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151. Tamoxifen and contralateral breast cancer in BRCA1 and BRCA2 carriers: an update

Author

Gronwald, Jacek, Tung, Nadine, Foulkes, William D., Offit, Kenneth, Gershoni, Ruth, Daly, Mary, Kim-Sing, Charmaine, Olsson, Hakan, Ainsworth, Peter, Eisen, Andrea, Saal, Howard, Friedman, Eitan, Olopade, Olufunmilayo, Osborne, Michael, Weitzel, Jeffrey, Lynch, Henry, Ghadirian, Parviz, Lubinski, Jan, Sun, Ping, Narod, Steven A., Gilchrist, D., Weber, B., Rebbeck, T., Isaacs, C., Neuhausen, S., Garber, J., Karlan, B., Fishman, D., Merajver, S., McKinnon, W., Wood, M., Evans, G., Moller, P., Pasini, B., Sweet, K., Eng, C., Rennert, G., Couch, F., McLennan, J., and Provencher, D.

Subjects
Oncology, Adult, Cancer Research, medicine.medical_specialty, Oophorectomy, Antineoplastic Agents, Hormonal, medicine.medical_treatment, breast cancer, BRCA1, BRCA2, tamoxifen, DNA Mutational Analysis, Genes, BRCA2, Genes, BRCA1, Breast Neoplasms, Risk Assessment, Functional Laterality, Breast cancer, Internal medicine, medicine, Odds Ratio, Humans, Genetic Predisposition to Disease, Risk factor, skin and connective tissue diseases, Retrospective Studies, Gynecology, business.industry, Case-control study, Retrospective cohort study, Neoplasms, Second Primary, Odds ratio, Middle Aged, Antiestrogen, medicine.disease, Pedigree, Tamoxifen, Premenopause, Case-Control Studies, Female, business, medicine.drug
Abstract

Women with a mutation in BRCA1 or BRCA2 face a lifetime risk of breast cancer of approximately 80%, and following the first diagnosis the 10-year risk of contralateral breast cancer is approximately 30%. It has been shown that both tamoxifen and oophorectomy prevent contralateral breast cancer, but it is not clear whether there is a benefit in giving tamoxifen to women who have previously undergone an oophorectomy. Furthermore, the relative degree of protection in BRCA1 and BRCA2 carriers has not been well evaluated. We studied 285 women with bilateral breast cancer and a BRCA1 or BRCA2 mutation, and 751 control women with unilateral breast cancer and a BRCA1 or BRCA2 mutation in a matched case-control study. Control women were of similar age and had a similar age of diagnosis of breast cancer and had been followed for as long as the case for a second primary breast cancer. The history of tamoxifen use for treating the first breast cancer was compared between bilateral and unilateral cases. The multivariate odds ratio for contralateral breast cancer associated with tamoxifen use was 0.50 for carriers of BRCA1 mutations (95% CI, 0.30-0.85) and was 0.42 for carriers of BRCA2 mutations (95% CI, 0.17-1.02). The protective effect of tamoxifen was not seen among women who had undergone an oophorectomy (OR = 0.83; 95%CI, 0.24-2.89) but this subgroup was small. In contrast, a strong protective effect of tamoxifen was apparent among women who were premenopausal or who had undergone natural menopause (OR = 0.44; 95% CI, 0.27-0.65).

Published
2005

155. A Nonsynonymous Polymorphism in IRS1 Modifies Risk of Developing Breast and Ovarian Cancers in BRCA1 and Ovarian Cancer in BRCA2 Mutation Carriers

Author

Ding, Yuan C, McGuffog, Lesley, Healey, Sue, Friedman, Eitan, Laitman, Yael, Paluch-Shimon, Shani, Kaufman, Bella, Liljegren, Annelie, Lindblom, Annika, Olsson, Hakan, Kristoffersson, Ulf, Stenmark Askmalm, Marie, Melin, Beatrice, Domchek, Susan M, Nathanson, Katherine L, Rebbeck, Timothy R, Jakubowska, Anna, Lubinski, Jan, Jaworska, Katarzyna, Durda, Katarzyna, Gronwald, Jacek, Huzarski, Tomasz, Cybulski, Cezary, Byrski, Tomasz, Osorio, Ana, Ramony Cajal, Teresa, Stavropoulou, Alexandra V, Benitez, Javier, Hamann, Ute, Rookus, Matti, Aalfs, Cora M, de Lange, Judith L, Meijers-Heijboer, Hanne E J, Oosterwijk, Jan C, van Asperen, Christi J, Gomez Garcia, Encarna B, Hoogerbrugge, Nicoline, Jager, Agnes, van der Luijt, Rob B, Easton, Douglas F, Peock, Susan, Frost, Debra, Ellis, Steve D, Platte, Radka, Fineberg, Elena, Evans, D Gareth, Lalloo, Fiona, Izatt, Louise, Eeles, Ros, Adlard, Julian, Davidson, Rosemarie, Eccles, Diana, Cole, Trevor, Cook, Jackie, Brewer, Carole, Tischkowitz, Marc, Godwin, Andrew K, Pathak, Harsh, Stoppa-Lyonnet, Dominique, Sinilnikova, Olga M, Mazoyer, Sylvie, Barjhoux, Laure, Leone, Melanie, Gauthier-Villars, Marion, Caux-Moncoutier, Virginie, de Pauw, Antoine, Hardouin, Agnes, Berthet, Pascaline, Dreyfus, Helene, Fert Ferrer, Sandra, Collonge-Rame, Marie-Agnes, Sokolowska, Johanna, Buys, Saundra, Daly, Mary, Miron, Alex, Terry, Mary Beth, Chung, Wendy, John, Esther M, Southey, Melissa, Goldgar, David, Singer, Christian F, Tea, Muy-Kheng Maria, Gschwantler-Kaulich, Daphne, Fink-Retter, Anneliese, Hansen, Thomas V O, Ejlertsen, Bent, Johannsson, Oskar T, Offit, Kenneth, Sarrel, Kara, Gaudet, Mia M, Vijai, Joseph, Robson, Mark, Piedmonte, Marion R, Andrews, Lesley, Cohn, David, DeMars, Leslie R, DiSilvestro, Paul, Rodriguez, Gustavo, Ewart Toland, Amanda, Montagna, Marco, Agata, Simona, Imyanitov, Evgeny, Isaacs, Claudine, Janavicius, Ramunas, Lazaro, Conxi, Blanco, Ignacio, Ramus, Susan J, Sucheston, Lara, Karlan, Beth Y, Gross, Jenny, Ganz, Patricia A, Beattie, Mary S, Schmutzler, Rita K, Wappenschmidt, Barbara, Meindl, Alfons, Arnold, Norbert, Niederacher, Dieter, Preisler-Adams, Sabine, Gadzicki, Dorotehea, Varon-Mateeva, Raymonda, Deissler, Helmut, Gehrig, Andrea, Sutter, Christian, Kast, Karin, Nevanlinna, Heli, Aittomaki, Kristiina, Spurdle, Amanda B, Beesley, Jonathan, Chen, Xiaoqing, Tomlinson, Gail E, Weitzel, Jeffrey, Garber, Judy E, Olopade, Olufunmilayo I, Rubinstein, Wendy S, Tung, Nadine, Blum, Joanne L, Narod, Steven A, Brummel, Sean, Gillen, Daniel L, Lindor, Noralane, Fredericksen, Zachary, Pankratz, Vernon S, Couch, Fergus J, Radice, Paolo, Peterlongo, Paolo, Greene, Mark H, Loud, Jennifer T, Mai, Phuong L, Andrulis, Irene L, Glendon, Gord, Gerdes, Anne-Marie, Birk Jensen, Uffe, Skytte, Anne-Bine, Caligo, Maria A, Lee, Andrew, Chenevix-Trench, Georgia, Antoniou, Antonis C, Neuhausen, Susan L, Ding, Yuan C, McGuffog, Lesley, Healey, Sue, Friedman, Eitan, Laitman, Yael, Paluch-Shimon, Shani, Kaufman, Bella, Liljegren, Annelie, Lindblom, Annika, Olsson, Hakan, Kristoffersson, Ulf, Stenmark Askmalm, Marie, Melin, Beatrice, Domchek, Susan M, Nathanson, Katherine L, Rebbeck, Timothy R, Jakubowska, Anna, Lubinski, Jan, Jaworska, Katarzyna, Durda, Katarzyna, Gronwald, Jacek, Huzarski, Tomasz, Cybulski, Cezary, Byrski, Tomasz, Osorio, Ana, Ramony Cajal, Teresa, Stavropoulou, Alexandra V, Benitez, Javier, Hamann, Ute, Rookus, Matti, Aalfs, Cora M, de Lange, Judith L, Meijers-Heijboer, Hanne E J, Oosterwijk, Jan C, van Asperen, Christi J, Gomez Garcia, Encarna B, Hoogerbrugge, Nicoline, Jager, Agnes, van der Luijt, Rob B, Easton, Douglas F, Peock, Susan, Frost, Debra, Ellis, Steve D, Platte, Radka, Fineberg, Elena, Evans, D Gareth, Lalloo, Fiona, Izatt, Louise, Eeles, Ros, Adlard, Julian, Davidson, Rosemarie, Eccles, Diana, Cole, Trevor, Cook, Jackie, Brewer, Carole, Tischkowitz, Marc, Godwin, Andrew K, Pathak, Harsh, Stoppa-Lyonnet, Dominique, Sinilnikova, Olga M, Mazoyer, Sylvie, Barjhoux, Laure, Leone, Melanie, Gauthier-Villars, Marion, Caux-Moncoutier, Virginie, de Pauw, Antoine, Hardouin, Agnes, Berthet, Pascaline, Dreyfus, Helene, Fert Ferrer, Sandra, Collonge-Rame, Marie-Agnes, Sokolowska, Johanna, Buys, Saundra, Daly, Mary, Miron, Alex, Terry, Mary Beth, Chung, Wendy, John, Esther M, Southey, Melissa, Goldgar, David, Singer, Christian F, Tea, Muy-Kheng Maria, Gschwantler-Kaulich, Daphne, Fink-Retter, Anneliese, Hansen, Thomas V O, Ejlertsen, Bent, Johannsson, Oskar T, Offit, Kenneth, Sarrel, Kara, Gaudet, Mia M, Vijai, Joseph, Robson, Mark, Piedmonte, Marion R, Andrews, Lesley, Cohn, David, DeMars, Leslie R, DiSilvestro, Paul, Rodriguez, Gustavo, Ewart Toland, Amanda, Montagna, Marco, Agata, Simona, Imyanitov, Evgeny, Isaacs, Claudine, Janavicius, Ramunas, Lazaro, Conxi, Blanco, Ignacio, Ramus, Susan J, Sucheston, Lara, Karlan, Beth Y, Gross, Jenny, Ganz, Patricia A, Beattie, Mary S, Schmutzler, Rita K, Wappenschmidt, Barbara, Meindl, Alfons, Arnold, Norbert, Niederacher, Dieter, Preisler-Adams, Sabine, Gadzicki, Dorotehea, Varon-Mateeva, Raymonda, Deissler, Helmut, Gehrig, Andrea, Sutter, Christian, Kast, Karin, Nevanlinna, Heli, Aittomaki, Kristiina, Spurdle, Amanda B, Beesley, Jonathan, Chen, Xiaoqing, Tomlinson, Gail E, Weitzel, Jeffrey, Garber, Judy E, Olopade, Olufunmilayo I, Rubinstein, Wendy S, Tung, Nadine, Blum, Joanne L, Narod, Steven A, Brummel, Sean, Gillen, Daniel L, Lindor, Noralane, Fredericksen, Zachary, Pankratz, Vernon S, Couch, Fergus J, Radice, Paolo, Peterlongo, Paolo, Greene, Mark H, Loud, Jennifer T, Mai, Phuong L, Andrulis, Irene L, Glendon, Gord, Gerdes, Anne-Marie, Birk Jensen, Uffe, Skytte, Anne-Bine, Caligo, Maria A, Lee, Andrew, Chenevix-Trench, Georgia, Antoniou, Antonis C, and Neuhausen, Susan L

Abstract

Background: We previously reported significant associations between genetic variants in insulin receptor substrate 1 (IRS1) and breast cancer risk in women carrying BRCA1 mutations. The objectives of this study were to investigate whether the IRS1 variants modified ovarian cancer risk and were associated with breast cancer risk in a larger cohort of BRCA1 and BRCA2 mutation carriers. less thanbrgreater than less thanbrgreater thanMethods: IRS1 rs1801123, rs1330645, and rs1801278 were genotyped in samples from 36 centers in the Consortium of Investigators of Modifiers of BRCA1/2 (CIMBA). Data were analyzed by a retrospective cohort approach modeling the associations with breast and ovarian cancer risks simultaneously. Analyses were stratified by BRCA1 and BRCA2 status and mutation class in BRCA1 carriers. less thanbrgreater than less thanbrgreater thanResults: Rs1801278 (Gly972Arg) was associated with ovarian cancer risk for both BRCA1 (HR, 1.43; 95% confidence interval (CI), 1.06-1.92; P = 0.019) and BRCA2 mutation carriers (HR, 2.21; 95% CI, 1.39-3.52, P = 0.0008). For BRCA1 mutation carriers, the breast cancer risk was higher in carriers with class II mutations than class I mutations (class II HR, 1.86; 95% CI, 1.28-2.70; class I HR, 0.86; 95%CI, 0.69-1.09; P-difference, 0.0006). Rs13306465 was associated with ovarian cancer risk in BRCA1 class II mutation carriers (HR, 2.42; P = 0.03). less thanbrgreater than less thanbrgreater thanConclusion: The IRS1 Gly972Arg single-nucleotide polymorphism, which affects insulin-like growth factor and insulin signaling, modifies ovarian cancer risk in BRCA1 and BRCA2 mutation carriers and breast cancer risk in BRCA1 class II mutation carriers. less thanbrgreater than less thanbrgreater thanImpact: These findings may prove useful for risk prediction for breast and ovarian cancers in BRCA1 and BRCA2 mutation carriers., Funding Agencies|NIH|R01CA74415P30CA033752|Israel cancer association||Mutua Madrilena Foundation||Red de Investigacion en Cancer|RD06/0020/1160|Spanish Ministry of Science and Innovation|FIS P1081120SAF2010-20493|Cancer Research UK|C1287/A10118C1287/A11990C5047/A8385|NIHR||NEYE Foundation||Clinical Genetics Branch, DCEG National Cancer Institute (NCI)||Community Oncology and Prevention Trials Program-COPTRG National Cancer Institute (NCI)||Russian Foundation for Basic Research|10-04-9211010-04-9260111-04-00227|Federal Agency for Science and Innovations|02.740.11.0780|Royal Society|JP090615|Research Council of Lithuania|LIG-19/2010|Institut Catala dOncologia (ICO)||Asociacion Espanola Contra el Cancer, Spanish Health Research Fund||Carlos III Health Institute||Catalan Health Institute||Autonomous Government of Catalonia|ISCIIIRETIC RD06/0020/1051PI10/01422PI10/314882009SGR290|American Cancer Society|120950-SIOP-06-258-06-COUN|German Cancer Aid|DKH 109076|Helsinki University Central Hospital||Academy of Finland|132473|Finnish Cancer Society||Sigrid Juselius Foundation||Canadian Institutes of Health Research||Canadian Breast Cancer Research Alliance|019511|NCI, under RFA|CA-06-503|Cancer Care Ontario|U01 CA69467|Cancer Prevention Institute of California|U01 CA69417|Columbia University|U01 CA69398|Fox Chase Cancer Center|U01 CA69631|Huntsman Cancer Institute|U01 CA69446|University of Melbourne|U01 CA69638|National Health and Medical Research Council of Australia||New South Wales Cancer Council||Victorian Health Promotion Foundation (Australia)||Victorian Breast Cancer Research Consortium||NITA|P01 CA16094R01 CA22435|National Institutes of Health|P30 CA13696P30 ES009089UL1 RR025764R01278978|National Center for Research Resources||National Center for Advancing Translational Sciences||NCI|P30 CA042014|NHMRC|145684288704454508|US NCI at the NIH|NO2-CP-11019-50N02-CP-65504|Westat, Inc.||Breast cancer Research Foundation||Komen Foundation for the Cure||Dutch Cancer Society

Published
2012
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156. Different fractions of human serum glycoproteins bind galectin-1 or galectin-8, and their ratio may provide a refined biomarker for pathophysiological conditions in cancer and inflammatory disease

Author

Carlsson, Michael C, Balog, Crina I A, Kilsgard, Ola, Hellmark, Thomas, Bakoush, Omran, Segelmark, Mårten, Ferno, Marten, Olsson, Hakan, Malmstrom, Johan, Wuhrer, Manfred, Leffler, Hakon, Carlsson, Michael C, Balog, Crina I A, Kilsgard, Ola, Hellmark, Thomas, Bakoush, Omran, Segelmark, Mårten, Ferno, Marten, Olsson, Hakan, Malmstrom, Johan, Wuhrer, Manfred, and Leffler, Hakon

Abstract

Background: Changes in glycosylation of serum proteins are common, and various glycoforms are being explored as biomarkers in cancer and inflammation. We recently showed that glycoforms detected by endogenous galectins not only provide potential biomarkers, but also have different functions when they encounter galectins in tissue cells. Now we have explored the use of a combination of two galectins with different specificities, to further increase biomarker sensitivity and specificity. less thanbrgreater than less thanbrgreater thanMethods: Sera from 14 women with metastatic breast cancer, 12 healthy controls, 14 patients with IgA-nephritis (IgAN), and 12 patients with other glomerulonephritis were fractionated by affinity chromatography on immobilized human galectin-1 or galectin-8N, and the protein amounts of the bound and unbound fractions for each galectin were determined. less thanbrgreater than less thanbrgreater thanResults: Each galectin bound largely different fractions of the serum glycoproteins, including different glycoforms of haptoglobin. In the cancer sera, the level of galectin-1 bound glycoproteins was higher and galectin-8N bound glycoproteins lower compared to the other patients groups, whereas in IgAN sera the level of galectin-8N bound glycoproteins were higher. less thanbrgreater than less thanbrgreater thanConclusion: The ratio of galectin-1 bound/galectin-8N bound glycoproteins showed high discriminatory power between cancer patients and healthy, with AUC of 0.98 in ROC analysis, and thus provides an interesting novel cancer biomarker candidate. less thanbrgreater than less thanbrgreater thanGeneral significance: The galectin-binding ability of a glycoprotein is not only a promising biomarker candidate but may also have a specific function when the glycoprotein encounters the galectin in tissue cells, and thus be related to the pathophysiological state of the patient. This article is part of a Special Issue entitled Glycoproteomics., Funding Agencies|Swedish Research Council (Vetenskapsradet)||Region Skane||Swedish Cancer Society||Lund University Hospital Foundation||Swedish Research Council|2008-3356|Swedish Foundation for Swedish Research|FFL4|Crafoord Foundation||Swedish Healthcare System

Published
2012
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157. Gene expression profiling of primary male breast cancers reveals two unique subgroups and identifies N-acetyltransferase-1 (NAT1) as a novel prognostic biomarker

Author

Johansson, Ida, Nilsson, Cecilia, Berglund, Pontus, Lauss, Martin, Ringner, Markus, Olsson, Hakan, Luts, Lena, Sim, Edith, Thorstensson, Sten, Fjallskog, Marie-Louise, Hedenfalk, Ingrid, Johansson, Ida, Nilsson, Cecilia, Berglund, Pontus, Lauss, Martin, Ringner, Markus, Olsson, Hakan, Luts, Lena, Sim, Edith, Thorstensson, Sten, Fjallskog, Marie-Louise, and Hedenfalk, Ingrid

Abstract

Introduction: Male breast cancer (MBC) is a rare and inadequately characterized disease. The aim of the present study was to characterize MBC tumors transcriptionally, to classify them into comprehensive subgroups, and to compare them with female breast cancer (FBC). less thanbrgreater than less thanbrgreater thanMethods: A total of 66 clinicopathologically well-annotated fresh frozen MBC tumors were analyzed using Illumina Human HT-12 bead arrays, and a tissue microarray with 220 MBC tumors was constructed for validation using immunohistochemistry. Two external gene expression datasets were used for comparison purposes: 37 MBCs and 359 FBCs. less thanbrgreater than less thanbrgreater thanResults: Using an unsupervised approach, we classified the MBC tumors into two subgroups, luminal M1 and luminal M2, respectively, with differences in tumor biological features and outcome, and which differed from the intrinsic subgroups described in FBC. The two subgroups were recapitulated in the external MBC dataset. Luminal M2 tumors were characterized by high expression of immune response genes and genes associated with estrogen receptor (ER) signaling. Luminal M1 tumors, on the other hand, despite being ER positive by immunohistochemistry showed a lower correlation to genes associated with ER signaling and displayed a more aggressive phenotype and worse prognosis. Validation of two of the most differentially expressed genes, class 1 human leukocyte antigen (HLA) and the metabolizing gene N-acetyltransferase-1 (NAT1), respectively, revealed significantly better survival associated with high expression of both markers (HLA, hazard ratio (HR) 3.6, P = 0.002; NAT1, HR 2.5, P = 0.033). Importantly, NAT1 remained significant in a multivariate analysis (HR 2.8, P = 0.040) and may thus be a novel prognostic marker in MBC. less thanbrgreater than less thanbrgreater thanConclusions: We have detected two unique and stable subgroups of MBC with differences in tumor biological features an, Funding Agencies|Swedish Cancer Society||G Nilsson Cancer Foundation||Mrs. B Kamprad Foundation||Lund University Hospital Research Foundation||SCIBLU Genomics center||governmental funding of clinical research within the national health services (ALF)||Lund University

Published
2012
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158. High-resolution genomic profiling of male breast cancer reveals differences hidden behind the similarities with female breast cancer

Author

Johansson, Ida, Nilsson, Cecilia, Berglund, Pontus, Strand, Carina, Jonsson, Goran, Staaf, Johan, Ringner, Markus, Nevanlinna, Heli, Barkardottir, Rosa B., Borg, Ake, Olsson, Hakan, Luts, Lena, Fjällskog, Marie-Louise, Hedenfalk, Ingrid, Johansson, Ida, Nilsson, Cecilia, Berglund, Pontus, Strand, Carina, Jonsson, Goran, Staaf, Johan, Ringner, Markus, Nevanlinna, Heli, Barkardottir, Rosa B., Borg, Ake, Olsson, Hakan, Luts, Lena, Fjällskog, Marie-Louise, and Hedenfalk, Ingrid

Abstract

Male breast cancer (MBC) is extremely rare and poorly characterized on the molecular level. Using high-resolution genomic data, we aimed to characterize MBC by genomic imbalances and to compare it with female breast cancer (FBC), and further to investigate whether the genomic profiles hold any prognostic information. Fifty-six fresh frozen MBC tumors were analyzed using high-resolution tiling BAC arrays. Significant regions in common between cases were assessed using Genomic Identification of Significant Targets in Cancer (GISTIC) analysis. A publicly available genomic data set of 359 FBC tumors was used for reference purposes. The data revealed a broad pattern of aberrations, confirming that MBC is a heterogeneous tumor type. Genomic gains were more common in MBC than in FBC and often involved whole chromosome arms, while losses of genomic material were less frequent. The most common aberrations were similar between the genders, but high-level amplifications were more common in FBC. We identified two genomic subgroups among MBCs; male-complex and male-simple. The male-complex subgroup displayed striking similarities with the previously reported luminal-complex FBC subgroup, while the male-simple subgroup seems to represent a new subgroup of breast cancer occurring only in men. There are many similarities between FBC and MBC with respect to genomic imbalances, but there are also distinct differences as revealed by high-resolution genomic profiling. MBC can be divided into two comprehensive genomic subgroups, which may be of prognostic value. The male-simple subgroup appears notably different from any genomic subgroup so far defined in FBC.

Published
2011
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159. Changes in Tree Growth, Biomass and Vegetation Over a 13-Year Period in the Swedish Sub-Arctic

Author

Hedenas, Henrik, Olsson, Hakan, Jonasson, Christer, Bergstedt, Johan, Dahlberg, Ulrika, Hedenas, Henrik, Olsson, Hakan, Jonasson, Christer, Bergstedt, Johan, and Dahlberg, Ulrika

Abstract

This study was conducted in the Swedish sub-Arctic, near Abisko, in order to assess the direction and scale of possible vegetation changes in the alpine-birch forest ecotone. We have re-surveyed shrub, tree and vegetation data at 549 plots grouped into 61 clusters. The plots were originally surveyed in 1997 and re-surveyed in 2010. Our study is unique for the area as we have quantitatively estimated a 19% increase in tree biomass mainly within the existing birch forest. We also found significant increases in the cover of two vegetation types-"birch forest-heath with mosses and "meadow with low herbs, while the cover of snowbed vegetation decreased significantly. The vegetation changes might be caused by climate, herbivory and past human impact but irrespective of the causes, the observed transition of the vegetation will have substantial effects on the mountain ecosystems., Funding Agencies|Swedish Environmental Protection Agency||IPY|512214-2008-188|Swedish National Forest Inventory||Abisko Arctic Scientific Research Station

Published
2011
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160. Genetic Variation at 9p22.2 and Ovarian Cancer Risk for BRCA1 and BRCA2 Mutation Carriers

Author

Ramus, Susan J, Kartsonaki, Christiana, A Gayther, Simon, D P Pharoah, Paul, M Sinilnikova, Olga, Beesley, Jonathan, Chen, Xiaoqing, McGuffog, Lesley, Healey, Sue, J Couch, Fergus, Wang, Xianshu, Fredericksen, Zachary, Peterlongo, Paolo, Manoukian, Siranoush, Peissel, Bernard, Zaffaroni, Daniela, Roversi, Gaia, Barile, Monica, Viel, Alessandra, Allavena, Anna, Ottini, Laura, Papi, Laura, Gismondi, Viviana, Capra, Fabio, Radice, Paolo, H Greene, Mark, L Mai, Phuong, L Andrulis, Irene, Glendon, Gord, Ozcelik, Hilmi, Thomassen, Mads, Gerdes, Anne-Marie, A Kruse, Torben, Cruger, Dorthe, Birk Jensen, Uffe, Adelaide Caligo, Maria, Olsson, Hakan, Lindblom, Annika, Arver, Brita, Karlsson, Per, Stenmark Askmalm, Marie, Borg, Ake, L Neuhausen, Susan, Chun Ding, Yuan, L Nathanson, Katherine, M Domchek, Susan, Jakubowska, Anna, Lubinski, Jan, Huzarski, Tomasz, Byrski, Tomasz, Gronwald, Jacek, Gorski, Bohdan, Cybulski, Cezary, Debniak, Tadeusz, Osorio, Ana, Tejada, Maria-Isabel, Benitez, Javier, Hamann, Ute, A Rookus, Matti, Verhoef, Senno, A Tilanus-Linthorst, Madeleine, P Vreeswijk, Maaike, Bodmer, Danielle, G E M Ausems, Margreet, A van Os, Theo, J Asperen, Christi, J Blok, Marinus, E J Meijers-Heijboer, Hanne, Peock, Susan, Cook, Margaret, Oliver, Clare, Frost, Debra, M Dunning, Alison, Gareth Evans, D, Eeles, Ros, Cole, Trevor, Hodgson, Shirley, J Morrison, Patrick, Porteous, Mary, John Kennedy, M, T Rogers, Mark, E Side, Lucy, Donaldson, Alan, Gregory, Helen, Godwin, Andrew, Moncoutier, Virginie, Castera, Laurent, Mazoyer, Sylvie, Bonadona, Valerie, Leroux, Dominique, Faivre, Laurence, Lidereau, Rosette, Nogues, Catherine, Bignon, Yves-Jean, Prieur, Fabienne, Collonge-Rame, Marie-Agnes, Venat-Bouvet, Laurence, Fert-Ferrer, Sandra, Miron, Alex, S Buys, Saundra, L Hopper, John, B Daly, Mary, M John, Esther, Beth Terry, Mary, Goldgar, David, V O Hansen, Thomas, Jonson, Lars, Ejlertsen, Bent, A Agnarsson, Bjarni, Offit, Kenneth, Kirchhoff, Tomas, Vijai, Joseph, V C Dutra-Clarke, Ana, A Przybylo, Jennifer, Montagna, Marco, Casella, Cinzia, N Imyanitov, Evgeny, Janavicius, Ramunas, Blanco, Ignacio, Lazaro, Conxi, B Moysich, Kirsten, Y Karlan, Beth, Gross, Jenny, Schmutzler, Rita, Wappenschmidt, Barbara, Meindl, Alfons, Fiebig, Britta, Sutter, Christian, Arnold, Norbert, Deissler, Helmut, Varon-Mateeva, Raymonda, Kast, Karin, Niederacher, Dieter, Gadzicki, Dorothea, Caldes, Trinidad, Nevanlinna, Heli, Aittomaeki, Kristiina, Simard, Jacques, Soucy, Penny, B Spurdle, Amanda, Holland, Helene, Chenevix-Trench, Georgia, F Easton, Douglas, C Antoniou, Antonis, Ramus, Susan J, Kartsonaki, Christiana, A Gayther, Simon, D P Pharoah, Paul, M Sinilnikova, Olga, Beesley, Jonathan, Chen, Xiaoqing, McGuffog, Lesley, Healey, Sue, J Couch, Fergus, Wang, Xianshu, Fredericksen, Zachary, Peterlongo, Paolo, Manoukian, Siranoush, Peissel, Bernard, Zaffaroni, Daniela, Roversi, Gaia, Barile, Monica, Viel, Alessandra, Allavena, Anna, Ottini, Laura, Papi, Laura, Gismondi, Viviana, Capra, Fabio, Radice, Paolo, H Greene, Mark, L Mai, Phuong, L Andrulis, Irene, Glendon, Gord, Ozcelik, Hilmi, Thomassen, Mads, Gerdes, Anne-Marie, A Kruse, Torben, Cruger, Dorthe, Birk Jensen, Uffe, Adelaide Caligo, Maria, Olsson, Hakan, Lindblom, Annika, Arver, Brita, Karlsson, Per, Stenmark Askmalm, Marie, Borg, Ake, L Neuhausen, Susan, Chun Ding, Yuan, L Nathanson, Katherine, M Domchek, Susan, Jakubowska, Anna, Lubinski, Jan, Huzarski, Tomasz, Byrski, Tomasz, Gronwald, Jacek, Gorski, Bohdan, Cybulski, Cezary, Debniak, Tadeusz, Osorio, Ana, Tejada, Maria-Isabel, Benitez, Javier, Hamann, Ute, A Rookus, Matti, Verhoef, Senno, A Tilanus-Linthorst, Madeleine, P Vreeswijk, Maaike, Bodmer, Danielle, G E M Ausems, Margreet, A van Os, Theo, J Asperen, Christi, J Blok, Marinus, E J Meijers-Heijboer, Hanne, Peock, Susan, Cook, Margaret, Oliver, Clare, Frost, Debra, M Dunning, Alison, Gareth Evans, D, Eeles, Ros, Cole, Trevor, Hodgson, Shirley, J Morrison, Patrick, Porteous, Mary, John Kennedy, M, T Rogers, Mark, E Side, Lucy, Donaldson, Alan, Gregory, Helen, Godwin, Andrew, Moncoutier, Virginie, Castera, Laurent, Mazoyer, Sylvie, Bonadona, Valerie, Leroux, Dominique, Faivre, Laurence, Lidereau, Rosette, Nogues, Catherine, Bignon, Yves-Jean, Prieur, Fabienne, Collonge-Rame, Marie-Agnes, Venat-Bouvet, Laurence, Fert-Ferrer, Sandra, Miron, Alex, S Buys, Saundra, L Hopper, John, B Daly, Mary, M John, Esther, Beth Terry, Mary, Goldgar, David, V O Hansen, Thomas, Jonson, Lars, Ejlertsen, Bent, A Agnarsson, Bjarni, Offit, Kenneth, Kirchhoff, Tomas, Vijai, Joseph, V C Dutra-Clarke, Ana, A Przybylo, Jennifer, Montagna, Marco, Casella, Cinzia, N Imyanitov, Evgeny, Janavicius, Ramunas, Blanco, Ignacio, Lazaro, Conxi, B Moysich, Kirsten, Y Karlan, Beth, Gross, Jenny, Schmutzler, Rita, Wappenschmidt, Barbara, Meindl, Alfons, Fiebig, Britta, Sutter, Christian, Arnold, Norbert, Deissler, Helmut, Varon-Mateeva, Raymonda, Kast, Karin, Niederacher, Dieter, Gadzicki, Dorothea, Caldes, Trinidad, Nevanlinna, Heli, Aittomaeki, Kristiina, Simard, Jacques, Soucy, Penny, B Spurdle, Amanda, Holland, Helene, Chenevix-Trench, Georgia, F Easton, Douglas, and C Antoniou, Antonis

Abstract

Background Germline mutations in the BRCA1 and BRCA2 genes are associated with increased risks of breast and ovarian cancers. Although several common variants have been associated with breast cancer susceptibility in mutation carriers, none have been associated with ovarian cancer susceptibility. A genome-wide association study recently identified an association between the rare allele of the single-nucleotide polymorphism (SNP) rs3814113 (ie, the C allele) at 9p22.2 and decreased risk of ovarian cancer for women in the general population. We evaluated the association of this SNP with ovarian cancer risk among BRCA1 or BRCA2 mutation carriers by use of data from the Consortium of Investigators of Modifiers of BRCA1/2. Methods We genotyped rs3814113 in 10 029 BRCA1 mutation carriers and 5837 BRCA2 mutation carriers. Associations with ovarian and breast cancer were assessed with a retrospective likelihood approach. All statistical tests were two-sided. Results The minor allele of rs3814113 was associated with a reduced risk of ovarian cancer among BRCA1 mutation carriers (per-allele hazard ratio of ovarian cancer = 0.78, 95% confidence interval = 0.72 to 0.85; P = 4.8 x 10(-9)) and BRCA2 mutation carriers (hazard ratio of ovarian cancer = 0.78, 95% confidence interval = 0.67 to 0.90; P = 5.5 x 10(-4)). This SNP was not associated with breast cancer risk among either BRCA1 or BRCA2 mutation carriers. BRCA1 mutation carriers with the TT genotype at SNP rs3814113 were predicted to have an ovarian cancer risk to age 80 years of 48%, and those with the CC genotype were predicted to have a risk of 33%. Conclusion Common genetic variation at the 9p22.2 locus was associated with decreased risk of ovarian cancer for carriers of a BRCA1 or BRCA2 mutation.

Published
2011
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161. Association of the Variants CASP8 D302H and CASP10 V410I with Breast and Ovarian Cancer Risk in BRCA1 and BRCA2 Mutation Carriers

Author

Engel, Christoph, Versmold, Beatrix, Wappenschmidt, Barbara, Simard, Jacques, Easton, Douglas F., Peock, Susan, Cook, Margaret, Oliver, Clare, Frost, Debra, Mayes, Rebecca, Evans, D. Gareth, Eeles, Rosalind, Paterson, Joan, Brewer, Carole, McGuffog, Lesley, Antoniou, Antonis C., Stoppa-Lyonnet, Dominique, Sinilnikova, Olga M., Barjhoux, Laure, Frenay, Marc, Michel, Cecile, Leroux, Dominique, Dreyfus, Helene, Toulas, Christine, Gladieff, Laurence, Uhrhammer, Nancy, Bignon, Yves-Jean, Meindl, Alfons, Arnold, Norbert, Varon-Mateeva, Raymonda, Niederacher, Dieter, Preisler-Adams, Sabine, Kast, Karin, Deissler, Helmut, Sutter, Christian, Gadzicki, Dorothea, Chenevix-Trench, Georgia, Spurdle, Amanda B., Chen, Xiaoqing, Beesley, Jonathan, Olsson, Hakan, Kristoffersson, Ulf, Ehrencrona, Hans, Liljegren, Annelie, van der Luijt, Rob B., van Os, Theo A., van Leeuwen, Flora E., Domchek, Susan M., Rebbeck, Timothy R., Nathanson, Katherine L., Osorio, Ana, Ramon y Cajal, Teresa, Konstantopoulou, Irene, Benitez, Javier, Friedman, Eitan, Kaufman, Bella, Laitman, Yael, Mai, Phuong L., Greene, Mark H., Nevanlinna, Heli, Aittomaki, Kristiina, Szabo, Csilla I., Caldes, Trinidad, Couch, Fergus J., Andrulis, Irene L., Godwin, Andrew K., Hamann, Ute, Schmutzler, Rita K., Engel, Christoph, Versmold, Beatrix, Wappenschmidt, Barbara, Simard, Jacques, Easton, Douglas F., Peock, Susan, Cook, Margaret, Oliver, Clare, Frost, Debra, Mayes, Rebecca, Evans, D. Gareth, Eeles, Rosalind, Paterson, Joan, Brewer, Carole, McGuffog, Lesley, Antoniou, Antonis C., Stoppa-Lyonnet, Dominique, Sinilnikova, Olga M., Barjhoux, Laure, Frenay, Marc, Michel, Cecile, Leroux, Dominique, Dreyfus, Helene, Toulas, Christine, Gladieff, Laurence, Uhrhammer, Nancy, Bignon, Yves-Jean, Meindl, Alfons, Arnold, Norbert, Varon-Mateeva, Raymonda, Niederacher, Dieter, Preisler-Adams, Sabine, Kast, Karin, Deissler, Helmut, Sutter, Christian, Gadzicki, Dorothea, Chenevix-Trench, Georgia, Spurdle, Amanda B., Chen, Xiaoqing, Beesley, Jonathan, Olsson, Hakan, Kristoffersson, Ulf, Ehrencrona, Hans, Liljegren, Annelie, van der Luijt, Rob B., van Os, Theo A., van Leeuwen, Flora E., Domchek, Susan M., Rebbeck, Timothy R., Nathanson, Katherine L., Osorio, Ana, Ramon y Cajal, Teresa, Konstantopoulou, Irene, Benitez, Javier, Friedman, Eitan, Kaufman, Bella, Laitman, Yael, Mai, Phuong L., Greene, Mark H., Nevanlinna, Heli, Aittomaki, Kristiina, Szabo, Csilla I., Caldes, Trinidad, Couch, Fergus J., Andrulis, Irene L., Godwin, Andrew K., Hamann, Ute, and Schmutzler, Rita K.

Abstract

Background: The genes caspase-8 (CASP8) and caspase-10 (CASP10) functionally cooperate and play a key role in the initiation of apoptosis. Suppression of apoptosis is one of the major mechanisms underlying the origin and progression of cancer. Previous case-control studies have indicated that the polymorphisms CASP8 D302H and CASP10 V410I are associated with a reduced risk of breast cancer in the general population. Methods: To evaluate whether the CASP8 D302H (CASP10 V410I) polymorphisms modify breast or ovarian cancer risk in BRCA1 and BRCA2 mutation carriers, we analyzed 7,353 (7,227) subjects of white European origin provided by 19 (18) study groups that participate in the Consortium of Investigators of Modifiers of BRCA1/2 (CIMBA). A weighted cohort approach was used to estimate hazard ratios (HR) and 95% confidence intervals (95% CI). Results: The minor allele of CASP8 D302H was significantly associated with a reduced risk of breast cancer (per-allele HR, 0.85; 95% CI, 0.76-0.97; P-trend = 0.011) and ovarian cancer (per-allele HR, 0.69; 95% CI, 0.53-0.89; P-trend = 0.004) for BRCA1 but not for BRCA2 mutation carriers. The CASP10 V410I polymorphism was not associated with breast or ovarian cancer risk for BRCA1 or BRCA2 mutation carriers. Conclusions: CASP8 D302H decreases breast and ovarian cancer risk for BRCA1 mutation carriers but not for BRCA2 mutation carriers. Impact: The combined application of these and other recently identified genetic risk modifiers could in the future allow better individual risk calculation and could aid in the individualized counseling and decision making with respect to preventive options in BRCA1 mutation carriers.

Published
2010
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163. 62

Author

Russell, James, primary, Vincent, Jean-Louis, additional, Kjølbye, Anne Louise, additional, Olsson, Hakan, additional, Blemings, Allan, additional, and Grundemar, Lars, additional

Published
2012
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167. Deletion of 14q in non-Hodgkin's lymphoma

Author

Kristoffersson, Ulf, primary, Heim, Sverre, additional, Johnsson, Anna, additional, Mandahl, Nils, additional, Olsson, Hakan, additional, Åkerman, Måns, additional, and Mitelman, Felix, additional

Published
2009
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177. ALOS PALSAR Calibration and Validation Results from Sweden

Author

Eriksson, Leif E.B., primary, Sandberg, Gustaf, additional, Ulander, Lars M.H., additional, Smith-Jonforsen, Gary, additional, Hallberg, Bjorn, additional, Folkesson, Klas, additional, Fransson, Johan E.S., additional, Magnusson, Mattias, additional, Olsson, Hakan, additional, Gustavsson, Anders, additional, and Flood, Bjorn, additional

Published
2007
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179. Chromosome 5 imbalance mapping in breast tumors from BRCA1 and BRCA2 mutation carriers and sporadic breast tumors

Author

Johannsdottir, Hrefna K., primary, Jonsson, Goran, additional, Johannesdottir, Gudrun, additional, Agnarsson, Bjarni A., additional, Eerola, Hannaleena, additional, Arason, Adalgeir, additional, Heikkila, Paivi, additional, Egilsson, Valgardur, additional, Olsson, Hakan, additional, Johannsson, Oskar Th., additional, Nevanlinna, Heli, additional, Borg, Ake, additional, and Barkardottir, Rosa B., additional

Published
2006
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181. Age at menarche and the risk of breast cancer in BRCA1 and BRCA2 mutation carriers

Author

Kotsopoulos, Joanne, primary, Lubinski, Jan, additional, Lynch, Henry T., additional, Neuhausen, Susan L., additional, Ghadirian, Parviz, additional, Isaacs, Claudine, additional, Weber, Barbara, additional, Kim-Sing, Charmaine, additional, Foulkes, William D., additional, Gershoni-Baruch, Ruth, additional, Ainsworth, Peter, additional, Friedman, Eitan, additional, Daly, Mary, additional, Garber, Judy E., additional, Karlan, Beth, additional, Olopade, Olufunmilayo I., additional, Tung, Nadine, additional, Saal, Howard M., additional, Eisen, Andrea, additional, Osborne, Michael, additional, Olsson, Hakan, additional, Gilchrist, Dawna, additional, Sun, Ping, additional, and Narod, Steven A., additional

Published
2005
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182. Functional characterization of a multi-cancer risk locus on chr5p15.33 reveals regulation of TERT by ZNF148

Author

Fang, Jun, Jia, Jinping, Makowski, Matthew, Xu, Mai, Wang, Zhaoming, Zhang, Tongwu, Hoskins, Jason W., Choi, Jiyeon, Han, Younghun, Zhang, Mingfeng, Thomas, Janelle, Kovacs, Michael, Collins, Irene, Dzyadyk, Marta, Thompson, Abbey, O'Neill, Maura, Das, Sudipto, Lan, Qi, Koster, Roelof, Canzian, Federico, Kooperberg, Charles, Arslan, Alan A, Bracci, Paige M, Buring, Julie, Duell, Eric J, Gallinger, Steven, Jacobs, Eric J, Kamineni, Aruna, Van Den Eeden, Stephen, Klein, Alison P, Kolonel, Laurence N, Li, Donghui, Olson, Sara H, Risch, Harvey A, Sesso, Howard D, Visvanathan, Kala, Zheng, Wei, Albanes, Demetrius, Austin, Melissa A, Boutron-Ruault, Marie-Christine, Bueno-de-Mesquita, H Bas, Cotterchio, Michelle, Gaziano, J Michael, Giovannucci, Edward L, Goggins, Michael, Gross, Myron, Hassan, Manal, Helzlsouer, Kathy J, Holly, Elizabeth A, Hunter, David J, Jenab, Mazda, Kaaks, Rudolf, Key, Timothy J, Khaw, Kay-Tee, Krogh, Vittorio, Kurtz, Robert C, LaCroix, Andrea, Le Marchand, Loic, Mannisto, Satu, Patel, Alpa V, Peeters, Petra H M, Riboli, Elio, Shu, Xiao-Ou, Sund, Malin, Thornquist, Mark, Tjønneland, Anne, Tobias, Geoffrey S, Trichopoulos, Dimitrios, Wactawski-Wende, Jean, Yu, Herbert, Yu, Kai, Zeleniuch-Jacquotte, Anne, Hoover, Robert, Hartge, Patricia, Fuchs, Charles, Chanock, Stephen J, Stevens, Victoria, Albanes, Demetrios, Caporaso, Neil E, Brennan, Paul, McKay, James, Wu, Xifeng, Hung, Rayjean J, McLaughlin, John R, Bickeboller, Heike, Risch, Angela, Wichmann, Erich, Houlston, Richard, Mann, Graham, Hopper, John, Aitken, Joanne, Armstrong, Bruce, Giles, Graham, Holland, Elizabeth, Kefford, Richard, Cust, Anne, Jenkins, Mark, Schmid, Helen, Puig, Susana, Aguilera, Paula, Badenas, Celia, Barreiro, Alicia, Carrera, Cristina, Gabriel, Daniel, Xavier, Pol Gimenez, Iglesias-Garcia, Pablo, Malvehy, Josep, Mila, Montse, Pigem, Ramon, Potrony, Miriam, Batille, Joan-AntonPuig, Marti, Gemma Tell, Hayward, Nick, Martin, Nicholas, Montgomery, Grant, Duffy, David, Whiteman, David, Gregor, Stuart Mac, Calista, Donato, Landi, Giorgi, Minghetti, Paola, Arcangeli, Fabio, Bertazzi, Pier Alberto, Ghiorzo, Paola, Scarra, Giovanna Bianchi, Pastorino, Lorenze, Bruno, William, Andreotti, Virginia, Queirolo, Paola, Spagnolo, Francesco, Mackie, Rona, Lang, Julie, Gruis, Nelleke, van Nieuwpoort, Frans A, Out, Coby, Bergman, Wilma, Kukutsch, Nicole, Bavinck, Jan Nico Bouwes, Bakker, Bert, van der Stoep, Nienke, ter Huurne, Jeanet, van der Rhee, Han, Bekkenk, Marcel, Snels, Dyon, van Praag, Marinus, Brochez, Lieve, Gerritsen, Rianne, Crijns, Marianne, Vasen, Hans, Janssen, Bart, Ingvar, Christian, Olsson, Hakan, Jonsson, Goran, Borg, Ake, Harbst, Katja, Nielsen, Kari, Zander, Anita Schmidt, Molvern, Anders, Helsing, Per, Andresen, Per Arne, Rootwelt, Helge, Akslen, Lars A, Bressac-de Paillerets, Brigitte, Demenais, Florence, Avril, Marie-Francoise, Chaudru, Valerie, Jeannin, Patricia, Lesueur, Fabienne, Maubec, Eve, Mohamdi, Hamida, Bossard, Myriam, Vaysse, Amaury, Boitier, Francoise, Caron, Oliver, Caux, Frederic, Dalle, Stephane, Dereure, Oliviier, Leroux, Dominique, Martin, Ludovic, Mateus, Christine, Robert, Caroline, Stoppa-Lyonnet, Dominique, Thomas, Luc, Wierzbicka, Eva, Elder, David, Ming, Michael, Mitra, Nandita, Debniak, Tadeusz, Lubinski, Jan, Hocevar, Marko, Novakovic, Srdjan, Peric, Barbara, Skerl, Petra, Hansson, Johan, Hoiom, Veronica, Freidman, Eitan, Azizi, Esther, Baron-Epel, Orna, Scope, Alon, Pavlotsky, Felix, Cohen-Manheim, Irit, Laitman, Yael, Harland, Mark, Randerson-Moor, Juliette, Laye, Jon, Davies, John, Nsengimana, Jeremie, O'Shea, Sally, Chan, May, Gascoyne, Jo, Tucker, Margaret A, Goldstein, Alisa M, Yang, Xiaohong R, Stolzenberg-Solomon, Rachael S., Kraft, Peter, Wolpin, Brian M., Jansen, Pascal W. T. C., Olson, Sara, McGlynn, Katherine A., Kanetsky, Peter A., Chatterjee, Nilanjan, Barrett, Jennifer H., Dunning, Alison M., Taylor, John C., Newton-Bishop, Julia A., Bishop, D. Timothy, Andresson, Thorkell, Petersen, Gloria M., Amos, Christopher I., Iles, Mark M., Nathanson, Katherine L., Landi, Maria Teresa, Vermeulen, Michiel, Brown, Kevin M., and Amundadottir, Laufey T.

Abstract

Genome wide association studies (GWAS) have mapped multiple independent cancer susceptibility loci to chr5p15.33. Here, we show that fine-mapping of pancreatic and testicular cancer GWAS within one of these loci (Region 2 in CLPTM1L) focuses the signal to nine highly correlated SNPs. Of these, rs36115365-C associated with increased pancreatic and testicular but decreased lung cancer and melanoma risk, and exhibited preferred protein-binding and enhanced regulatory activity. Transcriptional gene silencing of this regulatory element repressed TERT expression in an allele-specific manner. Proteomic analysis identifies allele-preferred binding of Zinc finger protein 148 (ZNF148) to rs36115365-C, further supported by binding of purified recombinant ZNF148. Knockdown of ZNF148 results in reduced TERT expression, telomerase activity and telomere length. Our results indicate that the association with chr5p15.33-Region 2 may be explained by rs36115365, a variant influencing TERT expression via ZNF148 in a manner consistent with elevated TERT in carriers of the C allele.

Published
2017
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184. Oral Contraceptives and the Risk of Hereditary Ovarian Cancer

Author

Narod, Steven A., primary, Risch, Harvey, additional, Moslehi, Roxana, additional, Dorum, Anne, additional, Neuhausen, Susan, additional, Olsson, Hakan, additional, Provencher, Diane, additional, Radice, Paolo, additional, Bishop, Susan, additional, Brunet, Jean-Sebastien, additional, and Ponder, Bruce A. J., additional

Published
1999
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187. Effect of Pregnancy on Prognosis for Young Women With Breast Cancer

Author

Guinee, Vincent F., primary, Olsson, Hakan, additional, Moller, Torgil, additional, Hess, Kenneth R., additional, Taylor, Sarah H., additional, Fahey, Thomas, additional, Gladikov, Juri V., additional, van den Blink, Joep W., additional, Bonichon, Francoise, additional, Dische, Stanley, additional, Yates, Jerome W., additional, and Cleton, Frans J., additional

Published
1995
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191. Prediction of forest stem volume using kriging adapted to detected edges.

Author

Wallerman, Jörgen, Joyce, Steve, Vencatasawmy, Coormaren P., and Olsson, Hakan

Subjects
FOREST management, PLANNING, GEOLOGICAL maps
Abstract

Investigates the application of a dynamic forestry planning in the prediction of forest stem volume. Creation of a high spatial resolution map from geopositioned field plot data; Dependence of the dynamic system on the accuracy of methods used in developing the map; Significance of the output from an edge-detection algorithm.

Published
2002
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192. Molecular stratification of metastatic melanoma using gene expression profiling : Prediction of survival outcome and benefit from molecular targeted therapy

Author

Cirenajwis, Helena, Ekedahl, Henrik, Lauss, Martin, Harbst, Katja, Carneiro, Ana, Enoksson, Jens, Rosengren, Frida, Werner-Hartman, Linda, Törngren, Therese, Kvist, Anders, Fredlund, Erik, Bendahl, Pär-Ola, Jirström, Karin, Lundgren, Lotta, Howlin, Jillian, Borg, Åke, Gruvberger-Saal, Sofia K., Saal, Lao H., Nielsen, Kari, Ringnér, Markus, Tsao, Hensin, Olsson, Håkan, Ingvar, Christian, Staaf, Johan, and Jönsson, Göran

Subjects
gene expression, melanoma, BRAF, BRAF inhibitor, mutation
Abstract

Melanoma is currently divided on a genetic level according to mutational status. However, this classification does not optimally predict prognosis. In prior studies, we have defined gene expression phenotypes (high-immune, pigmentation, proliferative and normal-like), which are predictive of survival outcome as well as informative of biology. Herein, we employed a population-based metastatic melanoma cohort and external cohorts to determine the prognostic and predictive significance of the gene expression phenotypes. We performed expression profiling on 214 cutaneous melanoma tumors and found an increased risk of developing distant metastases in the pigmentation (HR, 1.9; 95% CI, 1.05-3.28; P=0.03) and proliferative (HR, 2.8; 95% CI, 1.43-5.57; P=0.003) groups as compared to the high-immune response group. Further genetic characterization of melanomas using targeted deep-sequencing revealed similar mutational patterns across these phenotypes. We also used publicly available expression profiling data from melanoma patients treated with targeted or vaccine therapy in order to determine if our signatures predicted therapeutic response. In patients receiving targeted therapy, melanomas resistant to targeted therapy were enriched in the MITF-low proliferative subtype as compared to pre-treatment biopsies (P=0.02). In summary, the melanoma gene expression phenotypes are highly predictive of survival outcome and can further help to discriminate patients responding to targeted therapy.

Published
2015

193. Immunologic Proliferation Marker Ki-S2 as Prognostic Indicator for Lymph Node-Negative Breast Cancer

Author

Rudolf, Pierre, Alm, Per, Heidebrecht, Hans-Jurgen, Bolte, Hendrik, Ratjen, Virgo, Baldetorp, Bo, Ferno, Marten, Olsson, Hakan, and Parwaresch, Reza

Subjects
Breast cancer -- Physiological aspects, Cell proliferation -- Research, Health
Abstract

Background: Proper treatment of lymph node-negative breast cancer depends on an accurate prognosis. To improve prognostic models for this disease, we evaluated whether an immunohistochemical marker for proliferating cells, Ki-S2 (a monoclonal antibody that binds to a 100-kd nuclear protein expressed in S, G2, and M phases of the cell cycle), is an accurate indicator of prognosis. Methods: We studied 371 Swedish women with lymph node-negative breast cancer; the median follow-up time was 95 months. The fraction of tumor cells in S phase was assessed by flow cytometry, and tumor cell proliferation was measured immunohistochemically with the monoclonal antibodies Ki-S2 and Ki-S5 (directed against the nuclear antigen Ki-67). A combined prognostic index was calculated on the basis of the S-phase fraction, progesterone receptor content, and tumor size. Results: In multivariate analyses that did or did not (263 and 332 observations, respectively) include the S-phase fraction and the combined prognostic index, the Ki-S2 labeling index (percentage of antibody-stained tumor cell nuclei) emerged as the most statistically significant predictor of overall survival, disease-specific survival, and disease-free survival (all two-sided P [is less than] .0001). In the risk group defined by a Ki-S2 labeling index of 10% or less, life expectancy was not statistically significantly different from that of age-matched women without breast cancer, whereas the group with a high Ki-S2 labeling index had an increased risk of mortality of up to 20-fold. Conclusions: Cellular proliferation is a major determinant of the biologic behavior of breast cancer. Prognosis is apparently best indicated by the percentage of cells in S through M phases of the cell cycle. Measurement of the Ki-S2 labeling index of a tumor sample may improve a clinician's ability to make an accurate prognosis and to identify patients with a low risk of recurrence who may not need adjuvant therapy. [J Natl Cancer Inst 1999;91:271-8]

Published
1999

194. Immunologic proliferation marker Ki-S2 as prognostic indicator for lymph node-negative breast cancer.

Author

Rudolph, Pierre, Alm, Per, Heidebrecht, Hans-Jurgen, Bolte, Hendrik, Ratjen, Virgo, Baldetorp, Bo, Ferno, Marten, Olsson, Hakan, Parwaresch, Reza, Rudolph, P, Alm, P, Heidebrecht, H J, Bolte, H, Ratjen, V, Baldetorp, B, Fernö, M, Olsson, H, and Parwaresch, R

Subjects
IMMUNOHISTOCHEMISTRY, CELL proliferation, MONOCLONAL antibodies, PROGNOSIS, BREAST cancer
Abstract

Background: Proper treatment of lymph node-negative breast cancer depends on an accurate prognosis. To improve prognostic models for this disease, we evaluated whether an immunohistochemical marker for proliferating cells, Ki-S2 (a monoclonal antibody that binds to a 100-kd nuclear protein expressed in S, G2, and M phases of the cell cycle), is an accurate indicator of prognosis.Methods: We studied 371 Swedish women with lymph node-negative breast cancer; the median follow-up time was 95 months. The fraction of tumor cells in S phase was assessed by flow cytometry, and tumor cell proliferation was measured immunohistochemically with the monoclonal antibodies Ki-S2 and Ki-S5 (directed against the nuclear antigen Ki-67). A combined prognostic index was calculated on the basis of the S-phase fraction, progesterone receptor content, and tumor size.Results: In multivariate analyses that did or did not (263 and 332 observations, respectively) include the S-phase fraction and the combined prognostic index, the Ki-S2 labeling index (percentage of antibody-stained tumor cell nuclei) emerged as the most statistically significant predictor of overall survival, disease-specific survival, and disease-free survival (all two-sided P<.0001). In the risk group defined by a Ki-S2 labeling index of 10% or less, life expectancy was not statistically significantly different from that of age-matched women without breast cancer, whereas the group with a high Ki-S2 labeling index had an increased risk of mortality of up to 20-fold.Conclusions: Cellular proliferation is a major determinant of the biologic behavior of breast cancer. Prognosis is apparently best indicated by the percentage of cells in S through M phases of the cell cycle. Measurement of the Ki-S2 labeling index of a tumor sample may improve a clinician's ability to make an accurate prognosis and to identify patients with a low risk of recurrence who may not need adjuvant therapy. [ABSTRACT FROM AUTHOR]

Published
1999
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195. Breast Size in Relation to Endogenous Hormone Levels, Body Constitution, and Oral Contraceptive Use in Healthy Nulligravid Women Aged 19–25 Years.

Author

Jemström, Helena and Olsson, Hakan

Subjects
SIZE of breast, ORAL contraceptives, HUMAN constitution, SEX hormones, GONADOTROPIN, PROGESTERONE
Abstract

In 1993 and 1994, the relation between breast size and hormonal factors and body constitution was studied in 65 healthy nulligravid women aged 19–25 years. Twenty-five women were current oral contraceptive users, 20 women were former users, and 20 women had never used oral contraceptives. Breast size was strongly positively correlated with current oral contraceptive use during menstrual cycle days 5–10, as well as days 18–23. No significant effect of former oral contraceptive use was seen on breast size. A significant increase in breast size between cycle days 5–10 and days 18–23 was seen among current oral contraceptive users. Breast size was significantly positively correlated with body mass index (weight (kg)/height (m)2), height, and weight in nonusers (i.e., former and never users combined) but not in current users. In nonusers, during the follicular phase, breast size was significantly positively associated with insulin-like growth factor 1. During the luteal phase, larger breast sizes were significantly associated with higher 17β-estradiol and progesterone levels and lower testosterone levels among nonusers. In models for current users, large breast sizes were significantly associated with high prolactin and luteinizing hormone levels and low follicle-stimulating hormone levels during cycle days 5–10. During cycle days 18–23, larger breast sizes correlated with low endogenous progesterone levels. [ABSTRACT FROM AUTHOR]

Published
1997
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199. Re: High frequency of multiple melanomas and breast and pancreas carcinomas in CDKN2A mutation-positive melanoma families.

Author

Plna, Kamila, Hemminki, Kari, Olsson, Hakan, Andersson, Harald, Bladstrom, Anna, Borg, Ake, Ingvar, Christian, Moller, Torgil, Westerdahl, Johan, Plna, K, and Hemminki, K

Subjects
MELANOMA, GENETICS of breast cancer, BREAST tumors, GENETIC mutation, ONCOGENES, PANCREATIC tumors, SKIN tumors, DISEASE incidence
Abstract

Discusses the high frequency of multiple melanomas and breast and pancreas carcinomas among CDKN2A mutation-positive melanoma families in Sweden. Calculation of standardized incidence ratio; Interaction among parental susceptibility genes in the offspring.

Published
2001
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200. Genome-wide association study identifies three new melanoma susceptibility loci

Author

Barrett, Jennifer H., Iles, Mark M., Harland, Mark, Taylor, John C., Aitken, Joanne F., Andresen, Per Arne, Akslen, Lars A., Armstrong, Bruce K., Avril, Marie F., Azizi, Esther, Bakker, Bert, Bergman, Wilma, Bianchi-Scarrà, Giovanna, Bressac-de Paillerets, Brigitte, Calista, Donato, Cannon-Albright, Lisa A., Corda, Eve, Cust, Anne E., Debniak, Tadeusz, Duffy, David, Dunning, Alison M., Easton, Douglas F., Friedman, Eitan, Galan, Pilar, Ghiorzo, Paola, Giles, Graham G., Hansson, Johan, Hocevar, Marko, Höiom, Veronica, Hopper, John L., Ingvar, Christian, Janssen, Bart, Jenkins, Mark A., Jönsson, Göran, Kefford, Richard F., Landi, Giorgio, Landi, Maria Teresa, Lang, Julie, Lubinski, Jan, Mackie, Rona, Malvehy, J. (Josep), Martin, Nicholas G., Molven, Anders, Montgomery, Grant W., Nieuwpoort, Frans A. van, Novakovic, Srdjan, Olsson, Hakan, Pastorino, Lorenza, Puig i Sardà, Susana, Puig Butillé, Joan Anton, Randerson-Moor, Juliette, Snowden, Helen, Tuominen, Raider, Belle, Patricia van, Stoep, Nienke van der, Whiteman, David C., Zelenika, Diana, Han, Jiali, Fang, Shenying, Lee, Jeffrey E., Wei, Qingyi, Lathrop, G. Mark, Gillanders, Elizabeth M., Brown, Kevin M., Goldstein, Alisa M., Kanetsky, Peter A., Mann, Graham J., MacGregor, Stuart, Elder, David E., Amos, Christopher I., Hayward, Nicholas K., Gruis, Nelleke A., Demenais, Florence, Newton-Bishop, Julia, Bishop, D. Timothy, GenoMEL Consortium, and Universitat de Barcelona

Subjects
Genètica mèdica, Medical genetics, Skin cancer, Melanoma, Càncer de pell
Abstract

We report a genome-wide association study for melanoma that was conducted by the GenoMEL Consortium. Our discovery phase included 2,981 individuals with melanoma and 1,982 study-specific control individuals of European ancestry, as well as an additional 6,426 control subjects from French or British populations, all of whom were genotyped for 317,000 or 610,000 single-nucleotide polymorphisms (SNPs). Our analysis replicated previously known melanoma susceptibility loci. Seven new regions with at least one SNP with P < 10−5 and further local imputed or genotyped support were selected for replication using two other genome-wide studies (from Australia and Texas, USA). Additional replication came from case-control series from the UK and The Netherlands. Variants at three of the seven loci replicated at P < 10−3: an SNP in ATM (rs1801516, overall P = 3.4 × 10−9), an SNP in MX2 (rs45430, P = 2.9 × 10−9) and an SNP adjacent to CASP8 (rs13016963, P = 8.6 × 10−10). A fourth locus near CCND1 remains of potential interest, showing suggestive but inconclusive evidence of replication (rs1485993, overall P = 4.6 × 10−7 under a fixed-effects model and P = 1.2 × 10−3 under a random-effects model). These newly associated variants showed no association with nevus or pigmentation phenotypes in a large British case-control series.

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