participants with familial pancreatic cancer or with the BRCA2 gene mutation completed a baseline questionnaire prior to their first pancreatic cancer screening and genetic counseling session. Participants also completed questionnaires at 3- and 12-month follow-up. RESULTS: Cancer-related intrusive thoughts decreased significantly over time, whereas cancer-related worry decreased at 3 months and showed a small but significant increase at 1 year. Age and baseline distress exhibited moderator effects. Younger individuals showed a significant decrease in cancer-related intrusive thoughts, cancer-related avoidant thoughts, and cancer worry. Additionally, individuals with greater baseline distress showed a significant decrease in cancer-related intrusive thoughts over time. CONCLUSIONS: Analysis of the long-term effects of pancreatic cancer screening and genetic testing reveal psychological gains that are maintained at 1-year follow-up. This intervention is particularly effective for younger participants and individuals with greater baseline distress.

10 Article Pancreatic cancer risk counselling and screening: impact on perceived risk and psychological functioning. 2010

Maheu, Christine / Vodermaier, Andrea / Rothenmund, Heidi / Gallinger, Steve / Ardiles, Paola / Semotiuk, Kara / Holter, Spring / Thayalan, Saumea / Esplen, Mary Jane. ·York University, Toronto, ON, Canada. cmaheu@uhnres.utoronto.ca ·Fam Cancer · Pubmed #20623197.

ABSTRACT: Individuals at increased risk for pancreatic cancer who undergo screening can experience psychological and emotional distress. The objective of this study is to determine whether individuals participating in a pancreatic cancer screening program experience disruptions in risk perception, cancer-related anxiety or emotional distress. A pretestposttest design was used to examine perceived risk and psychological functioning of individuals participating in a pancreatic cancer screening protocol. The screening protocol includes genetic counselling, transcutaneous abdominal ultrasound, magnetic resonance imaging, and blood collection and eligible participants included individuals with a family history of pancreatic cancer or BRCA2 mutation carriers. At baseline, participants (n = 198) showed low to moderate levels of risk perception, pancreatic cancer-related anxiety, and general distress. Participants with familial pancreatic cancer (FPC) (n = 131) endorsed higher risk perception of pancreatic cancer than the BRCA2 carriers (n = 67) (perceived lifetime risk 42 vs. 15%), but did not differ on cancer worry or general distress prior to the first study appointment. From baseline to 3 months follow-up, no significant time or time by group interactions emerged on risk perception or general distress, but cancer worry decreased over time for the FPC group regardless of the number of affected relatives. Our findings indicate that participation in a pancreatic cancer screening program does not lead to a significant increase in risk perception, cancer worry, or general distress and that participants with high baseline levels of risk perception and distress may benefit from a more comprehensive risk assessment and psychological support.

11 Minor Analysis of the gene coding for the BRCA2-interacting protein PALB2 in familial and sporadic pancreatic cancer. 2009

Tischkowitz, Marc D / Sabbaghian, Nelly / Hamel, Nancy / Borgida, Ayelet / Rosner, Chaim / Taherian, Nassim / Srivastava, Archana / Holter, Spring / Rothenmund, Heidi / Ghadirian, Parviz / Foulkes, William D / Gallinger, Steven. · ·Gastroenterology · Pubmed #19635604.

ABSTRACT: -- No abstract --