Publications by authors named "Carrie L Snyder"

17 Publications

  • Page 1 of 1

Efficacy of proximal colectomy for surgical management of right-sided first colorectal cancer in Lynch Syndrome mutation carriers.

Am J Surg 2018 07 8;216(1):99-105. Epub 2017 Nov 8.

Division of Clinical Research and Evaluative Sciences, Creighton University, School of Medicine, 2500 California Plaza, Omaha, NE 68178, USA.

Background: This study analyzes the occurrence of colorectal cancer (CRC) in Lynch syndrome (LS) mutation carriers, interval until diagnosis of metachronous CRC, and survival after proximal colectomy (PC) compared with total (TC) and subtotal colectomy (STC) for right-sided first CRC in LS mutation carriers.

Methods: Sixty-four LS mutation carriers with right-sided first CRC treated with PC or TC + STC were confirmed by clinical records. Bivariate analyses were examined for significance and life tables were generated for risk of metachronous CRC and survival estimates following surgery.

Results: One of 16 (6.3%) mutation carriers treated with TC + STC developed subsequent CRC compared with 13/48 (27%) treated by PC. There was no significant difference in survival estimates between PC compared with TC + STC through 25 years after surgery.

Conclusion: Risk of subsequent CRC and survival estimates following PC and TC + STC should be considered in surgical management of right-sided first CRC in LS mutation carriers.
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http://dx.doi.org/10.1016/j.amjsurg.2017.11.003DOI Listing
July 2018

Introduction to special issue of Familial Cancer.

Fam Cancer 2016 07;15(3):357-8

, Omaha, NE, USA.

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http://dx.doi.org/10.1007/s10689-016-9909-1DOI Listing
July 2016

Should risk-reducing surgery in women from hereditary breast ovarian cancer families be confined to removal of the fallopian tubes with ovarian conservation?

Womens Health (Lond) 2015 Jul 6;11(4):423-7. Epub 2015 Aug 6.

Department of Preventive Medicine & Public Health, Creighton University, HLSB Room 202, 2500 California Plaza, Omaha, NE 68178, USA.

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http://dx.doi.org/10.2217/whe.15.26DOI Listing
July 2015

Endometrial cancers in mutation carriers from hereditary breast ovarian cancer syndrome kindreds: report from the Creighton University Hereditary Cancer Registry with review of the implications.

Int J Gynecol Cancer 2015 May;25(4):650-6

Departments of *Obstetrics and Gynecology, †Preventive Medicine and Public Health, and ‡Pathology, Creighton University School of Medicine, Omaha, NE.

Objective: The aim of this study was to categorize and report endometrial cancers in mutation carriers from hereditary breast ovarian cancer families.

Methods: Our Hereditary Cancer Registry was searched for gynecologic and peritoneal cancers linked to mutations in BRCA1 or BRCA2. Invasive cancers were registered in 101 mutation carriers with complete pathology reports. Efforts were made to secure diagnostic surgical pathology tissues for review. All records and available diagnostic slides were meticulously studied, and primary cancers were classified.

Findings: Eight malignancies were classified as primary endometrial cancers. Five of these were low- or intermediate-grade endometrioid carcinomas, and 3 were pure serous carcinomas or contained serous carcinoma elements mixed with high-grade endometrioid carcinoma. Breast cancers were diagnosed in 5 patients before and in 1 patient after endometrial carcinoma. Three endometrioid carcinomas were preceded by estrogen treatment, 2 for many years and the other for only 2 months, and 2 of the patients with serous carcinoma had been treated with tamoxifen.

Conclusions: The finding that 8 of gynecologic and peritoneal cancers in 101 mutation carriers were endometrial cancers with a smaller proportion of endometrioid carcinomas than reported in general populations is added to the current controversial literature on endometrial cancer, particularly regarding serous carcinomas, in hereditary breast ovarian cancer syndrome. Well-designed prospective programs for standardized surgical and pathologic handling, processing, and reporting are essential for working out the pathogenesis, true risks, and best management of this disease in carriers of deleterious BRCA1 and BRCA2 germline mutations.
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http://dx.doi.org/10.1097/IGC.0000000000000402DOI Listing
May 2015

Milestones of Lynch syndrome: 1895-2015.

Nat Rev Cancer 2015 03 12;15(3):181-94. Epub 2015 Feb 12.

Department of Medicine (Oncology), Stanford Cancer Institute, Stanford University, Grant Building S169, 1291 Welch Road, Stanford, California 94305, USA.

Lynch syndrome, which is now recognized as the most common hereditary colorectal cancer condition, is characterized by the predisposition to a spectrum of cancers, primarily colorectal cancer and endometrial cancer. We chronicle over a century of discoveries that revolutionized the diagnosis and clinical management of Lynch syndrome, beginning in 1895 with Warthin's observations of familial cancer clusters, through the clinical era led by Lynch and the genetic era heralded by the discovery of causative mutations in mismatch repair (MMR) genes, to ongoing challenges.
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http://dx.doi.org/10.1038/nrc3878DOI Listing
March 2015

Common variants at the 19p13.1 and ZNF365 loci are associated with ER subtypes of breast cancer and ovarian cancer risk in BRCA1 and BRCA2 mutation carriers.

Authors:
Fergus J Couch Mia M Gaudet Antonis C Antoniou Susan J Ramus Karoline B Kuchenbaecker Penny Soucy Jonathan Beesley Xiaoqing Chen Xianshu Wang Tomas Kirchhoff Lesley McGuffog Daniel Barrowdale Andrew Lee Sue Healey Olga M Sinilnikova Irene L Andrulis Hilmi Ozcelik Anna Marie Mulligan Mads Thomassen Anne-Marie Gerdes Uffe Birk Jensen Anne-Bine Skytte Torben A Kruse Maria A Caligo Anna von Wachenfeldt Gisela Barbany-Bustinza Niklas Loman Maria Soller Hans Ehrencrona Per Karlsson Katherine L Nathanson Timothy R Rebbeck Susan M Domchek Ania Jakubowska Jan Lubinski Katarzyna Jaworska Katarzyna Durda Elzbieta Zlowocka Tomasz Huzarski Tomasz Byrski Jacek Gronwald Cezary Cybulski Bohdan Górski Ana Osorio Mercedes Durán María Isabel Tejada Javier Benitez Ute Hamann Frans B L Hogervorst Theo A van Os Flora E van Leeuwen Hanne E J Meijers-Heijboer Juul Wijnen Marinus J Blok Marleen Kets Maartje J Hooning Rogier A Oldenburg Margreet G E M Ausems Susan Peock Debra Frost Steve D Ellis Radka Platte Elena Fineberg D Gareth Evans Chris Jacobs Rosalind A Eeles Julian Adlard Rosemarie Davidson Diana M Eccles Trevor Cole Jackie Cook Joan Paterson Carole Brewer Fiona Douglas Shirley V Hodgson Patrick J Morrison Lisa Walker Mary E Porteous M John Kennedy Lucy E Side Betsy Bove Andrew K Godwin Dominique Stoppa-Lyonnet Marion Fassy-Colcombet Laurent Castera François Cornelis Sylvie Mazoyer Mélanie Léoné Nadia Boutry-Kryza Brigitte Bressac-de Paillerets Olivier Caron Pascal Pujol Isabelle Coupier Capucine Delnatte Linda Akloul Henry T Lynch Carrie L Snyder Saundra S Buys Mary B Daly Marybeth Terry Wendy K Chung Esther M John Alexander Miron Melissa C Southey John L Hopper David E Goldgar Christian F Singer Christine Rappaport Muy-Kheng M Tea Anneliese Fink-Retter Thomas V O Hansen Finn C Nielsen Aðalgeir Arason Joseph Vijai Sohela Shah Kara Sarrel Mark E Robson Marion Piedmonte Kelly Phillips Jack Basil Wendy S Rubinstein John Boggess Katie Wakeley Amanda Ewart-Toland Marco Montagna Simona Agata Evgeny N Imyanitov Claudine Isaacs Ramunas Janavicius Conxi Lazaro Ignacio Blanco Lidia Feliubadalo Joan Brunet Simon A Gayther Paul P D Pharoah Kunle O Odunsi Beth Y Karlan Christine S Walsh Edith Olah Soo Hwang Teo Patricia A Ganz Mary S Beattie Elizabeth J van Rensburg Cecelia M Dorfling Orland Diez Ava Kwong Rita K Schmutzler Barbara Wappenschmidt Christoph Engel Alfons Meindl Nina Ditsch Norbert Arnold Simone Heidemann Dieter Niederacher Sabine Preisler-Adams Dorothea Gadzicki Raymonda Varon-Mateeva Helmut Deissler Andrea Gehrig Christian Sutter Karin Kast Britta Fiebig Wolfram Heinritz Trinidad Caldes Miguel de la Hoya Taru A Muranen Heli Nevanlinna Marc D Tischkowitz Amanda B Spurdle Susan L Neuhausen Yuan Chun Ding Noralane M Lindor Zachary Fredericksen V Shane Pankratz Paolo Peterlongo Siranoush Manoukian Bernard Peissel Daniela Zaffaroni Monica Barile Loris Bernard Alessandra Viel Giuseppe Giannini Liliana Varesco Paolo Radice Mark H Greene Phuong L Mai Douglas F Easton Georgia Chenevix-Trench Kenneth Offit Jacques Simard

Cancer Epidemiol Biomarkers Prev 2012 Apr 20;21(4):645-57. Epub 2012 Feb 20.

Departments of Laboratory Medicine and Pathology, Mayo Clinic, 200 First Street SW, Rochester, MN 55905, USA.

Background: Genome-wide association studies (GWAS) identified variants at 19p13.1 and ZNF365 (10q21.2) as risk factors for breast cancer among BRCA1 and BRCA2 mutation carriers, respectively. We explored associations with ovarian cancer and with breast cancer by tumor histopathology for these variants in mutation carriers from the Consortium of Investigators of Modifiers of BRCA1/2 (CIMBA).

Methods: Genotyping data for 12,599 BRCA1 and 7,132 BRCA2 mutation carriers from 40 studies were combined.

Results: We confirmed associations between rs8170 at 19p13.1 and breast cancer risk for BRCA1 mutation carriers [HR, 1.17; 95% confidence interval (CI), 1.07-1.27; P = 7.42 × 10(-4)] and between rs16917302 at ZNF365 (HR, 0.84; 95% CI, 0.73-0.97; P = 0.017) but not rs311499 at 20q13.3 (HR, 1.11; 95% CI, 0.94-1.31; P = 0.22) and breast cancer risk for BRCA2 mutation carriers. Analyses based on tumor histopathology showed that 19p13 variants were predominantly associated with estrogen receptor (ER)-negative breast cancer for both BRCA1 and BRCA2 mutation carriers, whereas rs16917302 at ZNF365 was mainly associated with ER-positive breast cancer for both BRCA1 and BRCA2 mutation carriers. We also found for the first time that rs67397200 at 19p13.1 was associated with an increased risk of ovarian cancer for BRCA1 (HR, 1.16; 95% CI, 1.05-1.29; P = 3.8 × 10(-4)) and BRCA2 mutation carriers (HR, 1.30; 95% CI, 1.10-1.52; P = 1.8 × 10(-3)).

Conclusions: 19p13.1 and ZNF365 are susceptibility loci for ovarian cancer and ER subtypes of breast cancer among BRCA1 and BRCA2 mutation carriers.

Impact: These findings can lead to an improved understanding of tumor development and may prove useful for breast and ovarian cancer risk prediction for BRCA1 and BRCA2 mutation carriers.
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http://dx.doi.org/10.1158/1055-9965.EPI-11-0888DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3319317PMC
April 2012

Modification of BRCA1-Associated Breast and Ovarian Cancer Risk by BRCA1-Interacting Genes.

Cancer Res 2011 Sep 28;71(17):5792-805. Epub 2011 Jul 28.

Abramson Cancer Center, Center for Clinical Epidemiology and Biostatistics, and Department of Medicine, The University of Pennsylvania Perleman School of Medicine, Philadelphia, Pennsylvania, USA.

Inherited BRCA1 mutations confer elevated cancer risk. Recent studies have identified genes that encode proteins that interact with BRCA1 as modifiers of BRCA1-associated breast cancer. We evaluated a comprehensive set of genes that encode most known BRCA1 interactors to evaluate the role of these genes as modifiers of cancer risk. A cohort of 2,825 BRCA1 mutation carriers was used to evaluate the association of haplotypes at ATM, BRCC36, BRCC45 (BRE), BRIP1 (BACH1/FANCJ), CTIP, ABRA1 (FAM175A), MERIT40, MRE11A, NBS1, PALB2 (FANCN), RAD50, RAD51, RAP80, and TOPBP1, and was associated with time to breast and ovarian cancer diagnosis. Statistically significant false discovery rate (FDR) adjusted P values for overall association of haplotypes (P(FDR)) with breast cancer were identified at ATM (P(FDR) = 0.029), BRCC45 (P(FDR) = 0.019), BRIP1 (P(FDR) = 0.008), CTIP (P(FDR) = 0.017), MERIT40 (P(FDR) = 0.019), NBS1 (P(FDR) = 0.003), RAD50 (P(FDR) = 0.014), and TOPBP1 (P(FDR) = 0.011). Haplotypes at ABRA1 (P(FDR) = 0.007), BRCC45 (P(FDR) = 0.016 and P(FDR) = 0.005 in two haplotype blocks), and RAP80 (P(FDR) < 0.001) were associated with ovarian cancer risk. Overall, the data suggest that genomic variation at multiple loci that encode proteins that interact biologically with BRCA1 are associated with modified breast cancer and ovarian cancer risk in women who carry BRCA1 mutations.
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http://dx.doi.org/10.1158/0008-5472.CAN-11-0773DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3170727PMC
September 2011

Familial plasma cell disorders and associated cancers.

Clin Lymphoma Myeloma Leuk 2011 Feb;11(1):80-1

Department of Preventive Medicine and Public Health, Creighton University, Omaha NE 68178, USA.

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http://dx.doi.org/10.3816/CLML.2011.n.013DOI Listing
February 2011

EPCAM deletions, Lynch syndrome, and cancer risk.

Lancet Oncol 2011 Jan;12(1):5-6

Department of Preventive Medicine and Public Health, Creighton University, 2500 California Plaza, Omaha, NE, USA.

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http://dx.doi.org/10.1016/S1470-2045(10)70291-6DOI Listing
January 2011

Family information service participation increases the rates of mutation testing among members of families with BRCA1/2 mutations.

Breast J 2009 Sep-Oct;15 Suppl 1:S20-4

Department of Preventive Medicine, Creighton University School of Medicine, Omaha, Nebraska 68178, USA.

Some members of hereditary breast-ovarian cancer (HBOC) families may not participate in BRCA testing to determine their mutation status in part because they are unaware of their cancer risk and the availability of BRCA testing. Participation in a family information service (FIS), of which we have provided more than 100 sessions during the past 30 years, has been seen to effectively allow family members to be educated regarding their cancer genetic risk and potential benefits from cancer control measures such as mutation testing. However, the effect of the FIS on the rate of mutation testing has not been studied. One thousand five hundred seventy-four eligible (>18-year old, at a 25% or higher pedigree risk) members from 60 extended HBOC families with BRCA1/2 mutations were invited to attend a FIS to learn about their risk and undergo genetic testing. The rates of mutation testing were compared between those who had attended an FIS, and those who had not with chi-squared test and logistic regression analysis. Seventy five percent (334/444) of FIS attendees had undergone mutation testing following or during an FIS which was significantly higher than the 33.8% (382/1130) rate among nonattendees (p < 0.0001). Logistic regression analysis showed that FIS attendance, breast-ovarian cancer history, gender, and age were significant variables for undertaking a mutation test. FIS attendance significantly increased the rate of mutation testing among high-risk family members.
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http://dx.doi.org/10.1111/j.1524-4741.2009.00807.xDOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2760017PMC
December 2009

Genetic counseling and the advanced practice oncology nursing role in a hereditary cancer prevention clinic: hereditary breast cancer focus (part I).

Breast J 2009 Sep-Oct;15 Suppl 1:S2-10

Department of Preventive Medicine, Creighton University, Omaha, Nebraska 68178, USA.

Interest in hereditary breast cancer has increased rapidly among all health care providers as well as the laity. A major problem for health care providers, however, is the time and skill required for gathering family history, interpreting the pedigree, and providing genetic counseling for the high-risk patient so that BRCA testing, when indicated, can be pursued and screening and prevention strategies employed by the patient. The fields of hereditary cancer and molecular biology have developed at a rate that makes it difficult for physicians to keep up with this explosive knowledge. Therefore, "Who is going to take care of all of these crucial matters for patient benefit?" is a germane question. Our experience has confirmed that the advanced practice oncology nurse who is interested in cancer genetics can become skilled at providing this service to the patient and his/her family. This study portrays the role of such an oncology nurse in meeting this important public health challenge, with special attention devoted to the logistics of this role in the rapidly emerging field of hereditary breast cancer.
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http://dx.doi.org/10.1111/j.1524-4741.2009.00802.xDOI Listing
December 2009

Genetic counseling and the advanced practice oncology nursing role in a hereditary cancer prevention clinic: hereditary breast cancer focus (part II).

Breast J 2009 Sep-Oct;15 Suppl 1:S11-9

Department of Preventive Medicine, Creighton University, Omaha, Nebraska 68178, USA.

Hereditary breast cancer (BC) is heterogeneous to the extent that no two high-risk patients can be considered as being the same. These individual differences are magnified further when patients' emotional response to all facets of hereditary BC are considered, particularly issues surrounding gene testing. A series of case histories have been provided that illustrate the wide range of attitudes, feelings, and emotional responses explained by patients when learning of their hereditary cancer risk status. The role of the oncology nurse-genetic counselor has been described in each of these family reports.
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http://dx.doi.org/10.1111/j.1524-4741.2009.00803.xDOI Listing
December 2009

Hereditary ovarian carcinoma: heterogeneity, molecular genetics, pathology, and management.

Mol Oncol 2009 Apr 21;3(2):97-137. Epub 2009 Feb 21.

Department of Preventive Medicine and Public Health, Creighton University School of Medicine, 2500 California Plaza, Omaha, NE 68178, USA.

Hereditary ovarian cancer accounts for at least 5% of the estimated 22,000 new cases of this disease during 2009. During this same time, over 15,000 will die from malignancy ascribed to ovarian origin. The bulk of these hereditary cases fits the hereditary breast-ovarian cancer syndrome, while virtually all of the remainder will be consonant with the Lynch syndrome, disorders which are autosomal dominantly inherited. Advances in molecular genetics have led to the identification of BRCA1 and BRCA2 gene mutations which predispose to the hereditary breast-ovarian cancer syndrome, and mutations in mismatch repair genes, the most common of which are MSH2 and MLH1, which predispose to Lynch syndrome. These discoveries enable relatively certain diagnosis, limited only by their variable penetrance, so that identification of mutation carriers through a comprehensive cancer family history might be possible. This paper reviews the subject of hereditary ovarian cancer, with particular attention to its molecular genetic basis, its pathology, and its phenotypic/genotypic heterogeneity.
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http://dx.doi.org/10.1016/j.molonc.2009.02.004DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2778287PMC
April 2009

BRCA1 and pancreatic cancer: pedigree findings and their causal relationships.

Cancer Genet Cytogenet 2005 Apr;158(2):119-25

Department of Preventive Medicine, Creighton University School of Medicine, 2500 California Plaza, Omaha, NE 68178, USA.

Anecdotal reports and series studies indicate that 5-10% of pancreatic cancer (PC) cases are familial. In addition, PC is associated with a variety of hereditary cancer syndromes. PC appears to be an integral cancer in the hereditary breast-ovarian cancer (HBOC) syndrome, with most notice given to the role of BRCA2. Our purpose is to call attention to BRCA1, which also predisposes to PC. Using data from our familial breast cancer registry, we identified 19 BRCA1/2 families that contain PC affecteds in the pedigrees, 15 with BRCA1 mutations and 4 with BRCA2 mutations. The association between BRCA2 and pancreatic cancer is well established; however, a definite link with pancreatic cancer in families carrying a BRCA1 mutation has been far less studied. Thus, the focus of this report is on 9 of the 15 BRCA1 families, in which PC affecteds were either confirmed carriers of the BRCA1 mutation or were inferred as probable obligate BRCA1 mutation carriers. The numbers are small, but nevertheless illustrate the finding of others of an apparent association between PC and BRCA1-mutation-bearing families. Given the dismal prognosis of PC, with the only current hope for survival being through surgical extirpation of the pancreas prior to metastasis, it is prudent that we realize the potential predisposition toward PC via BRCA1, in the hope of early diagnosis and prevention.
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http://dx.doi.org/10.1016/j.cancergencyto.2004.01.032DOI Listing
April 2005

Hereditary breast-ovarian cancer at the bedside: role of the medical oncologist.

J Clin Oncol 2003 Feb;21(4):740-53

Department of Preventive Medicine and Public Health, Creighton University School of Medicine, 2500 California Plaza, Omaha, NE 68178, USA.

Purpose: To provide practical considerations for diagnosing, counseling, and managing patients at high risk for hereditary breast cancer.

Design: We have studied 98 extended hereditary breast cancer (HBC)/hereditary breast-ovarian cancer (HBOC) families with BRCA1/2 germline mutations. From these families, 1,315 individuals were counseled and sampled for DNA testing. Herein, 716 of these individuals received their DNA test results in concert with genetic counseling. Several challenging pedigrees were selected from Creighton University's hereditary cancer family registry, as well as one family from Evanston/Northwestern Healthcare, to be discussed in this present report.

Results: Many obstacles were identified in diagnosis, counseling, and managing patients at high risk for HBC/HBOC. These obstacles were early noncancer death of key relatives, perception of insurance or employment discrimination, fear, anxiety, apprehension, reduced gene penetrance, and poor compliance. Other important issues such as physician culpability and malpractice implications for failure to collect or act on the cancer family history were identified.

Conclusion: When clinical gene testing emerged for BRCA1 and BRCA2, little was known about the efficacy of medical interventions. Potential barriers to uptake of testing were largely unexplored. Identification and referral of high-risk patients and families to genetic counseling can greatly enhance the care of the population at the highest risk for cancer. However, because premonitory physical stigmata are absent in most of these syndromes, an HBOC diagnosis may be missed unless a careful family history of cancer of the breast, ovary, or several integrally associated cancers is obtained.
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http://dx.doi.org/10.1200/JCO.2003.05.096DOI Listing
February 2003

Family with acute myelocytic leukemia, breast, ovarian, and gastrointestinal cancer.

Cancer Genet Cytogenet 2002 Aug;137(1):8-14

Department of Preventive Medicine and Public Health, Creighton University School of Medicine, 2500 California Plaza, Omaha, NE 68178, USA.

We report a multigeneration family in which hematologic cancers, particularly acute myelocytic leukemia (AML), and solid tumors were interspersed in cancer-prone lineages consistent with an autosomal dominant mode of genetic transmission. This combination of AML and solid tumors, in the absence of a known hereditary disorder such as the Li-Fraumeni syndrome, appears to be unique. This pedigree appears to support our hypothesis of a genetic susceptibility to both solid tumors and hematologic cancer in this kindred. Our study involved the genetic work-up of the family and the education of high-risk patients. Medical and pathology reports were retrieved for cross-referencing and verification of family reports. Blood collected through venipuncture and, when available, diagnostic bone marrow specimens were obtained for cytogenetic studies, inclusive of multiflour fluorescence in situ hybridization (M-FISH) and G-banding methods. Slides and tissue blocks were reviewed, when available. No constitutional chromosomal abnormality or rearrangement and no abnormal platelet count or function was identified in cancer-affected members or high-risk relatives in this family. However, two family members affected with AML exhibited abnormal acquired clones in their bone marrow specimens by both G-band studies and interphase FISH, both with a deletion of 5q.
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http://dx.doi.org/10.1016/s0165-4608(02)00537-xDOI Listing
August 2002