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Associations of Breast Cancer Risk Factors With Tumor Subtypes: A Pooled Analysis From the Breast Cancer Association Consortium Studies.

https://arctichealth.org/en/permalink/ahliterature99764
Source
J Natl Cancer Inst. 2010 Dec 29;
Publication Type
Article
Date
Dec-29-2010
Author
Xiaohong R Yang
Jenny Chang-Claude
Ellen L Goode
Fergus J Couch
Heli Nevanlinna
Roger L Milne
Mia Gaudet
Marjanka K Schmidt
Annegien Broeks
Angela Cox
Peter A Fasching
Rebecca Hein
Amanda B Spurdle
Fiona Blows
Kristy Driver
Dieter Flesch-Janys
Judith Heinz
Peter Sinn
Alina Vrieling
Tuomas Heikkinen
Kristiina Aittomäki
Päivi Heikkilä
Carl Blomqvist
Jolanta Lissowska
Beata Peplonska
Stephen Chanock
Jonine Figueroa
Louise Brinton
Per Hall
Kamila Czene
Keith Humphreys
Hatef Darabi
Jianjun Liu
Laura J Van 't Veer
Flora E van Leeuwen
Irene L Andrulis
Gord Glendon
Julia A Knight
Anna Marie Mulligan
Frances P O'Malley
Nayana Weerasooriya
Esther M John
Matthias W Beckmann
Arndt Hartmann
Sebastian B Weihbrecht
David L Wachter
Sebastian M Jud
Christian R Loehberg
Laura Baglietto
Dallas R English
Graham G Giles
Catriona A McLean
Gianluca Severi
Diether Lambrechts
Thijs Vandorpe
Caroline Weltens
Robert Paridaens
Ann Smeets
Patrick Neven
Hans Wildiers
Xianshu Wang
Janet E Olson
Victoria Cafourek
Zachary Fredericksen
Matthew Kosel
Celine Vachon
Helen E Cramp
Daniel Connley
Simon S Cross
Sabapathy P Balasubramanian
Malcolm W R Reed
Thilo Dörk
Michael Bremer
Andreas Meyer
Johann H Karstens
Aysun Ay
Tjoung-Won Park-Simon
Peter Hillemanns
Jose Ignacio Arias Pérez
Primitiva Menéndez Rodríguez
Pilar Zamora
Javier Benítez
Yon-Dschun Ko
Hans-Peter Fischer
Ute Hamann
Beate Pesch
Thomas Brüning
Christina Justenhoven
Hiltrud Brauch
Diana M Eccles
William J Tapper
Sue M Gerty
Elinor J Sawyer
Ian P Tomlinson
Angela Jones
Michael Kerin
Nicola Miller
Niall McInerney
Hoda Anton-Culver
Argyrios Ziogas
Chen-Yang Shen
Chia-Ni Hsiung
Pei-Ei Wu
Show-Lin Yang
Jyh-Cherng Yu
Shou-Tung Chen
Giu-Cheng Hsu
Christopher A Haiman
Brian E Henderson
Loic Le Marchand
Laurence N Kolonel
Annika Lindblom
Sara Margolin
Anna Jakubowska
Jan Lubinski
Tomasz Huzarski
Tomasz Byrski
Bohdan Górski
Jacek Gronwald
Maartje J Hooning
Antoinette Hollestelle
Ans M W van den Ouweland
Agnes Jager
Mieke Kriege
Madeleine M A Tilanus-Linthorst
Margriet Collée
Shan Wang-Gohrke
Katri Pylkäs
Arja Jukkola-Vuorinen
Kari Mononen
Mervi Grip
Pasi Hirvikoski
Robert Winqvist
Arto Mannermaa
Veli-Matti Kosma
Jaana Kauppinen
Vesa Kataja
Päivi Auvinen
Ylermi Soini
Reijo Sironen
Stig E Bojesen
David Dynnes Ørsted
Diljit Kaur-Knudsen
Henrik Flyger
Børge G Nordestgaard
Helene Holland
Georgia Chenevix-Trench
Siranoush Manoukian
Monica Barile
Paolo Radice
Susan E Hankinson
David J Hunter
Rulla Tamimi
Suleeporn Sangrajrang
Paul Brennan
James McKay
Fabrice Odefrey
Valerie Gaborieau
Peter Devilee
P E A Huijts
Raem Tollenaar
C. Seynaeve
Gillian S Dite
Carmel Apicella
John L Hopper
Fleur Hammet
Helen Tsimiklis
Letitia D Smith
Melissa C Southey
Manjeet K Humphreys
Douglas Easton
Paul Pharoah
Mark E Sherman
Montserrat Garcia-Closas
Author Affiliation
Affiliations of authors: Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Department of Health and Human Sciences, Rockville, MD (XRY, SC, JF, LBr, MES, MG-C); Section of Epidemiology and Genetics, Institute of Cancer Research, Sutton, Surrey, UK (MG-C); Division of Cancer Epidemiology, German Cancer Research Center, Heidelberg, Germany (JC-C, RH, AV); Department of Health Sciences Research (ELG, FJC, JEO, VC, ZF, MKo, CV); Department of Laboratory Medicine and Pathology (FJC, XW), Mayo Clinic, Rochester, MN; Department of Obstetrics and Gynecology (HN, THe), Department of Clinical Genetics (KA), Department of Pathology (PHe), and Department of Oncology (CB), Helsinki University Central Hospital, Helsinki, Finland; Genetic and Molecular Epidemiology Group (RLM), Human Cancer Genetic Group (JB), Spanish National Cancer Research Centre (CNIO), Madrid, Spain; Department of Epidemiology and Population Health, Albert Einstein College of Medicine, Bronx, NY (MGa); Amsterdam Breast Cancer Study, Netherlands Cancer Institute, Amsterdam, the Netherlands (MKS, AB, LJVV, FEvL); Institute for Cancer Studies, Department of Oncology (AC, DC,HEC), Academic Unit of Pathology (SCC), Academic Unit of Surgical Oncology, Department of Oncology (SPB, MWRR), University of Sheffield Medical School, Sheffield, UK; Division of Hematology and Oncology, David Geffen School of Medicine, University of California at Los Angeles, Los Angeles, CA (PAF); Department of Gynecology and Obstetrics, (MWB, SBW, SMJ, CRL), Institute of Pathology (AHa, DLW), University Breast Center Franconia, University Breast Center, University Hospital Erlangen, Erlangen, Germany; The Queensland Institute of Medical Research Post Office, Royal Brisbane Hospital, Herston, Queensland, Australia (ABS, HH, GC-T); Department of Oncology, University of Cambridge, Cambridge, UK (FB, KD, MKH, DE, PP, MG-C); Department of Medical Biometrics and Epidemiology, University Medical Center Hamburg-Eppendorf, Hamburg, Germany (DF-J, JH); Department of Pathology, University Hospital, Heidelberg, Germany (PS); Department of Cancer Epidemiology and Prevention, Cancer Center and M. Sklodowska-Curie Institute of Oncology, Warsaw, Poland (JLi); Department of Occupational and Environmental Epidemiology Nofer Institute of Occupational Medicine, Lodz, Poland (BP); Department of Medical Epidemiology and Biostatistics, Karolinska Institute, Stockholm, Sweden (PHa, KC, KH, HD); Human Genetics, Genome Institute of Singapore, Singapore, Singapore (JLi); Ontario Cancer Genetics Network (OCGN), Cancer Care Ontario, Toronto, ON, Canada (ILA, GG, NW); Departments of Molecular Genetics and Laboratory Medicine and Pathobiology, University of Toronto, Toronto, ON, Canada (ILA); Dalla Lana School of Public Health, University of Toronto, Prosserman Centre for Health Research, Samuel Lunenfeld Research Institute, Mount Sinai Hospital, Toronto, ON, Canada (JAK); Keenan Research Centre, Li Ka Shing Knowledge Institute of St. Michael's Hospital, and Laboratory Medicine and Pathobiology (AMM), Department of Pathology and Laboratory Medicine, Mount Sinai Hospital, and Laboratory Medicine and Pathobiology (FPOM), University of Toronto, Toronto, Ontario, Canada Northern California Cancer Center, Fremont, CA (EMJ); Department of Health Research and Policy, Stanford University School of Medicine and Stanford Cancer Center, Stanford, CA (EMJ); Cancer Epidemiology Centre, Cancer Council Victoria, Melbourne, Australia (LB, DRE, GGG, GS); Centre for Molecular, Environmental, Genetic, and Analytic Epidemiology, The University of Melbourne, Melbourne, Australia (LBa, DRE, GGG, GS, GSD, CA, JLH); The Alfred Hospital, Melbourne, Australia (CAM); Vesalius Research Center, KU Leuven and VIB, Leuven, Belgium (DL); Department of Radiotherapy, University Hospitals, Leuven, Belgium (TV, CW, RP, AS, PN, HW); Department of Obstetrics and Gynaecology (TD, AA, T-WP-S, PH), Department of Radiation Oncology (MB, AM, JHK), Hanover Medical School, Hanover, Germany (TD, MBr, AMe, JHK, AA, T-WP-S, PHi); Servicio Cirugía General (JIAP), Servicio de Anatomía Patológica (PMR), Hospital Monte Naranco, Oviedo, Spain Servicio de Oncología Médica, Hospital La Paz, Madrid, Spain (PZ); CIBERER, Madrid, Spain (JB); Department of Internal Medicine, Evangelische Kliniken Bonn gGmbH, Johanniter Krankenhaus, Bonn, Germany (Y-DK); Institute of Pathology, Medical Faculty of the University of Bonn, Bonn, Germany (H-PF); Molecular Genetics of Breast Cancer, Deutsches Krebsforschungszentrum (DKFZ), Heidelberg, Germany (UH); Institute for Prevention and Occupational Medicine of the German Social Accident Insurance (IPA), Bochum, Germany (BP, TBr ); Dr. Margarete Fischer-Bosch-Institute of Clinical Pharmacology, Stuttgart, Germany (CJ, HB); University of Tübingen, Tübingen, Germany (CJ, HB); University of Southampton School of Medicine, Southampton University Hospitals NHS Trust, Southampton (DME, WJT, SMG); Guy's, King's, St Thomas' Cancer Centre, Guy's Hospital, London, UK (EJS); Wellcome Trust Centre for Human Genetics, University of Oxford, Oxford, UK (EJS, IPT, AJo, NMc); Clinical Science Institute, University College Hospital, Galway, Ireland (MKe, NMc, NMi); Department of Epidemiology, University of California Irvine, Irvine (HA-C, AZ); Institute of Biomedical Sciences, Academia Sinica, Taipei, Taiwan (C-YS, C-NH, P-EW, S-LY); Graduate Institute of Environmental Science, China Medical University, Taichung, Taiwan (C-YS); Department of Surgery (J-CY), Department of Radiology (G-CH), Tri-Service General Hospital, Taipei, Taiwan (J-CY, G-CH); Department of Surgery, Changhua Christian Hospital, Changhua, Taiwan (S-TC); Department of Preventive Medicine, Keck School of Medicine and Norris Comprehensive Cancer Center, University of Southern California, Los Angeles, CA (CAH, BEH); Epidemiology Program, Cancer Research Center, University of Hawaii, Honolulu, HI (LLM, LNK); Department of Molecular Medicine and Surgery (AL), Department of Oncology and Pathology (SMa), Karolinska Institutet, Stockholm, Sweden; International Hereditary Cancer Centre, Department of Genetics and Pathology, Pomeranian Medical University, Szczecin, Poland (AJa, JLu, THu, TBy, BG, JG); Department of Medical Oncology Rotterdam Family Cancer Clinic, Erasmus University Medical Center, Rotterdam, the Netherlands (MJH, AHo, AMWvdO, AJa, MKr, MMAT-L, MC); Department of Obstetrics and Gynecology, University of Ulm, Ulm, Germany (SW-G); University of Oulu, Oulu University Hospital, Oulu, Finland (KP, AJ-V, KM, MGr, PHi, RW); Department of Pathology, Institute of Clinical Medicine, University of Eastern Finland and Kuopio University Hospital; Biocenter Kuopio, Kuopio, Finland (AMa, V-MK, JK, YS, RS); Department of Oncology, Vaasa Central Hospital, Vaasa, Finland (VK); Department of Oncology, Kuopio University Hospital, Kuopio, Finland (PA); The Peter MacCallum Cancer Centre, East Melbourne, Australia (kConFab); Department of Clinical Biochemistry and Department of Breast Surgery, Herlev University Hospital, University of Copenhagen, Copenhagen, Denmark (SEB, DDØ, DK-K, HF, BGN); Unit of Medical Genetics, Department of Preventive and Predictive Medicine (SMa), Unit of Genetic Susceptibility to Cancer, Department of Experimental Oncology and Molecular Medicine (PR), Fondazione IRCCS Istituto Nazionale Tumori (INT), Milan, Italy; Division of Cancer Prevention and Genetics, Istituto Europeo di Oncologia (IEO), Milan, Italy (MBa); Channing Laboratory, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA (SEH, DJH, RT); Department of Epidemiology, Harvard School of Public Health, Boston, MA (SEH, DJH, RT); Molecular Epidemiology Unit, National Cancer Institute, Ratchathewi, Bangkok, Thailand (SS); International Agency for Research on Cancer, Lyon, France (PB, JM, FO, VG); Department of Human Genetics (PD), Department of Pathology (PD), Department of Clinical Genetics (PEAH), Department of Surgical Oncology (RAEMT), Leiden University Medical Center, Leiden, the Netherlands; Department of Medical Oncology, Rotterdam Family Cancer Clinic, Erasmus MC-Daniel den Hoed Cancer Center, Rotterdam, the Netherlands (CS); The Genetic Epidemiology Laboratory, Department of Pathology, The University of Melbourne, Victoria, Australia (FH, HT, LDS, MCS).
Source
J Natl Cancer Inst. 2010 Dec 29;
Date
Dec-29-2010
Language
English
Publication Type
Article
Abstract
Background Previous studies have suggested that breast cancer risk factors are associated with estrogen receptor (ER) and progesterone receptor (PR) expression status of the tumors. Methods We pooled tumor marker and epidemiological risk factor data from 35?568 invasive breast cancer case patients from 34 studies participating in the Breast Cancer Association Consortium. Logistic regression models were used in case-case analyses to estimate associations between epidemiological risk factors and tumor subtypes, and case-control analyses to estimate associations between epidemiological risk factors and the risk of developing specific tumor subtypes in 12 population-based studies. All statistical tests were two-sided. Results In case-case analyses, of the epidemiological risk factors examined, early age at menarche (=12 years) was less frequent in case patients with PR(-) than PR(+) tumors (P = .001). Nulliparity (P = 3 × 10(-6)) and increasing age at first birth (P = 2 × 10(-9)) were less frequent in ER(-) than in ER(+) tumors. Obesity (body mass index [BMI] = 30 kg/m(2)) in younger women (=50 years) was more frequent in ER(-)/PR(-) than in ER(+)/PR(+) tumors (P = 1 × 10(-7)), whereas obesity in older women (>50 years) was less frequent in PR(-) than in PR(+) tumors (P = 6 × 10(-4)). The triple-negative (ER(-)/PR(-)/HER2(-)) or core basal phenotype (CBP; triple-negative and cytokeratins [CK]5/6(+) and/or epidermal growth factor receptor [EGFR](+)) accounted for much of the heterogeneity in parity-related variables and BMI in younger women. Case-control analyses showed that nulliparity, increasing age at first birth, and obesity in younger women showed the expected associations with the risk of ER(+) or PR(+) tumors but not triple-negative (nulliparity vs parity, odds ratio [OR] = 0.94, 95% confidence interval [CI] = 0.75 to 1.19, P = .61; 5-year increase in age at first full-term birth, OR = 0.95, 95% CI = 0.86 to 1.05, P = .34; obesity in younger women, OR = 1.36, 95% CI = 0.95 to 1.94, P = .09) or CBP tumors. Conclusions This study shows that reproductive factors and BMI are most clearly associated with hormone receptor-positive tumors and suggest that triple-negative or CBP tumors may have distinct etiology.
PubMed ID
21191117 View in PubMed
Less detail

Breast cancer-associated Abraxas mutation disrupts nuclear localization and DNA damage response functions.

https://arctichealth.org/en/permalink/ahliterature126768
Source
Sci Transl Med. 2012 Feb 22;4(122):122ra23
Publication Type
Article
Date
Feb-22-2012
Author
Szilvia Solyom
Bernadette Aressy
Katri Pylkäs
Jeffrey Patterson-Fortin
Jaana M Hartikainen
Anne Kallioniemi
Saila Kauppila
Jenni Nikkilä
Veli-Matti Kosma
Arto Mannermaa
Roger A Greenberg
Robert Winqvist
Author Affiliation
Laboratory of Cancer Genetics, Department of Clinical Genetics, Institute of Clinical Medicine and Biocenter Oulu, University of Oulu, Oulu University Hospital, Aapistie 5A, FI-90220 Oulu, Finland.
Source
Sci Transl Med. 2012 Feb 22;4(122):122ra23
Date
Feb-22-2012
Language
English
Publication Type
Article
Keywords
Adult
Amino Acid Sequence
Amino Acid Substitution - genetics
Base Sequence
Breast Neoplasms - genetics
Carrier Proteins - chemistry - genetics
Cell Line, Tumor
Cell Nucleus - metabolism
DNA Breaks, Double-Stranded
DNA Damage
Female
Finland
Genetic Testing
Heterozygote
Humans
Male
Molecular Sequence Data
Mutation - genetics
Pedigree
Protein Transport
Abstract
Breast cancer is the most common cancer in women in developed countries and has a well-established genetic component. Germline mutations in a network of genes encoding BRCA1, BRCA2, and their interacting partners confer hereditary susceptibility to breast cancer. Abraxas directly interacts with the BRCA1 BRCT (BRCA1 carboxyl-terminal) repeats and contributes to BRCA1-dependent DNA damage responses, making Abraxas a candidate for yet unexplained disease susceptibility. Here, we have screened 125 Northern Finnish breast cancer families for coding region and splice-site Abraxas mutations and genotyped three tagging single-nucleotide polymorphisms within the gene from 991 unselected breast cancer cases and 868 female controls for common cancer-associated variants. A novel heterozygous alteration, c.1082G>A (Arg361Gln), that results in abrogated nuclear localization and DNA response activities was identified in three breast cancer families and in one additional familial case from an unselected breast cancer cohort, but not in healthy controls (P = 0.002). On the basis of its exclusive occurrence in familial cancers, disease cosegregation, evolutionary conservation, and disruption of critical BRCA1 functions, the recurrent Abraxas c.1082G>A mutation connects to cancer predisposition. These findings contribute to the concept of a BRCA-centered tumor suppressor network and provide the identity of Abraxas as a new breast cancer susceptibility gene.
Notes
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PubMed ID
22357538 View in PubMed
Less detail

Evaluation of the need for routine clinical testing of PALB2 c.1592delT mutation in BRCA negative Northern Finnish breast cancer families.

https://arctichealth.org/en/permalink/ahliterature108069
Source
BMC Med Genet. 2013;14:82
Publication Type
Article
Date
2013
Author
Maria Haanpää
Katri Pylkäs
Jukka S Moilanen
Robert Winqvist
Author Affiliation
Laboratory of Cancer Genetics and Tumor Biology, Department of Clinical Chemistry and Biocenter Oulu, Institute of Diagnostics, University of Oulu, P,O, Box 5000, 90014 Oulu, Finland.
Source
BMC Med Genet. 2013;14:82
Date
2013
Language
English
Publication Type
Article
Keywords
Adult
Alleles
BRCA2 Protein - genetics
Breast Neoplasms - diagnosis - epidemiology - genetics
Cohort Studies
European Continental Ancestry Group - genetics
Female
Finland - epidemiology
Genetic Predisposition to Disease
Genetic Testing
Germ-Line Mutation
Heterozygote
Humans
Middle Aged
Nuclear Proteins - genetics
Pedigree
Risk factors
Tumor Suppressor Proteins - genetics
Ubiquitin-Protein Ligases - genetics
Abstract
Testing for mutations in the BRCA1 and BRCA2 genes among high-risk breast cancer patients has become a routine practice among clinical geneticists. Unfortunately, however, the genetic background of a majority of the cases coming to the clinics remains currently unexplained, making genetic counseling rather challenging. In recent years it has become evident world-wide that also women carrying a heterozygous germline mutation in PALB2 are at significantly increased risk of getting breast cancer. We have previously studied the clinical as well as biological impact of the PALB2 c.1592delT founder mutation occurring in about 1% of Finnish breast cancer patients unselected for their family history of disease, and our results demonstrated a 40% increased breast cancer risk by age 70 for female mutation carriers. Thus, this relatively common mutation in PALB2 is associated with a high risk of developing breast cancer. The aim of the current study was to analyze whether female index individuals of breast cancer families who had tested negative for germline mutations in BRCA1/BRCA2 as part of genetic counseling services should be offered mutation testing for PALB2 c.1592delT.
The study cohort consisted of altogether 223 individuals who had contacted the Department of Clinical Genetics at the Oulu University Hospital in Finland between the years 1997 and 2011 for counseling on hereditary breast and/or ovarian cancer risk. 101 of them met our inclusion criteria. Of these, 10 persons were now deceased, but 6 of them had participated in one of our previous studies on PALB2. Seventy (77%) of the remaining 91 persons responded positively to our study invitation. Chart review of updated pedigree data led to the exclusion of 14 further individuals not meeting the selection criteria.
Of the 56 alive affected female individuals screened for PALB2 c.1592delT, altogether two (3.6%) tested positive for this mutation. In addition, of the previously tested but now deceased 6 persons eligible for the current study, one more mutation carrier was observed. Therefore, overall 4.8% (3/62) of the tested individuals belonging to the Northern Finnish 1997-2011 study cohort turned out to be carriers of the PALB2 c.1592delT allele.
Given the potential benefits versus harms of this testing, the result of our study suggest that PALB2 c.1592delT should be a routine part of the genetic counseling protocol for Finnish high-risk breast cancer cases tested negative for mutations in BRCA1/BRCA2.
Notes
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PubMed ID
23941127 View in PubMed
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FANCM mutation c.5791C>T is a risk factor for triple-negative breast cancer in the Finnish population.

https://arctichealth.org/en/permalink/ahliterature292112
Source
Breast Cancer Res Treat. 2017 Nov; 166(1):217-226
Publication Type
Journal Article
Date
Nov-2017
Author
Johanna I Kiiski
Anna Tervasmäki
Liisa M Pelttari
Sofia Khan
Tuomo Mantere
Katri Pylkäs
Arto Mannermaa
Maria Tengström
Anders Kvist
Åke Borg
Veli-Matti Kosma
Anne Kallioniemi
Johanna Schleutker
Ralf Bützow
Carl Blomqvist
Kristiina Aittomäki
Robert Winqvist
Heli Nevanlinna
Author Affiliation
Department of Obstetrics and Gynecology, University of Helsinki and Helsinki University Hospital, Helsinki, Finland.
Source
Breast Cancer Res Treat. 2017 Nov; 166(1):217-226
Date
Nov-2017
Language
English
Publication Type
Journal Article
Keywords
Alleles
Case-Control Studies
DNA Helicases - genetics
DNA Repair
Female
Finland - epidemiology
Gene Duplication
Gene Frequency
Genetic Predisposition to Disease
Genotype
Humans
Mutation
Odds Ratio
Population Surveillance
Risk assessment
Risk factors
Sequence Deletion
Triple Negative Breast Neoplasms - epidemiology - genetics
Abstract
The FANCM c.5101C>T nonsense mutation was previously found to associate with breast cancer in the Finnish population, especially among triple-negative cases. Here, we studied the prevalence of three other FANCM variants: c.5791C>T, which has been reported to predispose to familial breast cancer, and the c.4025_4026delCT and c.5293dupA variants recently identified in Finnish cancer patients.
We genotyped the FANCM c.5791C>T mutation in 4806 invasive breast cancer patients, including BRCA1/2 mutation negative familial cases and unselected cases, and in 2734 healthy population controls from four different geographical areas of Finland. The association of the mutation with breast cancer risk among patient subgroups was statistically evaluated. We further analyzed the combined risk associated with c.5101C>T and c.5791C>T mutations. We also genotyped 526 unselected ovarian cancer patients for the c.5791C>T mutation and 862 familial breast cancer patients for the c.4025_4026delCT and c.5293dupA variants.
The frequency of the FANCM c.5791C>T mutation was higher among breast cancer cases than in controls (OR 1.94, 95% CI 0.87-4.32, P = 0.11), with a statistically significant association with triple-negative breast cancer (OR 5.14, 95% CI 1.65-16.0, P = 0.005). The combined analysis for c.5101C>T and c.5791C>T carriers confirmed a strong association with breast cancer (OR 1.86, 95% CI 1.32-2.49, P = 0.0002), especially among the triple-negative patients (OR 3.08, 95% CI 1.77-5.35, P = 0.00007). For the other variants, only one additional c.4025_4026delCT carrier and no c.5293dupA carriers were observed.
These results support the role of FANCM as a breast cancer susceptibility gene, particularly for triple-negative breast cancer.
Notes
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PubMed ID
28702895 View in PubMed
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Further evidence for the contribution of the RAD51C gene in hereditary breast and ovarian cancer susceptibility.

https://arctichealth.org/en/permalink/ahliterature101494
Source
Breast Cancer Res Treat. 2011 Jul 13;
Publication Type
Article
Date
Jul-13-2011
Author
Mikko Vuorela
Katri Pylkäs
Jaana M Hartikainen
Karin Sundfeldt
Annika Lindblom
Anna von Wachenfeldt Wäppling
Maria Haanpää
Ulla Puistola
Annika Rosengren
Maarit Anttila
Veli-Matti Kosma
Arto Mannermaa
Robert Winqvist
Author Affiliation
Laboratory of Cancer Genetics, Department of Clinical Genetics and Biocenter Oulu, University of Oulu, Oulu University Hospital, P.O. Box 5000, 90014, Oulu, Finland.
Source
Breast Cancer Res Treat. 2011 Jul 13;
Date
Jul-13-2011
Language
English
Publication Type
Article
Abstract
RAD51C, a RAD51 paralogue involved in homologous recombination, is a recently established Fanconi anemia and breast cancer predisposing factor. In the initial report, RAD51C mutations were shown to confer a high risk for both breast and ovarian tumors, but most of the replication studies published so far have failed to identify any additional susceptibility alleles. Here, we report a full mutation screening of the RAD51C gene in 147 Finnish familial breast cancer cases and in 232 unselected ovarian cancer cases originating from Finland and Sweden. In addition, in order to resolve whether common RAD51C SNPs are risk factors for breast cancer, we genotyped five tagging single nucleotide polymorphisms, rs12946522, rs304270, rs304283, rs17222691, and rs28363312, all located within the gene, from 993 Finnish breast cancer cases and 871 controls for cancer associated variants. Whereas, none of the studied common SNPs associated with breast cancer susceptibility, mutation analysis revealed two clearly pathogenic alterations. RAD51C c.-13_14del27 was observed in one familial breast cancer case and c.774delT in one unselected ovarian cancer case, thus confirming that RAD51C mutations are implicated in breast and ovarian cancer predisposition, although their overall frequency seems to be low. Independent identification of the very recently reported RAD51C c.774delT mutation in yet another patient originating from Sweden suggests that it might be a recurrent mutation in that population and should be studied further. The reliable estimation of the clinical implications of carrying a defective RAD51C allele still requires the identification of additional mutation positive families.
PubMed ID
21750962 View in PubMed
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Genome-wide search for breast cancer linkage in large Icelandic non-BRCA1/2 families.

https://arctichealth.org/en/permalink/ahliterature96318
Source
Breast Cancer Res. 2010 Jul 16;12(4):R50
Publication Type
Article
Date
Jul-16-2010
Author
Adalgeir Arason
Haukur Gunnarsson
Gudrun Johannesdottir
Kristjan Jonasson
Par-Ola Bendahl
Elizabeth Gillanders
Bjarni A Agnarsson
Goran Jonsson
Katri Pylkas
Aki Mustonen
Tuomas Heikkinen
Kristiina Aittomaki
Carl Blomqvist
Beatrice Melin
Oskar Th Johannsson
Pal Moller
Robert Winqvist
Heli Nevanlinna
Ake Borg
Rosa B Barkardottir
Source
Breast Cancer Res. 2010 Jul 16;12(4):R50
Date
Jul-16-2010
Language
English
Publication Type
Article
Abstract
ABSTRACT: INTRODUCTION: A significant proportion of high-risk breast cancer families are not explained by mutations in known genes. Recent genome-wide searches (GWS) have not revealed any single major locus reminiscent of BRCA1 and BRCA2, indicating that still unidentified genes may explain relatively few families each or interact in a way obscure to linkage analyses. This has drawn attention to possible benefits of studying populations where genetic heterogeneity might be reduced. We thus performed a GWS for linkage on nine Icelandic multiple-case non-BRCA1/2 families of desirable size for mapping highly penetrant loci. To follow up suggestive loci, an additional 13 families from other Nordic countries were genotyped for selected markers. METHODS: GWS was performed using 811 microsatellite markers providing about 5 centiMorgan (cM) resolution. Multipoint logarithm of odds (LOD) scores were calculated using parametric and nonparametric methods. For selected markers and cases, tumour tissue was compared to normal tissue to look for allelic loss indicative of a tumour suppressor gene. RESULTS: The three highest signals were located at chromosomes 6q, 2p and 14q. One family contributed suggestive LOD scores (LOD 2.63-3.03, dominant model) at all these regions, without consistent evidence of a tumour suppressor gene. Haplotypes in nine affected family members mapped the loci to 2p23.2-p21, 6q14.2-q23.2 and 14q21.3-24.3. No evidence of a highly penetrant locus was found among the remaining families. The heterogeneity LOD (HLOD) at the 6q, 2p and 14q loci in all families was 3.27, 1.66 and 1.24, respectively. The subset of 13 Nordic families showed supportive HLODs at chromosome 6q (ranging 0.34-1.37 by country subset). The 2p and 14q loci overlap with regions indicated by large families in previous GWS studies of breast cancer. CONCLUSIONS: Chromosomes 2p, 6q and 14q are candidate sites for genes contributing together to high breast cancer risk. A polygenic model is supported, suggesting the joint effect of genes in contributing to breast cancer risk to be rather common in non-BRCA1/2 families. For genetic counselling it would seem important to resolve the mode of genetic interaction.
PubMed ID
20637093 View in PubMed
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Mutation analysis of the AATF gene in breast cancer families.

https://arctichealth.org/en/permalink/ahliterature98554
Source
BMC Cancer. 2009;9:457
Publication Type
Article
Date
2009
Author
Maria Haanpää
Mervi Reiman
Jenni Nikkilä
Hannele Erkko
Katri Pylkäs
Robert Winqvist
Author Affiliation
Laboratory of Cancer Genetics, Oulu University Hospital, P,O, Box 22, FIN-90221 Oulu, Finland. maappi@mail.student.oulu.fi
Source
BMC Cancer. 2009;9:457
Date
2009
Language
English
Publication Type
Article
Keywords
Apoptosis Regulatory Proteins - analysis - genetics
Breast Neoplasms - genetics
DNA Mutational Analysis
Family
Female
Finland
Genetic Predisposition to Disease
Germ-Line Mutation
Humans
Mutation, Missense
Polymorphism, Single Nucleotide
Repressor Proteins - analysis - genetics
Abstract
BACKGROUND: About 5-10% of breast cancer is due to inherited disease predisposition. Many previously identified susceptibility factors are involved in the maintenance of genomic integrity. AATF plays an important role in the regulation of gene transcription and cell proliferation. It induces apoptosis by associating with p53. The checkpoint kinases ATM/ATR and CHEK2 interact with and phosphorylate AATF, enhancing its accumulation and stability. Based on its biological function, and direct interaction with several known breast cancer risk factors, AATF is a good candidate gene for being involved in heritable cancer susceptibility. METHODS: Here we have screened the entire coding region of AATF in affected index cases from 121 Finnish cancer families for germline defects, using conformation sensitive gel electrophoresis and direct sequencing. RESULTS: Altogether seven different sequence changes were observed, one missense variant and six intronic ones. Based on the in silico analyses of these sequence alterations, as well as their occurrence in cases and controls, none of them, however, were predicted to be pathogenic. CONCLUSIONS: To our knowledge, this is the first study reporting the mutation screening of the AATF gene in familial breast cancer cases. No evidence for the association with breast cancer was observed.
PubMed ID
20025740 View in PubMed
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Mutation screening of the RNF8, UBC13 and MMS2 genes in Northern Finnish breast cancer families.

https://arctichealth.org/en/permalink/ahliterature132816
Source
BMC Med Genet. 2011;12:98
Publication Type
Article
Date
2011
Author
Mikko Vuorela
Katri Pylkäs
Robert Winqvist
Author Affiliation
Department of Clinical Genetics and Biocenter Oulu, University of Oulu, Oulu University Hospital, Oulu, Finland.
Source
BMC Med Genet. 2011;12:98
Date
2011
Language
English
Publication Type
Article
Keywords
Adult
Aged
Aged, 80 and over
Base Sequence
Breast Neoplasms - genetics
DNA Mutational Analysis
DNA Primers - genetics
DNA, Neoplasm - genetics
DNA-Binding Proteins - genetics
Female
Finland
Genetic Predisposition to Disease
Genetic Testing
Germ-Line Mutation
Heterozygote
Humans
Ligases - genetics
Middle Aged
Ubiquitin-Conjugating Enzymes - genetics
Abstract
Currently known susceptibility genes such as BRCA1 and BRCA2 explain less than 25% of familial aggregation of breast cancer, which suggests the involvement of additional susceptibility genes. RNF8, UBC13 and MMS2 are involved in the DNA damage response pathway and play important roles in BRCA1-mediated DNA damage recognition. Based on the evidence that several players in the ubiquitin-mediated BRCA1-dependent DDR seem to contribute to breast cancer predisposition, RNF8, UBC13 and MMS2 were considered plausible candidate genes for susceptibility to breast cancer.
The entire coding region and splice junctions of RNF8, UBC13 and MMS2 genes were screened for mutations in affected index cases from 123 Northern Finnish breast cancer families by using conformation sensitive gel electrophoresis, high resolution melting (HRM) analysis and direct sequencing.
Mutation analysis revealed several changes in RNF8 and UBC13, whereas no aberrations were observed in MMS2. None of the found sequence changes appeared to associate with breast cancer susceptibility.
The present data suggest that mutations in RNF8, UBC13 and MMS2 genes unlikely make any sizeable contribution to breast cancer predisposition in Northern Finland.
Notes
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PubMed ID
21774837 View in PubMed
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Primary Myocardial Fibrosis as an Alternative Phenotype Pathway of Inherited Cardiac Structural Disorders.

https://arctichealth.org/en/permalink/ahliterature302642
Source
Circulation. 2018 06 19; 137(25):2716-2726
Publication Type
Journal Article
Research Support, Non-U.S. Gov't
Date
06-19-2018
Author
M Juhani Junttila
Lauri Holmström
Katri Pylkäs
Tuomo Mantere
Kari Kaikkonen
Katja Porvari
Marja-Leena Kortelainen
Lasse Pakanen
Risto Kerkelä
Robert J Myerburg
Heikki V Huikuri
Author Affiliation
Research Unit of Internal Medicine, University of Oulu and University Hospital of Oulu, Finland (M.J.J., L.H., K.K., H.V.H.) juhani.junttila@oulu.fi.
Source
Circulation. 2018 06 19; 137(25):2716-2726
Date
06-19-2018
Language
English
Publication Type
Journal Article
Research Support, Non-U.S. Gov't
Keywords
Adult
Aged
Arrhythmogenic Right Ventricular Dysplasia - genetics - mortality - pathology
Autopsy - methods
Cardiomyopathy, Dilated - genetics - mortality - pathology
Cardiomyopathy, Hypertrophic - genetics - mortality - pathology
Cause of Death
Death, Sudden, Cardiac - epidemiology - pathology
Female
Fibrosis
Finland - epidemiology
Gene Frequency
Genetic Predisposition to Disease
Genetic Variation
Heredity
Humans
Male
Middle Aged
Myocardium - pathology
Pathology, Molecular
Phenotype
Registries
Risk assessment
Risk factors
Abstract
Myocardial fibrosis is a common postmortem finding among young individuals with sudden cardiac death. Because there is no known single cause, we tested the hypothesis that some cases of myocardial fibrosis in the absence of identifiable causes (primary myocardial fibrosis [PMF]) are associated with genetic variants.
Tissue was obtained at autopsy from 4031 consecutive individuals with sudden cardiac death in Northern Finland, among whom PMF was the only structural finding in 145 subjects with sudden cardiac death. We performed targeted next-generation sequencing using a panel of 174 genes associated with myocardial structure and ion channel function when autopsies did not identify a secondary basis for myocardial fibrosis. All variants with an effect on protein and with a minor allele frequency
Notes
CommentIn: Circulation. 2018 Jun 19;137(25):2727-2729 PMID 29915099
PubMed ID
29915098 View in PubMed
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Screening for large genomic rearrangements in the FANCA gene reveals extensive deletion in a Finnish breast cancer family.

https://arctichealth.org/en/permalink/ahliterature137888
Source
Cancer Lett. 2011 Mar 28;302(2):113-8
Publication Type
Article
Date
Mar-28-2011
Author
Szilvia Solyom
Robert Winqvist
Jenni Nikkilä
Katrin Rapakko
Pasi Hirvikoski
Hannaleena Kokkonen
Katri Pylkäs
Author Affiliation
Laboratory of Cancer Genetics, Department of Clinical Genetics and Biocenter Oulu, University of Oulu, Oulu University Hospital, University of Oulu, Oulu, Finland.
Source
Cancer Lett. 2011 Mar 28;302(2):113-8
Date
Mar-28-2011
Language
English
Publication Type
Article
Keywords
Breast Neoplasms - genetics
Fanconi Anemia - genetics
Female
Finland - epidemiology
Genetic Predisposition to Disease
Humans
Mass Screening
Sequence Deletion
Abstract
A portion of familial breast cancer cases are caused by mutations in the same genes that are inactivated in the downstream part of Fanconi anemia (FA) signaling pathway. Here we have assessed the FANCA gene for breast cancer susceptibility by examining blood DNA for aberrations from 100 Northern Finnish breast cancer families using the MLPA method. We identified a novel heterozygous deletion, removing the promoter and 12 exons of the gene in one family. This allele was absent from 124 controls. We conclude that FANCA deletions might contribute to breast cancer susceptibility, potentially in combination with other germline mutations. To our knowledge, this is the first study reporting a large deletion in an upstream FA gene in familial breast cancer.
PubMed ID
21236561 View in PubMed
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