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A “hiányzó örökletesség” problémája: a poligénes emlőrákhajlam új elemeinek azonosítása
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Ezen az oldalon az NKFI Elektronikus Pályázatkezelő Rendszerében nyilvánosságra hozott projektjeit tekintheti meg.
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Projekt adatai |
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| azonosító |
112228 |
| típus |
K |
| Vezető kutató |
Oláh Edit |
| magyar cím |
A “hiányzó örökletesség” problémája: a poligénes emlőrákhajlam új elemeinek azonosítása |
| Angol cím |
The “missing heritability”: identifying novel elements of the polygenic breast cancer susceptibility |
| magyar kulcsszavak |
emlőrákra hajlamosító gének, poligénes daganathajlam, emlőrákszindrómák, BRCA1, BRCA2, DNS hibajavító gének, DNS hibatoleráló gének, NGS |
| angol kulcsszavak |
breast cancer susceptibility genes, polygenic susceptibility to cancer, breast cancer syndromes, BRCA1, BRCA2, DNA repair genes, DNA damage tolerance genes, NGS |
| megadott besorolás |
| Tumorbiológia (Orvosi és Biológiai Tudományok Kollégiuma) | 50 % | | Ortelius tudományág: Onkológia | | Sejtgenetika (Orvosi és Biológiai Tudományok Kollégiuma) | 50 % | | Ortelius tudományág: Molekuláris genetika |
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| zsűri |
Immun-, Tumor- és Mikrobiológia |
| Kutatóhely |
Molekuláris Genetikai Osztály (Országos Onkológiai Intézet) |
| résztvevők |
Antal Péter
Bozsik Anikó
Gézsi András
Mátrai Zoltán
Mórocz Mónika
Papp János
Pócza Tímea
Udvarhelyi Nóra Klára
Vaszkó Tibor
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| projekt kezdete |
2015-01-01 |
| projekt vége |
2018-12-31 |
| aktuális összeg (MFt) |
38.148 |
| FTE (kutatóév egyenérték) |
10.00 |
| állapot |
lezárult projekt |
magyar összefoglaló A kutatás összefoglalója, célkitűzései szakemberek számára
Itt írja le a kutatás fő célkitűzéseit a témában jártas szakember számára.
Az emlőrákra hajlamosító genetikai faktorok nagy része még emlőrák halmozódást mutató családokban is ismeretlen. A kutatás célja olyan gének azonosítása, amelyek öröklött megváltozásai hozzájárulnak az emlőrák iránti genetikai fogékonysághoz. A cél megvalósítását három, az újgenerációs szekvenáláson alapuló módszer alkalmazásával tervezzük. Az első, funkcionális alapú megközelítés keretében a genom integritásának fenntartásában szerepet játszó gének exonjai kerülnek vizsgálatra. Ebbe a géncsoportba tartoznak a DNS hibatolerancia génjei, valamint azok, amelyek a DNS sérülések által kiváltott ellenőrzőpont aktiválódása során a replikációs villa stabilizálásában vesznek részt. A második, lokalizációs alapú megközelítésben azon gének exonjait vizsgáljuk, amelyek a genomszintű asszociációs vizsgálatok (GWAS) során azonosított SNP-k közelében helyezkednek el. Harmadikként egy olyan új, RNS-szekvenáláson alapuló módszer kifejlesztését tervezzük, amely alkalmazása révén azonosítani tudjuk azokat a genetikai változásokat, amelyek a transzláció korai terminációját, és az érintett mRNS lebomlását okozzák.
Néhány újonnan azonosított variánst in vitro funkcionális vizsgálatoknak vetünk alá, hogy validáljuk azok hatását a sejtek proliferációjára, az apoptózisra, és – a genom integritásának fenntartásában szerepet játszó gének esetében – a homológ rekombinációra. A daganatos fenotípust várhatóan módosító variánsok vizsgálatához a BRCA mutációt és a kérdéses variánst egyaránt hordozók fenotípusát hasonlítjuk a csak BRCA mutációt hordozókéhoz. Ugyancsak célkitűzéseink közé tartozik a beteg- és kontrollcsoport között szignifikánsan eltérő gyakoriságot mutató variánsmintázatok keresése.
Mi a kutatás alapkérdése?
Ebben a részben írja le röviden, hogy mi a kutatás segítségével megválaszolni kívánt probléma, mi a kutatás kiinduló hipotézise, milyen kérdéseket válaszolnak meg a kísérletek.
Jól ismert, hogy a genetikai hajlam a gyakori daganatok, köztük az emlőrák kiemelt kockázati tényezője, de a tumorok kialakulására hajlamosító gének jelentős része még nem ismert: ezt a részt nevezzük ‘hiányzó örökletességnek’. Az emlőrák halmozódását mutató családok több mint felében a hajlamosító tényező ugyancsak azonosítatlan. Kutatásunk során a még ismeretlen genetikai tényezőkkel kapcsolatban négy hipotézist állítottunk fel. Az első értelmében a keresett variánsok egy része a genom integritásában szerepet játszó géneket érinti. Második feltevésünk, hogy a teljes genomra kiterjedő asszociációs vizsgálatok által kijelölt területeken valóban találhatók hajlamosító gének, amelyeknek a daganatképződésben betöltött szerepe eddig ismert funkcióik alapján nem merült fel. Harmadik hipotézisünk szerint a hajlamosító tényezők egy része olyan szabályozó területeken található, amelyeket az ilyen allélek keresése során csak ritkán vizsgálnak. Ezek azonosítására egy új, RNS-szekvenáláson alapuló módszer kifejlesztését tervezzük, amely alkalmas olyan genetikai tényezők felfedésére, amelyek aktiválódása a transzláció idő előtti terminációját, és az érintett mRNS molekula lebomlását okozza. Negyedik hipotézisünk szerint a ‘hiányzó örökletesség’ hátterében nem csak egyedi variánsok, hanem több variáns által alkotott mintázatok is állhatnak. A fenti feltevéseket ismert családi háttérrel és negatív BRCA mutációs státusszal rendelkező daganatos, valamint egészséges kontroll minták újgenerációs szekvenálásával teszteljük. Néhány ígéretes variánst funkcionális vizsgálatnak vetünk alá, hogy megerősítsük a szekvenálás adatainak statisztikai értékelése során levont következtetéseket.
Mi a kutatás jelentősége?
Röviden írja le, milyen új perspektívát nyitnak az alapkutatásban az elért eredmények, milyen társadalmi hasznosíthatóságnak teremtik meg a tudományos alapját. Mutassa be, hogy a megpályázott kutatási területen lévő hazai és a nemzetközi versenytársaihoz képest melyek az egyediségei és erősségei a pályázatának!
Projektünk eredményeként az ismert gének kockázatnövelő hatásának pontosabb megbecslésén túl az örökletes emlőrákhajlam molekuláris alapjainak jobb megértését elősegítő fontos ismeretekre számíthatunk. Emellett olyan új gének azonosítását is várjuk, amelyeket eddig nem hoztak kapcsolatba ezen megbetegedések kockázatával.
A szekvenálási eredmények értékelése révén ritka patogén variánsok azonosítását várjuk. Elképzelhető, hogy ezek a variánsok a vártnál nagyobb számban fordulnak elő bizonyos génekben és/vagy útvonalakon, ezáltal akár új támadáspontokat is kijelölhetőek lesznek a daganatellenes terápiák számára. A nagyszámú gén vizsgálata miatt több ígéretes hajlamosító variáns azonosítására számíthatunk.
Törekszünk egy új, RNS szekvenáláson alapuló módszer kifejlesztésére, amelynek alkalmazásával lehetőség nyílik olyan genetikai változások azonosítására, amelyek a transzláció idő előtti terminációjához, és ezáltal az érintett mRNS eliminációjához vezetnek. Feltételezzük, hogy e módszerrel képesek leszünk káros genetikai változások lokalizálására olyan régiókban is, amelyeket a ‘hiányzó örökletesség’ okainak keresése során nem vizsgálnak. Ez a módszer a teljes genom szekvenálását is helyettesítheti olyan esetekben, amikor a cél retrotranszpozon szekvenciák exonizációja, vagy a transzkripció szomszédos génekbe történő átolvasása okainak azonosítása.
Mivel az örökletes daganatos megbetegedések jó modellként szolgálnak a sporadikus esetekhez is, a tervezett kutatás során azonosított variánsokkal kapcsolatos ismeretek felhasználhatók a sporadikus megbetegedések etiológiájának jobb megértéséhez.
A projekt során nyert ismereteink várhatóan növelik a molekuláris genetikai diagnosztikai vizsgálatok hatékonyságát, akár azonnal érezhető segítséget nyújtva a nagy kockázattal élők számára. Potenciális eredményeink hozzájárulhatnak olyan modellek kialakításához, amelyek segítik a daganat korai diagnózisát és az egyéni kockázat pontosabb felmérését.
A rákkutatás ezen kompetitív területén számítunk várható eredményeink rangos folyóiratokban történő publikálására.
A tervezett alapkutatás lehetővé teszi a jelenleg is folyó hazai és nemzetközi együttműködéseink folytatását.
A kutatás összefoglalója, célkitűzései laikusok számára
Ebben a fejezetben írja le a kutatás fő célkitűzéseit alapműveltséggel rendelkező laikusok számára. Ez az összefoglaló a döntéshozók, a média, illetve az érdeklődők tájékoztatása szempontjából különösen fontos az NKFI Hivatal számára.
A rákbetegség nem öröklődik, de a daganatok kialakulására hajlamosító genetikai tényezők örökölhetők. A BRCA1 és BRCA2 gének örökölt génhibái az emlőrákra való hajlam ismert kulcstényezői. Az emlőrák hátterében álló molekuláris genetikai változások megértésében az utóbbi évtizedben jelentős előrelépés történt. Ennek ellenére a daganatok halmozódását mutató emlőrákos családok jelentős részében a feltételezett hajlamosító tényezőket nem sikerült azonosítani. Ezt a jelenséget nevezzük ‘hiányzó örökletességnek’. Jelen kutatásaink célja, hogy az utóbbi években bekövetkezett jelentős tudományos és technológiai fejlődés eredményeinek alkalmazásával felfedjünk és azonosítsunk néhány, az emlőrák iránti hajlamban szerepet játszó genetikai tényezőt. A javasolt kutatás egy modern, rendkívül hatékony technika, az ún. újgenerációs szekvenálás alkalmazásával fogja vizsgálni a negatív BRCA mutációs státusszal rendelkező emlőrákos családok DNS és RNS mintáit, alapozva részben a BRCA1/2 és más hajlamosító géneket érintő saját kutatási eredményeinkre, részben az emlőrákra hajlamosító genetikai tényezők kutatása során eddigiekben feltárt tudásanyagra. A kutatás során nyert ismereteink közvetlenül hozzájárulhatnak a molekuláris genetikai diagnosztikai vizsgálatok hatékonyságához, a nagy genetikai kockázattal élők számára esetleg azonnal érezhető módon. Egyúttal lehetővé teszik olyan modellek felépítését, amelyek hozzásegíthetnek a daganat korai diagnózisához és az egyéni kockázat pontosabb felméréséhez. A nyert információk hasznosnak bizonyulhatnak olyan további kutatások megalapozásához, amelyek a daganatok kialakulásában szerepet játszó molekuláris kölcsönhatások tisztására irányulnak.
| angol összefoglaló Summary of the research and its aims for experts
Describe the major aims of the research for experts.
A considerable part of the genetic factors of breast cancer susceptibility is still unknown even in breast cancer families. The AIM of the research is to identify genes whose variants may contribute to cancer susceptibility by implementing three different approaches. First, in a function-based approach, the exome of genes participating in the maintenance of genomic integrity will be examined. The tested genes include DNA damage tolerance genes and those taking part in the stabilization of the replication forks in response to DNA damage checkpoint activation. Second, in a localization-based search, the exome of genes residing in a certain constrained neighborhood of SNPs identified by genome-wide association studies (GWAS) will be tested. Third, we plan to develop a novel, RNA-Seq-based method which is expected to be applicable to localize genetic changes resulting in the usage of premature translation termination codon and, in turn, the degradation of the impaired mRNA by nonsense-mediated mRNA decay (NMD). All three approaches will utilize next generation sequencing technology to identify potential pathogenic variants. Selected newly identified variants will then be tested in functional assays in cell cultures to validate their impact on proliferation, apoptosis and, in the case of genes contributing to the maintenance of genomic integrity, homologous recombination (HR). The potential disease-modifying role of the variants will also be tested by comparison of phenotypes of BRCA mutation carriers with or without the variant. Variant patterns with significantly different frequencies between cases and controls will also be searched.
What is the major research question?
Describe here briefly the problem to be solved by the research, the starting hypothesis, and the questions addressed by the experiments.
It is widely accepted, that genetic susceptibility is a major risk factor for most common cancers, including breast cancer. However, a considerable fraction of cancer susceptibility genes has not yet been identified. For example, the heritability has yet been unaccounted for in more than half of the families with multiple cases of breast cancer. We hypothesize, that some of the still unidentified genetic factors are associated with genes that have a role in the maintenance of genome integrity. Another hypothesis of the proposed work is that the regions designated by genome-wide association studies really contain susceptibility genes, whose role in tumor predisposition may not even be suspected on the basis of their already known functions. We also hypothesize that some susceptibility factors reside in regulatory and/or deep intronic regions, which are not routinely examined when searching for cancer predisposing alleles. The identification of such factors, whose activation leads to premature translation termination and, eventually, the decay of the affected mRNAs, is aimed at by a novel RNA-Seq-based method that we plan to develop. Our fourth hypothesis is that part of the ‘missing heritability’ is linked to variant patterns rather than single alternative variants. The listed hypotheses will be tested by genotyping BRCA1/2 mutation negative cancer cases with known family history and healthy controls by either targeted re-sequencing or RNA-Seq. Some promising variants will also undergo functional studies to corroborate the results obtained by the biostatistical evaluation of next generation sequencing data.
What is the significance of the research?
Describe the new perspectives opened by the results achieved, including the scientific basics of potential societal applications. Please describe the unique strengths of your proposal in comparison to your domestic and international competitors in the given field.
In addition to confirm the contribution of known susceptibility genes to breast cancer risk, we anticipate substantial novel findings in understanding the molecular basis of heritable breast cancer susceptibility. We also foresee to identify novel variants and/or genes that have not yet been linked to breast cancer risk. Rare pathogenic variants lying in the coding region of genes are expected to be found by appropriately filtering the sequencing results. It is possible that such rare variants are enriched in certain genes and/or pathways, which can pinpoint new targets that may be efficiently treated with anticancer drugs. Since a large number of genes will be examined, we expect to hit upon several promising disease-causing variants. We also expect the successful development of a novel method able to identify genetic changes which lead to premature translation termination and, consequently, the elimination of the affected mRNA. We predict that such an approach may help to find pathogenic genetic changes localized in regions generally not studied when searching for factors responsible for ‘missing heritability’. Such a method may replace whole genome sequencing when, for example, the genome-wide identification of exonization of retrotransposon sequences or spreading of transcription to a neighboring gene due to the impairment of the transcription termination signal is aimed at.
Since familial/hereditary cancer is a good model of the more frequent sporadic cases, the variants which will have been revealed by this study may also contribute to the etiology of sporadic cancers, thus strengthening the significance of our findings. The knowledge expected to be gained from the completion of the proposed project would directly enhance the efficiency of molecular genetic testing with immediate benefits of high-risk individuals, and make it possible to develop models for early detection, diagnosis and risk prediction.
We are confident that our results will be published in highly prestigious scientific journals and have an impact on the competitive research of breast cancer susceptibility.
The basic research activity makes also possible the continuation of our ongoing domestic and international collaborations.
Summary and aims of the research for the public
Describe here the major aims of the research for an audience with average background information. This summary is especially important for NRDI Office in order to inform decision-makers, media, and others.
Cancer cannot be inherited, but genetic variants making someone susceptible to develop a tumor during his or her lifetime, can. BRCA1 and BRCA2 genes are key players of breast cancer susceptibility. In spite of the rapid progression made during the past decade to uncover the molecular mechanism of tumorigenesis in breast cancer, a large fraction of tumor susceptibility genes in breast cancer families has not yet been discovered. The lack of this knowledge is called ‘missing heritability’. The aim of this research project is to unravel and validate several new inherited genetic factors by utilize some of the scientific and technological advances implemented during the past five years. Based partly on our previous and recent research on BRCA1, BRCA2 and other tumour suppressor genes, partly on the latest remarkable research results on the field of genetic susceptibility to breast cancer, the proposed research will be realised using the most up-to-date high-throughput technique, namely next-generation sequencing, on DNA/RNA samples of patients from breast cancer families with known negative BRCA1 & BRCA2 mutation status. In the case of a successful completion, the knowledge collected might directly enhance the efficiency of molecular genetic testing, offer immediate benefits to high-risk individuals, and make it possible to develop models for early detection, diagnosis and risk prediction. The gathered information is also expected to be utilized in the substantiation of further research activity which aims at dissecting the multi-faceted molecular interactions underlying tumour formation.
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| Singer Christian F, Balmaña Judith, Bürki Nicole, Delaloge Suzette, Filieri Maria Elisabetta, Gerdes Anna-Marie, Grindedal Eli Marie, Han Sileni, Johansson Oskar, Kaufman Bella, Krajc Mateja, Loman Niklas, Olah Edith, Paluch-Shimon Shani, Plavetic Natalija Dedic, Pohlodek Kamil, Rhiem Kerstin, Teixeira Manuel, Evans D Gareth: Genetic counselling and testing of susceptibility genes for therapeutic decision-making in breast cancer-an European consensus statement and expert recommendations., EUROPEAN JOURNAL OF CANCER 106: pp. 54-60., 2019 | | Szollár András, Újhelyi Mihály, Polgár Csaba, Oláh Edit, Pukancsik Dávid, Rubovszky Gábor, Udvarhelyi Nóra, Kovács Tibor, Sávolt Ákos, Kenessey István, Mátrai Zoltán: A long-term retrospective comparative study of the oncological outcomes of 598 very young (≤35 years) and young (36–45 years) breast cancer patients, EUROPEAN JOURNAL OF SURGICAL ONCOLOGY, 2019 | | Lakeman Inge M M, Hilbers Florentine S, Rodríguez-Girondo Mar, Lee Andrew, Vreeswijk Maaike P G, Hollestelle Antoinette, Seynaeve Caroline, Meijers-Heijboer Hanne, Oosterwijk Jan C, Hoogerbrugge Nicoline, Olah Edith, Vasen Hans F A, van Asperen Christi J, Devilee Peter: Addition of a 161-SNP polygenic risk score to family history-based risk prediction: impact on clinical management in non- BRCA1/2 breast cancer families, JOURNAL OF MEDICAL GENETICS p. jmedgenet-2019-106072., 2019 | | Jiang Xia, Finucane Hilary K., Schumacher Fredrick R., Schmit Stephanie L., Tyrer Jonathan P., Han Younghun, Michailidou Kyriaki, Lesseur Corina, Kuchenbaecker Karoline B., Dennis Joe, Conti David V., Casey Graham, Gaudet Mia M., Huyghe Jeroen R., Albanes Demetrius, Aldrich Melinda C., Andrew Angeline S., Andrulis Irene L., Anton-Culver Hoda, Antoniou Antonis C., Antonenkova Natalia N., Arnold Susanne M., Aronson Kristan J., Arun Banu K., Bandera Elisa V., Barkardottir Rosa B., Barnes Daniel R., Batra Jyotsna, Beckmann Matthias W., Benitez Javier, Benlloch Sara, Berchuck Andrew, Berndt Sonja I., Bickeböller Heike, Bien Stephanie A., Blomqvist Carl, Boccia Stefania, Bogdanova Natalia V., Bojesen Stig E., Bolla Manjeet K., Brauch Hiltrud, Brenner Hermann, Brenton James D., Brook Mark N., Brunet Joan, Brunnström Hans, Buchanan Daniel D., Burwinkel Barbara, Butzow Ralf, Cadoni Gabriella, Caldés Trinidad, Caligo Maria A., Campbell Ian, Campbell Peter T., Cancel-Tassin Géraldine, Cannon-Albright Lisa, Campa Daniele, Caporaso Neil, Carvalho André L., Chan Andrew T., Chang-Claude Jenny, Chanock Stephen J., Chen Chu, Christiani David C., Claes Kathleen B. 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J, Lee A, Lee E, Lee JW, Lee MH, Lejbkowicz F, Lesueur F, Li J, Lilyquist J, Lincoln A, Lindblom A, Lissowska J, Lo WY, Loibl S, Long J, Loud JT, Lubinski J, Luccarini C, Lush M, MacInnis RJ, Maishman T, Makalic E, Kostovska IM, Malone KE, Manoukian S, Manson JE, Margolin S, Martens JWM, Martinez ME, Matsuo K, Mavroudis D, Mazoyer S, McLean C, Meijers-Heijboer H, Menéndez P, Meyer J, Miao H, Miller A, Miller N, Mitchell G, Montagna M, Muir K, Mulligan AM, Mulot C, Nadesan S, Nathanson KL; NBSC Collaborators, Neuhausen SL, Nevanlinna H, Nevelsteen I, Niederacher D, Nielsen SF, Nordestgaard BG, Norman A, Nussbaum RL, Olah E, Olopade OI, Olson JE, Olswold C, Ong KR, Oosterwijk JC, Orr N, Osorio A, Pankratz VS, Papi L, Park-Simon TW, Paulsson-Karlsson Y, Lloyd R, Pedersen IS, Peissel B, Peixoto A, Perez JIA, Peterlongo P, Peto J, Pfeiler G, Phelan CM, Pinchev M, Plaseska-Karanfilska D, Poppe B, Porteous ME, Prentice R, Presneau N, Prokofieva D, Pugh E, Pujana MA, Pylkäs K, Rack B, Radice P, Rahman N, Rantala J, Rappaport-Fuerhauser C, Rennert G, Rennert HS, Rhenius V, Rhiem K, Richardson A, Rodriguez GC, Romero A, Romm J, Rookus MA, Rudolph A, Ruediger T, Saloustros E, Sanders J, Sandler DP, Sangrajrang S, Sawyer EJ, Schmidt DF, Schoemaker MJ, Schumacher F, Schürmann P, Schwentner L, Scott C, Scott RJ, Seal S, Senter L, Seynaeve C, Shah M, Sharma P, Shen CY, Sheng X, Shimelis H, Shrubsole MJ, Shu XO, Side LE, Singer CF, Sohn C, Southey MC, Spinelli JJ, Spurdle AB, Stegmaier C, Stoppa-Lyonnet D, Sukiennicki G, Surowy H, Sutter C, Swerdlow A, Szabo CI, Tamimi RM, Tan YY, Taylor JA, Tejada MI, Tengström M, Teo SH, Terry MB, Tessier DC, Teulé A, Thöne K, Thull DL, Tibiletti MG, Tihomirova L, Tischkowitz M, Toland AE, Tollenaar RAEM, Tomlinson I, Tong L, Torres D, Tranchant M, Truong T, Tucker K, Tung N, Tyrer J, Ulmer HU, Vachon C, van Asperen CJ, Van Den Berg D, van den Ouweland AMW, van Rensburg EJ, Varesco L, Varon-Mateeva R, Vega A, Viel A, Vijai J, Vincent D, Vollenweider J, Walker L, Wang Z, Wang-Gohrke S, Wappenschmidt B, Weinberg CR, Weitzel JN, Wendt C, Wesseling J, Whittemore AS, Wijnen JT, Willett W, Winqvist R, Wolk A, Wu AH, Xia L, Yang XR, Yannoukakos D, Zaffaroni D, Zheng W, Zhu B, Ziogas A, Ziv E, Zorn KK, Gago-Dominguez M, Mannermaa A, Olsson H, Teixeira MR, Stone J, Offit K, Ottini L, Park SK, Thomassen M, Hall P, Meindl A, Schmutzler RK, Droit A, Bader GD, Pharoah PDP, Couch FJ, Easton DF, Kraft P, Chenevix-Trench G, García-Closas M, Schmidt MK, Antoniou AC, Simard J: Identification of ten variants associated with risk of estrogen-receptor-negative breast cancer, Nat Genet, 2017 | | Phelan CM, Kuchenbaecker KB, Tyrer JP, Kar SP, Lawrenson K, Winham SJ, Dennis J, Pirie A, Riggan MJ, Chornokur G, Earp MA, Lyra PC Jr, Lee JM, Coetzee S, Beesley J, McGuffog L, Soucy P, Dicks E, Lee A, Barrowdale D, Lecarpentier J, Leslie G, Aalfs CM, Aben KK, Adams M, Adlard J, Andrulis IL, Anton-Culver H, Antonenkova N; AOCS study group., Aravantinos G, Arnold N, Arun BK, Arver B, Azzollini J, Balmaña J, Banerjee SN, Barjhoux L, Barkardottir RB, Bean Y, Beckmann MW, Beeghly-Fadiel A, Benitez J, Bermisheva M, Bernardini MQ, Birrer MJ, Bjorge L, Black A, Blankstein K, Blok MJ, Bodelon C, Bogdanova N, Bojesen A, Bonanni B, Borg Å, Bradbury AR, Brenton JD, Brewer C, Brinton L, Broberg P, Brooks-Wilson A, Bruinsma F, Brunet J, Buecher B, Butzow R, Buys SS, Caldes T, Caligo MA, Campbell I, Cannioto R, Carney ME, Cescon T, Chan SB, Chang-Claude J, Chanock S, Chen XQ, Chiew YE, Chiquette J, Chung WK, Claes KB, Conner T, Cook LS, Cook J, Cramer DW, Cunningham JM, D'Aloisio AA, Daly MB, Damiola F, Damirovna SD, Dansonka-Mieszkowska A, Dao F, Davidson R, DeFazio A, Delnatte C, Doheny KF, Diez O, Ding YC, Doherty JA, Domchek SM, Dorfling CM, Dörk T, Dossus L, Duran M, Dürst M, Dworniczak B, Eccles D, Edwards T, Eeles R, Eilber U, Ejlertsen B, Ekici AB, Ellis S, Elvira M; EMBRACE Study., Eng KH, Engel C, Evans DG, Fasching PA, Ferguson S, Ferrer SF, Flanagan JM, Fogarty ZC, Fortner RT, Fostira F, Foulkes WD, Fountzilas G, Fridley BL, Friebel TM, Friedman E, Frost D, Ganz PA, Garber J, García MJ, Garcia-Barberan V, Gehrig A; GEMO Study Collaborators., Gentry-Maharaj A, Gerdes AM, Giles GG, Glasspool R, Glendon G, Godwin AK, Goldgar DE, Goranova T, Gore M, Greene MH, Gronwald J, Gruber S, Hahnen E, Haiman CA, Håkansson N, Hamann U, Hansen TV, Harrington PA, Harris HR, Hauke J; HEBON Study., Hein A, Henderson A, Hildebrandt MA, Hillemanns P, Hodgson S, Høgdall CK, Høgdall E, Hogervorst FB, Holland H, Hooning MJ, Hosking K, Huang RY, Hulick PJ, Hung J, Hunter DJ, Huntsman DG, Huzarski T, Imyanitov EN, Isaacs C, Iversen ES, Izatt L, Izquierdo A, Jakubowska A, James P, Janavicius R, Jernetz M, Jensen A, Jensen UB, John EM, Johnatty S, Jones ME, Kannisto P, Karlan BY, Karnezis A, Kast K; KConFab Investigators., Kennedy CJ, Khusnutdinova E, Kiemeney LA, Kiiski JI, Kim SW, Kjaer SK, Köbel M, Kopperud RK, Kruse TA, Kupryjanczyk J, Kwong A, Laitman Y, Lambrechts D, Larrañaga N, Larson MC, Lazaro C, Le ND, Le Marchand L, Lee JW, Lele SB, Leminen A, Leroux D, Lester J, Lesueur F, Levine DA, Liang D, Liebrich C, Lilyquist J, Lipworth L, Lissowska J, Lu KH, Lubinński J, Luccarini C, Lundvall L, Mai PL, Mendoza-Fandiño G, Manoukian S, Massuger LF, May T, Mazoyer S, McAlpine JN, McGuire V, McLaughlin JR, McNeish I, Meijers-Heijboer H, Meindl A, Menon U, Mensenkamp AR, Merritt MA, Milne RL, Mitchell G, Modugno F, Moes-Sosnowska J, Moffitt M, Montagna M, Moysich KB, Mulligan AM, Musinsky J, Nathanson KL, Nedergaard L, Ness RB, Neuhausen SL, Nevanlinna H, Niederacher D, Nussbaum RL, Odunsi K, Olah E, Olopade OI, Olsson H, Olswold C, O'Malley DM, Ong KR, Onland-Moret NC; OPAL study group., Orr N, Orsulic S, Osorio A, Palli D, Papi L, Park-Simon TW, Paul J, Pearce CL, Pedersen IS, Peeters PH, Peissel B, Peixoto A, Pejovic T, Pelttari LM, Permuth JB, Peterlongo P, Pezzani L, Pfeiler G, Phillips KA, Piedmonte 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V, Dowsett M, Pharoah PD, Simard J, Hall P, García-Closas M, Vachon C, Chenevix-Trench G, Antoniou AC, Easton DF, Edwards SL: Breast cancer risk variants at 6q25 display different phenotype associations and regulate ESR1, RMND1 and CCDC170, Nat Genet, 2016 | | Hamdi Y, Soucy P, Kuchenbaeker KB, Pastinen T, Droit A, Lemaçon A, Adlard J, Aittomäki K, Andrulis IL, Arason A, Arnold N, Arun BK, Azzollini J, Bane A, Barjhoux L, Barrowdale D, Benitez J, Berthet P, Blok MJ, Bobolis K, Bonadona V, Bonanni B, Bradbury AR, Brewer C, Buecher B, Buys SS, Caligo MA, Chiquette J, Chung WK, Claes KB, Daly MB, Damiola F, Davidson R, De la Hoya M, De Leeneer K, Diez O, Ding YC, Dolcetti R, Domchek SM, Dorfling CM, Eccles D, Eeles R, Einbeigi Z, Ejlertsen B; EMBRACE, Engel C, Gareth Evans D, Feliubadalo L, Foretova L, Fostira F, Foulkes WD, Fountzilas G, Friedman E, Frost D, Ganschow P, Ganz PA, Garber J, Gayther SA; GEMO Study Collaborators, Gerdes AM, Glendon G, Godwin AK, Goldgar DE, Greene MH, 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Thomassen M, Tihomirova L, Tischkowitz M, Tognazzo S, Toland AE, Tung N, van den Ouweland AM, van der Luijt RB, van Engelen K, van Rensburg EJ, Varon-Mateeva R, Wappenschmidt B, Wijnen JT, Rebbeck T, Chenevix-Trench G, Offit K, Couch FJ, Nord S, Easton DF, Antoniou AC, Simard J: Association of breast cancer risk in BRCA1 and BRCA2 mutation carriers with genetic variants showing differential allelic expression: identification of a modifier of brea, Breast Cancer Res Treat, 2016 | | Lawrenson K, Kar S, McCue K, Kuchenbaeker K, Michailidou K, Tyrer J, Beesley J, Ramus SJ, Li Q, Delgado MK, Lee JM, Aittomäki K, Andrulis IL, Anton-Culver H, Arndt V, Arun BK, Arver B, Bandera EV, Barile M, Barkardottir RB, Barrowdale D, Beckmann MW, Benitez J, Berchuck A, Bisogna M, Bjorge L, Blomqvist C, Blot W, Bogdanova N, Bojesen A, Bojesen SE, Bolla MK, Bonanni B, Børresen-Dale AL, Brauch H, Brennan P, Brenner H, Bruinsma F, Brunet J, Buhari SA, Burwinkel B, Butzow R, Buys SS, Cai Q, Caldes T, Campbell I, Canniotto R, Chang-Claude J, Chiquette J, Choi JY, Claes KB, GEMO Study Collaborators, Cook LS, Cox A, Cramer DW, Cross SS, Cybulski C, Czene K, Daly MB, Damiola F, Dansonka-Mieszkowska A, Darabi H, Dennis J, Devilee P, Diez O, Doherty JA, Domchek SM, Dorfling CM, Dörk T, Dumont M, Ehrencrona H, Ejlertsen B, Ellis S, EMBRACE, Engel C, Lee E, Evans DG, Fasching PA, Feliubadalo L, Figueroa J, Flesch-Janys D, Fletcher O, Flyger H, Foretova L, Fostira F, Foulkes WD, Fridley BL, Friedman E, Frost D, Gambino G, Ganz PA, Garber J, García-Closas M, Gentry-Maharaj A, Ghoussaini M, Giles GG, Glasspool R, Godwin AK, Goldberg MS, Goldgar DE, González-Neira A, Goode EL, Goodman MT, Greene MH, Gronwald J, Guénel P, Haiman CA, Hall P, Hallberg E, Hamann U, Hansen TV, Harrington PA, Hartman M, Hassan N, Healey S, Hereditary Breast and Ovarian Cancer Research Group Netherlands (HEBON), Heitz F, Herzog J, Høgdall E, Høgdall CK, Hogervorst FB, Hollestelle A, Hopper JL, Hulick PJ, Huzarski T, Imyanitov EN, KConFab Investigators, Australian Ovarian Cancer Study Group, Isaacs C, Ito H, Jakubowska A, Janavicius R, Jensen A, John EM, Johnson N, Kabisch M, Kang D, Kapuscinski M, Karlan BY, Khan S, Kiemeney LA, Kjaer SK, Knight JA, Konstantopoulou I, Kosma VM, Kristensen V, Kupryjanczyk J, Kwong A, de la Hoya M, Laitman Y, Lambrechts D, Le N, De Leeneer K, Lester J, Levine DA, Li J, Lindblom A, Long J, Lophatananon A, Loud JT, Lu K, Lubinski J, Mannermaa A, Manoukian S, Le Marchand L, Margolin S, Marme F, Massuger LF, Matsuo K, Mazoyer S, McGuffog L, McLean C, McNeish I, Meindl A, Menon U, Mensenkamp AR, Milne RL, Montagna M, Moysich KB, Muir K, Mulligan AM, Nathanson KL, Ness RB, Neuhausen SL, Nevanlinna H, Nord S, Nussbaum RL, Odunsi K, Offit K, Olah E, Olopade OI, Olson JE, Olswold C, O'Malley D, Orlow I, Orr N, Osorio A, Park SK, Pearce CL, Pejovic T, Peterlongo P, Pfeiler G, Phelan CM, Poole EM, Pylkäs K, Radice P, Rantala J, Rashid MU, Rennert G, Rhenius V, Rhiem K, Risch HA, 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susceptibility locus, Nat Commun, 2016 | | Ovarian Cancer Association Consortium, Breast Cancer Association Consortium, and Consortium of Modifiers of BRCA1 and BRCA2, Hollestelle A, van der Baan FH, Berchuck A, Johnatty SE, Aben KK, Agnarsson BA, Aittomäki K, Alducci E, Andrulis IL, Anton-Culver H, Antonenkova NN, Antoniou AC, Apicella C, Arndt V, Arnold N, Arun BK, Arver B, Ashworth A; Australian Ovarian Cancer Study Group, Baglietto L, Balleine R, Bandera EV, Barrowdale D, Bean YT, Beckmann L, Beckmann MW, Benitez J, Berger A, Berger R, Beuselinck B, Bisogna M, Bjorge L, Blomqvist C, Bogdanova NV, Bojesen A, Bojesen SE, Bolla MK, Bonanni B, Brand JS, Brauch H; Breast Cancer Family Register, Brenner H, Brinton L, Brooks-Wilson A, Bruinsma F, Brunet J, Brüning T, Budzilowska A, Bunker CH, Burwinkel B, Butzow R, Buys SS, Caligo MA, Campbell I, Carter J, Chang-Claude J, Chanock SJ, Claes KB, Collée JM, Cook LS, Couch FJ, Cox A, Cramer D, Cross SS, Cunningham JM, Cybulski C, Czene K, Damiola F, Dansonka-Mieszkowska A, Darabi H, de la Hoya M, deFazio A, Dennis J, Devilee P, Dicks EM, Diez O, Doherty JA, Domchek SM, Dorfling CM, Dörk T, Silva ID, du Bois A, Dumont M, Dunning AM, Duran M, Easton DF, Eccles D, Edwards RP, Ehrencrona H, Ejlertsen B, Ekici AB, Ellis SD; EMBRACE, Engel C, Eriksson M, Fasching PA, Feliubadalo L, Figueroa J, Flesch-Janys D, Fletcher O, Fontaine A, Fortuzzi S, Fostira F, Fridley BL, Friebel T, Friedman E, Friel G, Frost D, Garber J, García-Closas M, Gayther SA; GEMO Study Collaborators; GENICA Network, Gentry-Maharaj A, Gerdes AM, Giles GG, Glasspool R, Glendon G, Godwin AK, Goodman MT, Gore M, Greene MH, Grip M, Gronwald J, Gschwantler Kaulich D, Guénel P, Guzman SR, Haeberle L, Haiman CA, Hall P, Halverson SL, Hamann U, Hansen TV, Harter P, Hartikainen JM, Healey S; HEBON, Hein A, Heitz F, Henderson BE, Herzog J, T Hildebrandt MA, Høgdall CK, Høgdall E, Hogervorst FB, Hopper JL, Humphreys K, Huzarski T, Imyanitov EN, Isaacs C, Jakubowska A, Janavicius R, Jaworska K, Jensen A, Jensen UB, Johnson N, Jukkola-Vuorinen A, Kabisch M, Karlan BY, Kataja V, Kauff N; KConFab Investigators, Kelemen LE, Kerin MJ, Kiemeney LA, Kjaer SK, Knight JA, Knol-Bout JP, Konstantopoulou I, Kosma VM, Krakstad C, Kristensen V, Kuchenbaecker KB, Kupryjanczyk J, Laitman Y, Lambrechts D, Lambrechts S, Larson MC, Lasa A, Laurent-Puig P, Lazaro C, Le ND, Le Marchand L, Leminen A, Lester J, Levine DA, Li J, Liang D, Lindblom A, Lindor N, Lissowska J, Long J, Lu KH, Lubinski J, Lundvall L, Lurie G, Mai PL, Mannermaa A, Margolin S, Mariette F, Marme F, Martens JW, Massuger LF, Maugard C, Mazoyer S, McGuffog L, McGuire V, McLean C, McNeish I, Meindl A, Menegaux F, Menéndez P, Menkiszak J, Menon U, Mensenkamp AR, Miller N, Milne RL, Modugno F, Montagna M, Moysich KB, Müller H, Mulligan AM, Muranen TA, Narod SA, Nathanson KL, Ness RB, Neuhausen SL, Nevanlinna H, Neven P, Nielsen FC, Nielsen SF, Nordestgaard BG, Nussbaum RL, Odunsi K, Offit K, Olah E, Olopade OI, Olson JE, Olson SH, Oosterwijk JC, Orlow I, Orr N, Orsulic S, Osorio A, Ottini L, Paul J, Pearce CL, Pedersen IS, Peissel B, Pejovic T, Pelttari LM, Perkins J, Permuth-Wey J, Peterlongo P, Peto J, Phelan CM, Phillips KA, Piedmonte M, Pike MC, Platte R, Plisiecka-Halasa J, Poole EM, Poppe B, Pylkäs K, Radice P, Ramus SJ, Rebbeck TR, Reed MW, Rennert G, Risch HA, Robson M, Rodriguez GC, Romero A, Rossing MA, Rothstein JH, Rudolph A, Runnebaum I, Salani R, Salvesen HB, Sawyer EJ, Schildkraut JM, Schmidt MK, Schmutzler RK, Schneeweiss A, Schoemaker MJ, Schrauder MG, Schumacher F, Schwaab I, Scuvera G, Sellers TA, Severi G, Seynaeve CM, Shah M, Shrubsole M, Siddiqui N, Sieh W, Simard J, Singer CF, Sinilnikova OM, Smeets D, Sohn C, Soller M, Song H, Soucy P, Southey MC, Stegmaier C, Stoppa-Lyonnet D, Sucheston L; SWE-BRCA, Swerdlow A, Tangen IL, Tea MK, Teixeira MR, Terry KL, Terry MB, Thomassen M, Thompson PJ, Tihomirova L, Tischkowitz M, Toland AE, Tollenaar RA, Tomlinson I, Torres D, Truong T, Tsimiklis H, Tung N, Tworoger SS, Tyrer JP, Vachon CM, Van 't Veer LJ, van Altena AM, Van Asperen CJ, van den Berg D, van den Ouweland AM, van Doorn HC, Van Nieuwenhuysen E, van Rensburg EJ, Vergote I, Verhoef S, Vierkant RA, Vijai J, Vitonis AF, von Wachenfeldt A, Walsh C, Wang Q, Wang-Gohrke S, Wappenschmidt B, Weischer M, Weitzel JN, Weltens C, Wentzensen N, Whittemore AS, Wilkens LR, Winqvist R, Wu AH, Wu X, Yang HP, Zaffaroni D, Pilar Zamora M, Zheng W, Ziogas A, Chenevix-Trench G, Pharoah PD, Rookus MA, Hooning MJ, Goode EL: No clinical utility of KRAS variant rs61764370 for ovarian or breast cancer, Gynecol Oncol, 2016 | | Papp J, Kovacs ME, Matrai Z, Orosz E, Kasler M, Borresen-Dale AL, Olah E: Contribution of APC and MUTYH mutations to familial adenomatous polyposis susceptibility in Hungary, Fam Cancer, 2016 | | Silvestri V, Barrowdale D, Mulligan AM, Neuhausen SL, Fox S, Karlan BY, Mitchell G, James P, Thull DL, Zorn KK, Carter NJ, Nathanson KL, Domchek SM, Rebbeck TR, Ramus SJ, Nussbaum RL, Olopade OI, Rantala J, Yoon SY, Caligo MA, Spugnesi L, Bojesen A, Pedersen IS, Thomassen M, Jensen UB, Toland AE, Senter L, Andrulis IL, Glendon G, Hulick PJ, Imyanitov EN, Greene MH, Mai PL, Singer CF, Rappaport-Fuerhauser C, Kramer G, Vijai J, Offit K, Robson M, Lincoln A, Jacobs L, Machackova E, Foretova L, Navratilova M, Vasickova P, Couch FJ, Hallberg E, Ruddy KJ, Sharma P, Kim SW; kConFab Investigators, Teixeira MR, Pinto P, Montagna M, Matricardi L, Arason A, Johannsson OT, Barkardottir RB, Jakubowska A, Lubinski J, Izquierdo A, Pujana MA, Balmaña J, Diez O, Ivady G, Papp J, Olah E, Kwong A; Hereditary Breast and Ovarian Cancer Research Group Netherlands (HEBON), Nevanlinna H, Aittomäki K, Perez Segura P, Caldes T, Van Maerken T, Poppe B, Claes KB, Isaacs C, Elan C, Lasset C, Stoppa-Lyonnet D, Barjhoux L, Belotti M, Meindl A, Gehrig A, Sutter C, Engel C, Niederacher D, Steinemann D, Hahnen E, Kast K, Arnold N, Varon-Mateeva R, Wand D, 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Kuchenbaecker KB, Beesley J, Adlard J, Agnarsson BA, Andrulis IL, Arun BK, Barjhoux L, Belotti M, Benitez J, Berger A, Bojesen A, Bonanni B, Brewer C, Caldes T, Caligo MA, Campbell I, Chan SB, Claes KB, Cohn DE, Cook J, Daly MB, Damiola F, Davidson R, Pauw Ad, Delnatte C, Diez O, Domchek SM, Dumont M, Durda K, Dworniczak B, Easton DF, Eccles D, Edwinsdotter Ardnor C, Eeles R, Ejlertsen B, Ellis S, Evans DG, Feliubadalo L, Fostira F, Foulkes WD, Friedman E, Frost D, Gaddam P, Ganz PA, Garber J, Garcia-Barberan V, Gauthier-Villars M, Gehrig A, Gerdes AM, Giraud S, Godwin AK, Goldgar DE, Hake CR, Hansen TV, Healey S, Hodgson S, Hogervorst FB, Houdayer C, Hulick PJ, Imyanitov EN, Isaacs C, Izatt L, Izquierdo A, Jacobs L, Jakubowska A, Janavicius R, Jaworska-Bieniek K, Jensen UB, John EM, Vijai J, Karlan BY, Kast K, Investigators K, Khan S, Kwong A, Laitman Y, Lester J, Lesueur F, Liljegren A, Lubinski J, Mai PL, Manoukian S, Mazoyer S, Meindl A, Mensenkamp AR, Montagna M, Nathanson KL, Neuhausen SL, Nevanlinna H, Niederacher D, Olah E, Olopade OI, Ong KR, Osorio A, Park SK, Paulsson-Karlsson Y, Pedersen IS, Peissel B, Peterlongo P, Pfeiler G, Phelan CM, Piedmonte M, Poppe B, Pujana MA, Radice P, Rennert G, Rodriguez GC, Rookus MA, Ross EA, Schmutzler RK, Simard J, Singer CF, Slavin TP, Soucy P, Southey M, Steinemann D, Stoppa-Lyonnet D, Sukiennicki G, Sutter C, Szabo CI, Tea MK, Teixeira MR, Teo SH, Terry MB, Thomassen M, Tibiletti MG, Tihomirova L, Tognazzo S, van Rensburg EJ, Varesco L, Varon-Mateeva R, Vratimos A, Weitzel JN, McGuffog L, Kirk J, Toland AE, Hamann U, Lindor N, Ramus SJ, Greene MH, Couch FJ, Offit K, Pharoah PD, Chenevix-Trench G, Antoniou AC: Fine-Scale Mapping at 9p22.2 Identifies Candidate Causal Variants That Modify Ovarian Cancer Risk in BRCA1 and BRCA2 Mutation CarriersBRCA1 and BRCA2 Mutation Carriers, PLoS ONE, 2016 | | Zeng C, Guo X, Long J, Kuchenbaecker KB, Droit A, Michailidou K, Ghoussaini M, Kar S, Freeman A, Hopper JL, Milne RL, Bolla MK, Wang Q, Dennis J, Agata S, Ahmed S, Aittomäki K, Andrulis IL, Anton-Culver H, Antonenkova NN, Arason A, Arndt V, Arun BK, Arver B, Bacot F, Barrowdale D, Baynes C, Beeghly-Fadiel A, Benitez J, Bermisheva M, Blomqvist C, Blot WJ, Bogdanova NV, Bojesen SE, Bonanni B, Borresen-Dale AL, Brand JS, Brauch H, Brennan P, Brenner H, Broeks A, Brüning T, Burwinkel B, Buys SS, Cai Q, Caldes T, Campbell I, Carpenter J, Chang-Claude J, Choi JY, Claes KB, Clarke C, Cox A, Cross SS, Czene K, Daly MB, de la Hoya M, De Leeneer K, Devilee P, Diez O, Domchek SM, Doody M, Dorfling CM, Dörk T, Dos-Santos-Silva I, Dumont M, Dwek M, Dworniczak B, Egan K, Eilber U, Einbeigi Z, Ejlertsen B, Ellis S, Frost D, Lalloo F, EMBRACE, Fasching PA, Figueroa J, Flyger H, Friedlander M, Friedman E, Gambino G, Gao YT, Garber J, García-Closas M, Gehrig A, Damiola F, Lesueur F, Mazoyer S, Stoppa-Lyonnet D, behalf of GEMO Study Collaborators, Giles GG, Godwin AK, Goldgar DE, González-Neira A, Greene MH, Guénel P, 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AL, Kristensen V, Salvesen HB, Bjorge L, Bandera EV, Risch H, Zheng W, Beeghly-Fadiel A, Cai H, Pylkäs K, Tollenaar RA, Ouweland AM, Andrulis IL, Knight JA; OCGN, Narod S, Devilee P, Winqvist R, Figueroa J, Greene MH, Mai PL, Loud JT, García-Closas M, Schoemaker MJ, Czene K, Darabi H, McNeish I, Siddiquil N, Glasspool R, Kwong A, Park SK, Teo SH, Yoon SY, Matsuo K, Hosono S, Woo YL, Gao YT, Foretova L, Singer CF, Rappaport-Feurhauser C, Friedman E, Laitman Y, Rennert G, Imyanitov EN, Hulick PJ, Olopade OI, Senter L, Olah E, Doherty JA, Schildkraut J, Koppert LB, Kiemeney LA, Massuger LF, Cook LS, Pejovic T, Li J, Borg A, Öfverholm A, Rossing MA, Wentzensen N, Henriksson K, Cox A, Cross SS, Pasini BJ, Shah M, Kabisch M, Torres D, Jakubowska A, Lubinski J, Gronwald J, Agnarsson BA, Kupryjanczyk J, Moes-Sosnowska J, Fostira F, Konstantopoulou I, Slager S, Jones M; PRostate cancer AssoCiation group To Investigate Cancer Associated aLterations in the genome, Antoniou AC, Berchuck A, Swerdlow A, Chenevix-Trench G, Dunning AM, Pharoah PD, Hall P, Easton DF, Couch FJ, Spurdle AB, Goldgar DE: BRCA2 Polymorphic Stop Codon K3326X and the Risk of Breast, Prostate, and Ovarian Cancers, J Natl Cancer Inst Epub 2015 Nov 19., 2015 | | Dunning AM, Michailidou K, Kuchenbaecker KB, Thompson D, French JD, Beesley J, Healey CS, Kar S, Pooley KA, Lopez-Knowles E, Dicks E, Barrowdale D, Sinnott-Armstrong NA, Sallari RC, Hillman KM, Kaufmann S, Sivakumaran H, Moradi Marjaneh M, Lee JS, Hills M, Jarosz M, Drury S, Canisius S, Bolla MK, Dennis J, Wang Q, Hopper JL, Southey MC, Broeks A, Schmidt MK, Lophatananon A, Muir K, Beckmann MW, Fasching PA, Dos-Santos-Silva I, Peto J, Sawyer EJ, Tomlinson I, Burwinkel B, Marme F, Guénel P, Truong T, Bojesen SE, Flyger H, González-Neira A, Perez JI, Anton-Culver H, Eunjung L, Arndt V, Brenner H, Meindl A, Schmutzler RK, Brauch H, Hamann U, Aittomäki K, Blomqvist C, Ito H, Matsuo K, Bogdanova N, Dörk T, Lindblom A, Margolin S, Kosma VM, Mannermaa 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Khaw KT, Helland Å, Haakensen V, Dowsett M, Pharoah PD, Simard J, Hall P, García-Closas M, Vachon C, Chenevix-Trench G, Antoniou AC, Easton DF, Edwards SL: Breast cancer risk variants at 6q25 display different phenotype associations and regulate ESR1, RMND1 and CCDC170, NATURE GENETICS 48(4): 374-386, 2016 | | Ovarian Cancer Association Consortium, Breast Cancer Association Consortium, and Consortium of Modifiers of BRCA1 and BRCA2, Hollestelle A, van der Baan FH, Berchuck A, Johnatty SE, Aben KK, Agnarsson BA, Aittomäki K, Alducci E, Andrulis IL, Anton-Culver H, Antonenkova NN, Antoniou AC, Apicella C, Arndt V, Arnold N, Arun BK, Arver B, Ashworth A; Australian Ovarian Cancer Study Group, Baglietto L, Balleine R, Bandera EV, Barrowdale D, Bean YT, Beckmann L, Beckmann MW, Benitez J, Berger A, Berger R, Beuselinck B, Bisogna M, Bjorge L, Blomqvist C, Bogdanova NV, Bojesen A, Bojesen SE, Bolla MK, Bonanni B, Brand JS, Brauch H; Breast Cancer Family Register, Brenner H, Brinton L, 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MM, Phelan CM, Greene MH, Mai PL, Rennert G, Mulligan AM, Glendon G, Tchatchou S, Andrulis IL, Toland AE, Bojesen A, Pedersen IS, Thomassen M, Jensen UB, Laitman Y, Rantala J, von Wachenfeldt A, Ehrencrona H, Askmalm MS, Borg Å, Kuchenbaecker KB, McGuffog L, Barrowdale D, Healey S, Lee A, Pharoah PD, Chenevix-Trench G, Antoniou AC, Friedman E; on behalf of EMBRACE; on behalf of GEMO Study Collaborators; on behalf of HEBON; on behalf of KConFab Investigators: Candidate Genetic Modifiers for Breast and Ovarian Cancer Risk in BRCA1 and BRCA2 Mutation Carriers, CANDER EPIDEM BIOMAR PREV 24(1): 308-316, 2015 | | Rebbeck TR, Mitra N, Wan F, Sinilnikova OM, Healey S, McGuffog L, Mazoyer S, Chenevix-Trench G, Easton DF, Antoniou AC, Nathanson KL, CIMBA Consortium, Laitman Y, Kushnir A, Paluch-Shimon S, Berger R, Zidan J, Friedman E, Ehrencrona H, Stenmark-Askmalm M, Einbeigi Z, Loman N, Harbst K, Rantala J, Melin B, Huo D, Olopade OI, Seldon J, Ganz PA, Nussbaum RL, Chan SB, Odunsi K, Gayther 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Goldgar DE, Buys SS, Janavicius R, Dorfling CM, van Rensburg EJ, Neuhausen SL, Ding YC, Hansen TV, Jønson L, Gerdes AM, Ejlertsen B, Barrowdale D, Dennis J, Benitez J, Osorio A, Garcia MJ, Komenaka I, Weitzel JN, Ganschow P, Peterlongo P, Bernard L, Viel A, Bonanni B, Peissel B, Manoukian S, Radice P, Papi L, Ottini L, Fostira F, Konstantopoulou I, Garber J, Frost D, Perkins J, Platte R, Ellis S, EMBRACE, Godwin AK, Schmutzler RK, Meindl A, Engel C, Sutter C, Sinilnikova OM, GEMO Study Collaborators, Damiola F, Mazoyer S, Stoppa-Lyonnet D, Claes K, De Leeneer K, Kirk J, Rodriguez GC, Piedmonte M, O'Malley DM, de la Hoya M, Caldes T, Aittomäki K, Nevanlinna H, Collée JM, Rookus MA, Oosterwijk JC, Breast Cancer Family Registry, Tihomirova L, Tung N, Hamann U, Isaccs C, Tischkowitz M, Imyanitov EN, Caligo MA, Campbell IG, Hogervorst FB, HEBON, Olah E, Diez O, Blanco I, Brunet J, Lazaro C, Pujana MA, Jakubowska A, Gronwald J, Lubinski J, Sukiennicki G, Barkardottir RB, Plante M, Simard J, Soucy P, Montagna M, Tognazzo S, Teixeira MR, KConFab Investigators, Pankratz VS, Wang X, Lindor N, Szabo CI, Kauff N, Vijai J, Aghajanian CA, Pfeiler G, Berger A, Singer CF, Tea MK, Phelan CM, Greene MH, Mai PL, Rennert G, Mulligan AM, Tchatchou S, Andrulis IL, Glendon G, Toland AE, Jensen UB, Kruse TA, Thomassen M, Bojesen A, Zidan J, Friedman E, Laitman Y, Soller M, Liljegren A, Arver B, Einbeigi Z, Stenmark-Askmalm M, Olopade OI, Nussbaum RL, Rebbeck TR, Nathanson KL, Domchek SM, Lu KH, Karlan BY, Walsh C, Lester J, Australian Cancer Study (Ovarian Cancer Investigators), Australian Ovarian Cancer Study Group, Hein A, Ekici AB, Beckmann MW, Fasching PA, Lambrechts D, Van Nieuwenhuysen E, Vergote I, Lambrechts S, Dicks E, Doherty JA, Wicklund KG, Rossing MA, Rudolph A, Chang-Claude J, Wang-Gohrke S, Eilber U, Moysich KB, Odunsi K, Sucheston L, Lele S, Wilkens LR, Goodman MT, Thompson PJ, Shvetsov YB, Runnebaum IB, Dürst M, Hillemanns P, Dörk T, Antonenkova N, Bogdanova N, Leminen A, 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A, Anton-Culver H, Gentry-Maharaj A, Menon U, Harrington P, Lee AW, Wu AH, Pearce CL, Coetzee G, Pike MC, Dansonka-Mieszkowska A, Timorek A, Rzepecka IK, Kupryjanczyk J, Freedman M, Noushmehr H, Easton DF, Offit K, Couch FJ, Gayther S, Pharoah PP, Antoniou AC, Chenevix-Trench G, the Consortium of Investigators of Modifiers of BRCA1, BRCA2: Identification of six new susceptibility loci for invasive epithelial ovarian cancer, NATURE GENETICS 47(2): 164-171, 2015 | | Blanco I, Kuchenbaecker K, Cuadras D, Wang X, Barrowdale D, de Garibay GR, Librado P, Sánchez-Gracia A, Rozas J, Bonifaci N, McGuffog L, Pankratz VS, Islam A, Mateo F, Berenguer A, Petit A, Català I, Brunet J, Feliubadaló L, Tornero E, Benítez J, Osorio A, Cajal TR, Nevanlinna H, Aittomäki K, Arun BK, Toland AE, Karlan BY, Walsh C, Lester J, Greene MH, Mai PL, Nussbaum RL, Andrulis IL, Domchek SM, Nathanson KL, Rebbeck TR, Barkardottir RB, Jakubowska A, Lubinski J, Durda K, Jaworska-Bieniek K, Claes K, Van Maerken T, Díez O, 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