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2. Description of selected characteristics of familial glioma patients – Results from the Gliogene Consortium

Author

Sadetzki, Siegal, Bruchim, Revital, Oberman, Bernice, Armstrong, Georgina N, Lau, Ching C, Claus, Elizabeth B, Barnholtz-Sloan, Jill S, Il’yasova, Dora, Schildkraut, Joellen, Johansen, Christoffer, Houlston, Richard S, Shete, Sanjay, Amos, Christopher I, Bernstein, Jonine L, Olson, Sara H, Jenkins, Robert B, Lachance, Daniel, Vick, Nicholas A, Merrell, Ryan, Wrensch, Margaret, Davis, Faith G, McCarthy, Bridget J, Lai, Rose, Melin, Beatrice S, Bondy, Melissa L, and Consortium, Gliogene

Subjects
Brain Disorders, Cancer, Clinical Research, Neurosciences, Rare Diseases, Brain Cancer, Adolescent, Adult, Age Factors, Aged, Aged, 80 and over, Child, Child, Preschool, Denmark, Family Health, Female, Glioma, Humans, Incidence, Infant, Israel, Male, Middle Aged, Neoplasm Grading, Pedigree, Prevalence, Sex Factors, Sweden, United States, Young Adult, Familial glioma, Clinical characteristics, Genetic counselling, Gliogene Consortium, Oncology and Carcinogenesis, Public Health and Health Services, Oncology & Carcinogenesis
Abstract

BackgroundWhile certain inherited syndromes (e.g. Neurofibromatosis or Li-Fraumeni) are associated with an increased risk of glioma, most familial gliomas are non-syndromic. This study describes the demographic and clinical characteristics of the largest series of non-syndromic glioma families ascertained from 14 centres in the United States (US), Europe and Israel as part of the Gliogene Consortium.MethodsFamilies with 2 or more verified gliomas were recruited between January 2007 and February 2011. Distributions of demographic characteristics and clinical variables of gliomas in the families were described based on information derived from personal questionnaires.FindingsThe study population comprised 841 glioma patients identified in 376 families (9797 individuals). There were more cases of glioma among males, with a male to female ratio of 1.25. In most families (83%), 2 gliomas were reported, with 3 and 4 gliomas in 13% and 3% of the families, respectively. For families with 2 gliomas, 57% were among 1st-degree relatives, and 31.5% among 2nd-degree relatives. Overall, the mean (±standard deviation [SD]) diagnosis age was 49.4 (±18.7) years. In 48% of families with 2 gliomas, at least one was diagnosed at

Published
2013

3. A Variable Age of Onset Segregation Model for Linkage Analysis, with Correction for Ascertainment, Applied to Glioma

Author

Sun, Xiangqing, Vengoechea, Jaime, Elston, Robert, Chen, Yanwen, Amos, Christopher I, Armstrong, Georgina, Bernstein, Jonine L, Claus, Elizabeth, Davis, Faith, Houlston, Richard S, Il'yasova, Dora, Jenkins, Robert B, Johansen, Christoffer, Lai, Rose, Lau, Ching C, Liu, Yanhong, McCarthy, Bridget J, Olson, Sara H, Sadetzki, Siegal, Schildkraut, Joellen, Shete, Sanjay, Yu, Robert, Vick, Nicholas A, Merrell, Ryan, Wrensch, Margaret, Yang, Ping, Melin, Beatrice, Bondy, Melissa L, Barnholtz-Sloan, Jill S, and Consortium, on behalf of the Gliogene

Subjects
Epidemiology, Health Sciences, Clinical Research, Neurosciences, Rare Diseases, Brain Disorders, Genetics, Human Genome, Adult, Age of Onset, Brain Neoplasms, Female, Gene Frequency, Genetic Linkage, Glioma, Humans, Likelihood Functions, Lod Score, Male, Middle Aged, Models, Genetic, Pedigree, Prevalence, United States, Gliogene Consortium, Medical and Health Sciences, Biomedical and clinical sciences, Health sciences
Abstract

BackgroundWe propose a 2-step model-based approach, with correction for ascertainment, to linkage analysis of a binary trait with variable age of onset and apply it to a set of multiplex pedigrees segregating for adult glioma.MethodsFirst, we fit segregation models by formulating the likelihood for a person to have a bivariate phenotype, affection status and age of onset, along with other covariates, and from these we estimate population trait allele frequencies and penetrance parameters as a function of age (N = 281 multiplex glioma pedigrees). Second, the best fitting models are used as trait models in multipoint linkage analysis (N = 74 informative multiplex glioma pedigrees). To correct for ascertainment, a prevalence constraint is used in the likelihood of the segregation models for all 281 pedigrees. Then the trait allele frequencies are reestimated for the pedigree founders of the subset of 74 pedigrees chosen for linkage analysis.ResultsUsing the best-fitting segregation models in model-based multipoint linkage analysis, we identified 2 separate peaks on chromosome 17; the first agreed with a region identified by Shete and colleagues who used model-free affected-only linkage analysis, but with a narrowed peak: and the second agreed with a second region they found but had a larger maximum log of the odds (LOD).ConclusionsOur approach was able to narrow the linkage peak previously published for glioma.ImpactWe provide a practical solution to model-based linkage analysis for disease affection status with variable age of onset for the kinds of pedigree data often collected for linkage analysis.

Published
2012

4. Insight in glioma susceptibility through an analysis of 6p22.3, 12p13.33-12.1, 17q22-23.2 and 18q23 SNP genotypes in familial and non-familial glioma

Author

Liu, Yanhong, Melin, Beatrice S, Rajaraman, Preetha, Wang, Zhaoming, Linet, Martha, Shete, Sanjay, Amos, Christopher I, Lau, Ching C, Scheurer, Michael E, Tsavachidis, Spiridon, Armstrong, Georgina N, Houlston, Richard S, Hosking, Fay J, Claus, Elizabeth B, Barnholtz-Sloan, Jill, Lai, Rose, Il’yasova, Dora, Schildkraut, Joellen, Sadetzki, Siegal, Johansen, Christoffer, Bernstein, Jonine L, Olson, Sara H, Jenkins, Robert B, LaChance, Daniel, Vick, Nicholas A, Wrensch, Margaret, Davis, Faith, McCarthy, Bridget J, Andersson, Ulrika, Thompson, Patricia A, Chanock, Stephen, The Gliogene Consortium, and Bondy, Melissa L

Subjects
Biological Sciences, Biomedical and Clinical Sciences, Genetics, Human Genome, Cancer, Brain Disorders, Clinical Research, Brain Cancer, Neurosciences, Rare Diseases, Aetiology, 2.1 Biological and endogenous factors, Adolescent, Adult, Brain Neoplasms, Chromosome Mapping, Female, Genetic Predisposition to Disease, Glioma, Haplotypes, Humans, Male, Middle Aged, Polymorphism, Single Nucleotide, Gliogene Consortium, Complementary and Alternative Medicine, Paediatrics and Reproductive Medicine, Genetics & Heredity, Reproductive medicine
Abstract

The risk of glioma has consistently been shown to be increased twofold in relatives of patients with primary brain tumors (PBT). A recent genome-wide linkage study of glioma families provided evidence for a disease locus on 17q12-21.32, with the possibility of four additional risk loci at 6p22.3, 12p13.33-12.1, 17q22-23.2, and 18q23. To identify the underlying genetic variants responsible for the linkage signals, we compared the genotype frequencies of 5,122 SNPs mapping to these five regions in 88 glioma cases with and 1,100 cases without a family history of PBT (discovery study). An additional series of 84 familial and 903 non-familial cases were used to replicate associations. In the discovery study, 12 SNPs showed significant associations with family history of PBT (P < 0.001). In the replication study, two of the 12 SNPs were confirmed: 12p13.33-12.1 PRMT8 rs17780102 (P = 0.031) and 17q12-21.32 SPOP rs650461 (P = 0.025). In the combined analysis of discovery and replication studies, the strongest associations were attained at four SNPs: 12p13.33-12.1 PRMT8 rs17780102 (P = 0.0001), SOX5 rs7305773 (P = 0.0001) and STKY1 rs2418087 (P = 0.0003), and 17q12-21.32 SPOP rs6504618 (P = 0.0006). Further, a significant gene-dosage effect was found for increased risk of family history of PBT with these four SNPs in the combined data set (P(trend)

Published
2012

5. Data from A Variable Age of Onset Segregation Model for Linkage Analysis, with Correction for Ascertainment, Applied to Glioma

Author

Sun, Xiangqing, primary, Vengoechea, Jaime, primary, Elston, Robert, primary, Chen, Yanwen, primary, Amos, Christopher I., primary, Armstrong, Georgina, primary, Bernstein, Jonine L., primary, Claus, Elizabeth, primary, Davis, Faith, primary, Houlston, Richard S., primary, Il'yasova, Dora, primary, Jenkins, Robert B., primary, Johansen, Christoffer, primary, Lai, Rose, primary, Lau, Ching C., primary, Liu, Yanhong, primary, McCarthy, Bridget J., primary, Olson, Sara H., primary, Sadetzki, Siegal, primary, Schildkraut, Joellen, primary, Shete, Sanjay, primary, Yu, Robert, primary, Vick, Nicholas A., primary, Merrell, Ryan, primary, Wrensch, Margaret, primary, Yang, Ping, primary, Melin, Beatrice, primary, Bondy, Melissa L., primary, and Barnholtz-Sloan, Jill S., primary

Published
2023
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6. Supplementary Methods from A Variable Age of Onset Segregation Model for Linkage Analysis, with Correction for Ascertainment, Applied to Glioma

Author

Sun, Xiangqing, primary, Vengoechea, Jaime, primary, Elston, Robert, primary, Chen, Yanwen, primary, Amos, Christopher I., primary, Armstrong, Georgina, primary, Bernstein, Jonine L., primary, Claus, Elizabeth, primary, Davis, Faith, primary, Houlston, Richard S., primary, Il'yasova, Dora, primary, Jenkins, Robert B., primary, Johansen, Christoffer, primary, Lai, Rose, primary, Lau, Ching C., primary, Liu, Yanhong, primary, McCarthy, Bridget J., primary, Olson, Sara H., primary, Sadetzki, Siegal, primary, Schildkraut, Joellen, primary, Shete, Sanjay, primary, Yu, Robert, primary, Vick, Nicholas A., primary, Merrell, Ryan, primary, Wrensch, Margaret, primary, Yang, Ping, primary, Melin, Beatrice, primary, Bondy, Melissa L., primary, and Barnholtz-Sloan, Jill S., primary

Published
2023
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7. Supplementary Table 1 from A Variable Age of Onset Segregation Model for Linkage Analysis, with Correction for Ascertainment, Applied to Glioma

Author

Sun, Xiangqing, primary, Vengoechea, Jaime, primary, Elston, Robert, primary, Chen, Yanwen, primary, Amos, Christopher I., primary, Armstrong, Georgina, primary, Bernstein, Jonine L., primary, Claus, Elizabeth, primary, Davis, Faith, primary, Houlston, Richard S., primary, Il'yasova, Dora, primary, Jenkins, Robert B., primary, Johansen, Christoffer, primary, Lai, Rose, primary, Lau, Ching C., primary, Liu, Yanhong, primary, McCarthy, Bridget J., primary, Olson, Sara H., primary, Sadetzki, Siegal, primary, Schildkraut, Joellen, primary, Shete, Sanjay, primary, Yu, Robert, primary, Vick, Nicholas A., primary, Merrell, Ryan, primary, Wrensch, Margaret, primary, Yang, Ping, primary, Melin, Beatrice, primary, Bondy, Melissa L., primary, and Barnholtz-Sloan, Jill S., primary

Published
2023
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8. Supplementary Figure 4 from A Variable Age of Onset Segregation Model for Linkage Analysis, with Correction for Ascertainment, Applied to Glioma

Author

Sun, Xiangqing, primary, Vengoechea, Jaime, primary, Elston, Robert, primary, Chen, Yanwen, primary, Amos, Christopher I., primary, Armstrong, Georgina, primary, Bernstein, Jonine L., primary, Claus, Elizabeth, primary, Davis, Faith, primary, Houlston, Richard S., primary, Il'yasova, Dora, primary, Jenkins, Robert B., primary, Johansen, Christoffer, primary, Lai, Rose, primary, Lau, Ching C., primary, Liu, Yanhong, primary, McCarthy, Bridget J., primary, Olson, Sara H., primary, Sadetzki, Siegal, primary, Schildkraut, Joellen, primary, Shete, Sanjay, primary, Yu, Robert, primary, Vick, Nicholas A., primary, Merrell, Ryan, primary, Wrensch, Margaret, primary, Yang, Ping, primary, Melin, Beatrice, primary, Bondy, Melissa L., primary, and Barnholtz-Sloan, Jill S., primary

Published
2023
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9. Supplementary Figure 3 from A Variable Age of Onset Segregation Model for Linkage Analysis, with Correction for Ascertainment, Applied to Glioma

Author

Sun, Xiangqing, primary, Vengoechea, Jaime, primary, Elston, Robert, primary, Chen, Yanwen, primary, Amos, Christopher I., primary, Armstrong, Georgina, primary, Bernstein, Jonine L., primary, Claus, Elizabeth, primary, Davis, Faith, primary, Houlston, Richard S., primary, Il'yasova, Dora, primary, Jenkins, Robert B., primary, Johansen, Christoffer, primary, Lai, Rose, primary, Lau, Ching C., primary, Liu, Yanhong, primary, McCarthy, Bridget J., primary, Olson, Sara H., primary, Sadetzki, Siegal, primary, Schildkraut, Joellen, primary, Shete, Sanjay, primary, Yu, Robert, primary, Vick, Nicholas A., primary, Merrell, Ryan, primary, Wrensch, Margaret, primary, Yang, Ping, primary, Melin, Beatrice, primary, Bondy, Melissa L., primary, and Barnholtz-Sloan, Jill S., primary

Published
2023
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10. Supplementary Figure 1 from A Variable Age of Onset Segregation Model for Linkage Analysis, with Correction for Ascertainment, Applied to Glioma

Author

Sun, Xiangqing, primary, Vengoechea, Jaime, primary, Elston, Robert, primary, Chen, Yanwen, primary, Amos, Christopher I., primary, Armstrong, Georgina, primary, Bernstein, Jonine L., primary, Claus, Elizabeth, primary, Davis, Faith, primary, Houlston, Richard S., primary, Il'yasova, Dora, primary, Jenkins, Robert B., primary, Johansen, Christoffer, primary, Lai, Rose, primary, Lau, Ching C., primary, Liu, Yanhong, primary, McCarthy, Bridget J., primary, Olson, Sara H., primary, Sadetzki, Siegal, primary, Schildkraut, Joellen, primary, Shete, Sanjay, primary, Yu, Robert, primary, Vick, Nicholas A., primary, Merrell, Ryan, primary, Wrensch, Margaret, primary, Yang, Ping, primary, Melin, Beatrice, primary, Bondy, Melissa L., primary, and Barnholtz-Sloan, Jill S., primary

Published
2023
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11. Supplementary Figure 2 from A Variable Age of Onset Segregation Model for Linkage Analysis, with Correction for Ascertainment, Applied to Glioma

Author

Sun, Xiangqing, primary, Vengoechea, Jaime, primary, Elston, Robert, primary, Chen, Yanwen, primary, Amos, Christopher I., primary, Armstrong, Georgina, primary, Bernstein, Jonine L., primary, Claus, Elizabeth, primary, Davis, Faith, primary, Houlston, Richard S., primary, Il'yasova, Dora, primary, Jenkins, Robert B., primary, Johansen, Christoffer, primary, Lai, Rose, primary, Lau, Ching C., primary, Liu, Yanhong, primary, McCarthy, Bridget J., primary, Olson, Sara H., primary, Sadetzki, Siegal, primary, Schildkraut, Joellen, primary, Shete, Sanjay, primary, Yu, Robert, primary, Vick, Nicholas A., primary, Merrell, Ryan, primary, Wrensch, Margaret, primary, Yang, Ping, primary, Melin, Beatrice, primary, Bondy, Melissa L., primary, and Barnholtz-Sloan, Jill S., primary

Published
2023
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22. Germline rearrangements in families with strong family history of glioma and malignant melanoma, colon, and breast cancer

Author

Andersson, Ulrika, Wibom, Carl, Cederquist, Kristina, Aradottir, Steina, Borg, Åke, Armstrong, Georgina N., Shete, Sanjay, Lau, Ching C., Bainbridge, Matthew N., Claus, Elizabeth B., Barnholtz-Sloan, Jill, Lai, Rose, Il'yasova, Dora, Houlston, Richard S., Schildkraut, Joellen, Bernstein, Jonine L., Olson, Sara H., Jenkins, Robert B., Lachance, Daniel H., Wrensch, Margaret, Davis, Faith G., Merrell, Ryan, Johansen, Christoffer, Sadetzki, Siegal, Bondy, Melissa L., Melin, Beatrice S., Adatto, Phyllis, Morice, Fabian, Payen, Sam, McQuinn, Lacey, McGaha, Rebecca, Guerra, Sandra, Paith, Leslie, Roth, Katherine, Zeng, Dong, Zhang, Hui, Yung, Alfred, Aldape, Kenneth, Gilbert, Mark, Weinberger, Jeffrey, Colman, Howard, Conrad, Charles, de Groot, John, Forman, Arthur, Groves, Morris, Levin, Victor, Loghin, Monica, Puduvalli, Vinay, Sawaya, Raymond, Heimberger, Amy, Lang, Frederick, Levine, Nicholas, Tolentino, Lori, Saunders, Kate, Thach, Thu-Trang, Iacono, Donna Dello, Sloan, Andrew, Gerson, Stanton, Selman, Warren, Bambakidis, Nicholas, Hart, David, Miller, Jonathan, Hoffer, Alan, Cohen, Mark, Rogers, Lisa, Nock, Charles J, Wolinsky, Yingli, Devine, Karen, Fulop, Jordonna, Barrett, Wendi, Shimmel, Kristen, Ostrom, Quinn, Barnett, Gene, Rosenfeld, Steven, Vogelbaum, Michael, Weil, Robert, Ahluwalia, Manmeet, Peereboom, David, Staugaitis, Susan, Schilero, Cathy, Brewer, Cathy, Smolenski, Kathy, McGraw, Mary, Naska, Theresa, Ram, Zvi, Blumenthal, Deborah T., Bokstein, Felix, Umansky, Felix, Zaaroor, Menashe, Cohen, Avi, Tzuk-Shina, Tzeela, Voldby, Bo, Laursen, René, Andersen, Claus, Brennum, Jannick, Henriksen, Matilde Bille, Marzouk, Maya, Davis, Mary Elizabeth, Boland, Eamon, Smith, Marcel, Eze, Ogechukwu, Way, Mahalia, Lada, Pat, Miedzianowski, Nancy, Frechette, Michelle, Paleologos, Nina, Byström, Gudrun, Svedberg, Eva, Huggert, Sara, Kimdal, Mikael, Sandström, Monica, Brännström, Nikolina, Hayat, Amina, Tihan, Tarik, Zheng, Shichun, Berger, Mitchel, Butowski, Nicholas, Chang, Susan, Clarke, Jennifer, Prados, Michael, Rice, Terri, Sison, Jeannette, Kivett, Valerie, Duo, Xiaoqin, Hansen, Helen, Hsuang, George, Lamela, Rosito, Ramos, Christian, Patoka, Joe, Wagenman, Katherine, Zhou, Mi, Klein, Adam, McGee, Nora, Pfefferle, Jon, Wilson, Callie, Morris, Pagan, Hughes, Mary, Britt-Williams, Marlin, Foft, Jessica, Madsen, Julia, Polony, Csaba, McCarthy, Bridget, Zahora, Candice, Villano, John, Engelhard, Herbert, Borg, Ake, Chanock, Stephen K, Collins, Peter, Elston, Robert, Kleihues, Paul, Kruchko, Carol, Petersen, Gloria, Plon, Sharon, Thompson, Patricia, Johansen, C., Sadetzki, S., Melin, B., Scheurer, Michael E., Liu, Yanhong, Yu, Robert K., Aldape, Kenneth D., Gilbert, Mark R., Weinberg, Jeffrey, Hosking, Fay J., Robertson, Lindsay, Papaemmanuil, Elli, Sloan, Andrew E., McKean-Cowdin, Roberta, Yechezkel, Galit Hirsh, Bruchim, Revital Bar-Sade, Aslanov, Lili, Kosteljanetz, Michael, Broholm, Helle, Schubert, Erica, DeAngelis, Lisa, Yang, Ping, Rynearson, Amanda, Henriksson, Roger, Lada, Patricia, Wiencke, John, Wiemels, Joe, McCoy, Lucie, and McCarthy, Bridget J.

Subjects
Male, Cancer Research, Neurologi, Colorectal cancer, Bioinformatics, Germline, 0302 clinical medicine, glioma, Medicine, TP53, Family history, Melanoma, family history, 0303 health sciences, Brain Neoplasms, MLH1, Nuclear Proteins, CDKN2A/B, Middle Aged, Pedigree, 3. Good health, MutS Homolog 2 Protein, Neurology, Oncology, Child, Preschool, 030220 oncology & carcinogenesis, Basic and Translational Investigations, Colonic Neoplasms, Female, MutL Protein Homolog 1, Adult, Breast Neoplasms, Young Adult, 03 medical and health sciences, Germline mutation, Breast cancer, Glioma, Humans, Genetic Predisposition to Disease, neoplasms, Cyclin-Dependent Kinase Inhibitor p16, Germ-Line Mutation, Adaptor Proteins, Signal Transducing, Cyclin-Dependent Kinase Inhibitor p15, 030304 developmental biology, Cancer och onkologi, business.industry, Cancer, medicine.disease, MSH2, nervous system diseases, Checkpoint Kinase 2, Cancer and Oncology, Cancer research, Neurology (clinical), Tumor Suppressor Protein p53, business
Abstract

Background: Although familial susceptibility to glioma is known, the genetic basis for this susceptibility remains unidentified in the majority of glioma-specific families. An alternative approach to identifying such genes is to examine cancer pedigrees, which include glioma as one of several cancer phenotypes, to determine whether common chromosomal modifications might account for the familial aggregation of glioma and other cancers. Methods: Germline rearrangements in 146 glioma families (from the Gliogene Consortium; http://www.gliogene.org/) were examined using multiplex ligation-dependent probe amplification. These families all had at least 2 verified glioma cases and a third reported or verified glioma case in the same family or 2 glioma cases in the family with at least one family member affected with melanoma, colon, or breast cancer. The genomic areas covering TP53, CDKN2A, MLH1, and MSH2 were selected because these genes have been previously reported to be associated with cancer pedigrees known to include glioma. Results: We detected a single structural rearrangement, a deletion of exons 1-6 in MSH2, in the proband of one family with 3 cases with glioma and one relative with colon cancer. Conclusions: Large deletions and duplications are rare events in familial glioma cases, even in families with a strong family history of cancers that may be involved in known cancer syndromes. Meeting Abstract: P04.02 published in the same journal, Vol. 16, Suppl. 2.

Published
2014

25. Consensus Conference on Cancer Registration of Brain and Central Nervous System Tumors1

Author

McCarthy, Bridget J. and Kruchko, Carol

Subjects
Central Nervous System Neoplasms, Humans, Registries, Meeting Report
Abstract

The passage of Public Law 107–260, the Benign Brain Tumor Cancer Registries Amendment Act, in October 2002 has made the collection of all primary brain tumors a reality. However, at the first Consensus Conference on Brain Tumor Definition for Registration in 2002, and during the development of training materials for benign brain tumor collection, several issues were identified that were tabled for future discussion. These and other issues were addressed at the subsequent 2003 Consensus Conference on Cancer Registration of Brain and Central Nervous System Tumors, at which the Central Brain Tumor Registry of the United States facilitated a discussion among epidemiologists, neurosurgeons, and neuro-pathologists. Multidisciplinary consensus was reached on four points, for which the following recommendations were made: (1) amend the histology coding scheme for cysts and tumor-like lesions that currently have a code in the third edition of the International Classification of Disease for Oncology (ICDO), (2) collect data on all instances of specific cysts and tumor-like lesions that are located in brain and other CNS sites but currently lack ICDO codes, (3) establish a new ICDO topography site for skull base tumors for the brain and CNS, and (4) collect data on genetic syndromes in patients diagnosed with brain or CNS tumors. We view this conference as part of a continuing process. Because classification of primary intracranial and other CNS tumors is dynamic, and the registration and coding of these tumors will need to be periodically reviewed.

Published
2005

26. Consensus Conference on Brain Tumor Definition for registration. November 10, 2000

Author

McCarthy, Bridget J., Surawicz, Tanya, Bruner, Janet M., Kruchko, Carol, and Davis, Faith

Subjects
Brain Neoplasms, Humans, Registries, United States, Research Article
Abstract

The Consensus Conference on Brain Tumor Definition was facilitated by the Central Brain Tumor Registry of the United States and held on November 10, 2000, in Chicago, Illinois, to reach multidisciplinary agreement on a standard definition of brain tumors for collecting and comparing data in the U.S. The Brain Tumor Working Group, convened in 1998 to determine the status of brain tumor collection in the U.S., outlined 4 recommendations of which the first 2 guided the discussion for the Consensus Conference: (1) standardization of a definition of primary brain tumors that is based on site alone, rather than on site and behavior, and that can be used by surveillance organizations in collecting these tumors; and (2) development of a reporting scheme that can be used for comparing estimates of primary brain tumors across registries. Consensus was reached on the collection of all primary brain tumor histologies found and reported in the brain or CNS ICD-O site codes (C70.0-C72.9 and C75.1-C75.3), including those coded benign and uncertain as well as those coded malignant. In addition, a comprehensive listing of histologies occurring in the brain and CNS, based on the CBTRUS grouping scheme, was formulated to provide a template for reporting in accordance with the second recommendation of the Brain Tumor Working Group. With consensus achieved on the first 2 recommendations, the stage is set to move forward in estimating additional resources necessary for the collection of these tumors, including funding, training for cancer registrars, identifying quality control measures, and developing computerized edit checks, as outlined in the last 2 recommendations of the Brain Tumor Working Group.

Published
2002

27. Risk factors for oligodendroglial tumors : A pooled international study

Author

McCarthy, Bridget J, Rankin, Kristin M, Aldape, Ken, Bondy, Melissa L, Brännström, Thomas, Broholm, Helle, Feychting, Maria, Il'yasova, Dora, Inskip, Peter D, Johansen, Christoffer, Melin, Beatrice, Ruder, Avima M, Butler, Mary Ann, Scheurer, Michael E, Schüz, Joachim, Schwartzbaum, Judith A, Wrensch, Margaret R, Davis, Faith G, McCarthy, Bridget J, Rankin, Kristin M, Aldape, Ken, Bondy, Melissa L, Brännström, Thomas, Broholm, Helle, Feychting, Maria, Il'yasova, Dora, Inskip, Peter D, Johansen, Christoffer, Melin, Beatrice, Ruder, Avima M, Butler, Mary Ann, Scheurer, Michael E, Schüz, Joachim, Schwartzbaum, Judith A, Wrensch, Margaret R, and Davis, Faith G

Abstract

Oligodendroglial tumors are rare subtypes of brain tumors and are often combined with other glial tumors in epidemiological analyses. However, different demographic associations and clinical characteristics suggest potentially different risk factors. The purpose of this study was to investigate possible risk factors for oligodendroglial tumors (including oligodendroglioma, anaplastic oligodendroglioma, and mixed glioma). Data from 7 case-control studies (5 US and 2 Scandinavian) were pooled. Unconditional logistic regression was used to calculate odds ratios (ORs) and 95% confidence intervals (CIs), adjusted for age group, gender, and study site. Data on 617 cases and 1260 controls were available for analyses. Using data from all 7 studies, history of allergies and/or asthma was associated with a decreased risk of anaplastic oligodendroglioma (OR = 0.6; 95% CI: 0.4-0.9), and history of asthma only was associated with a decreased risk of oligodendroglioma (OR = 0.5; 95% CI: 0.3-0.9) and anaplastic oligodendroglioma (OR = 0.3; 95% CI: 0.1-0.9). A family history of brain tumors was associated with an increased risk of anaplastic oligodendroglioma (OR = 2.2; 95% CI: 1.1-4.5). Having had chicken pox was associated with a decreased risk of oligodendroglioma (OR = 0.6; 95% CI: 0.4-0.9) and anaplastic oligodendroglioma (OR = 0.5; 95% CI: 0.3-0.9) in the US studies. Although there is some overlap in risk factors between oligodendroglial tumors and gliomas as a group, it is likely that additional factors specific to oligodendroglial tumors have yet to be identified. Large, multi-institution international studies will be necessary to better characterize these etiological risk factors.

Published
2011
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28. Genome-wide high-density SNP linkage search for glioma susceptibility loci : results from the gliogene consortium

Author

Shete, Sanjay, Lau, Ching C, Houlston, Richard S, Claus, Elizabeth B, Barnholtz-Sloan, Jill, Lai, Rose, Il'yasova, Dora, Schildkraut, Joellen, Sadetzki, Siegal, Johansen, Christoffer, Bernstein, Jonine L, Olson, Sara H, Jenkins, Robert B, Yang, Ping, Vick, Nicholas A, Wrensch, Margaret, Davis, Faith G, McCarthy, Bridget J, Leung, Eastwood Hon-Chiu, Davis, Caleb, Cheng, Rita, Hosking, Fay J, Armstrong, Georgina N, Liu, Yanhong, Yu, Robert K, Henriksson, Roger, Melin, Beatrice S, Bondy, Melissa L, Shete, Sanjay, Lau, Ching C, Houlston, Richard S, Claus, Elizabeth B, Barnholtz-Sloan, Jill, Lai, Rose, Il'yasova, Dora, Schildkraut, Joellen, Sadetzki, Siegal, Johansen, Christoffer, Bernstein, Jonine L, Olson, Sara H, Jenkins, Robert B, Yang, Ping, Vick, Nicholas A, Wrensch, Margaret, Davis, Faith G, McCarthy, Bridget J, Leung, Eastwood Hon-Chiu, Davis, Caleb, Cheng, Rita, Hosking, Fay J, Armstrong, Georgina N, Liu, Yanhong, Yu, Robert K, Henriksson, Roger, Melin, Beatrice S, and Bondy, Melissa L

Abstract

Gliomas, which generally have a poor prognosis, are the most common primary malignant brain tumors in adults. Recent genome-wide association studies have shown that inherited susceptibility plays a role in the development of glioma. Although first-degree relatives of patients exhibit a two-fold increased risk of glioma, the search for susceptibility loci in familial forms of the disease has been challenging because the disease is relatively rare, fatal, and heterogeneous, making it difficult to collect sufficient biosamples from families for statistical power. To address this challenge, the Genetic Epidemiology of Glioma International Consortium (Gliogene) was formed to collect DNA samples from families with two or more cases of histologically confirmed glioma. In this study, we present results obtained from 46 U.S. families in which multipoint linkage analyses were undertaken using nonparametric (model-free) methods. After removal of high linkage disequilibrium single-nucleotide polymorphism, we obtained a maximum nonparametric linkage score (NPL) of 3.39 (P = 0.0005) at 17q12-21.32 and the Z-score of 4.20 (P = 0.000007). To replicate our findings, we genotyped 29 independent U.S. families and obtained a maximum NPL score of 1.26 (P = 0.008) and the Z-score of 1.47 (P = 0.035). Accounting for the genetic heterogeneity using the ordered subset analysis approach, the combined analyses of 75 families resulted in a maximum NPL score of 3.81 (P = 0.00001). The genomic regions we have implicated in this study may offer novel insights into glioma susceptibility, focusing future work to identify genes that cause familial glioma. Cancer Res; 71(24); 7568-75. (C) 2011 AACR.

Published
2011
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29. A Case for the Worldwide Collection of Primary Benign Brain Tumors.

Author

McCarthy, Bridget J, Schellinger, Kate A, Propp, Jennifer M, Kruchko, Carol, Malmer, Beatrice, McCarthy, Bridget J, Schellinger, Kate A, Propp, Jennifer M, Kruchko, Carol, and Malmer, Beatrice

Abstract

Background: Incidence data on malignant tumors are reported by the International Agency for Research on Cancer, with 189,485 new malignant brain tumors globally in 2002. However, collection and reporting of benign brain tumors are not universal. The objective here is to encourage the collection of primary benign brain tumors worldwide. Methods: Worldwide numbers of primary benign brain tumors were estimated through published articles and cancer registry reports presenting directly or indirectly reported benign incidence rates or frequencies for regions or countries. Results: An estimated 186,678 benign brain tumors were diagnosed worldwide in 2002. The estimated numbers of benign brain tumors were higher in females than males (105,918 vs. 80,759). Since many countries do not report primary benign brain tumors, the incidence rate estimates vary significantly by region. Conclusions: This is the first survey to assess worldwide numbers of benign brain tumors. Under-reporting, non-standardized collection, lack of age-adjustment, and other causes of the varying incidence rates must be considered. However, the estimated number of benign brain tumors approximately equals, and could exceed, the number of malignant brain tumors globally. Registration of primary benign brain histologies in different geographical areas and ethnicities could provide clues to the underlying causes of these tumors.

Published
2009
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30. Issues of diagnostic review in brain tumor studies : from the brain tumor epidemiology consortium

Author

Davis, Faith G, Malmer, Beatrice, Aldape, Ken, Barnholtz-Sloan, Jill S, Bondy, Melissa L, Brännström, Thomas, Bruner, Janet M, Burger, Peter C, Collins, V Peter, Inskip, Peter D, Kruchko, Carol, McCarthy, Bridget J, McLendon, Roger E, Sadetzki, Siegal, Tihan, Tarik, Wrensch, Margaret R, Buffler, Patricia A, Davis, Faith G, Malmer, Beatrice, Aldape, Ken, Barnholtz-Sloan, Jill S, Bondy, Melissa L, Brännström, Thomas, Bruner, Janet M, Burger, Peter C, Collins, V Peter, Inskip, Peter D, Kruchko, Carol, McCarthy, Bridget J, McLendon, Roger E, Sadetzki, Siegal, Tihan, Tarik, Wrensch, Margaret R, and Buffler, Patricia A

Abstract

Epidemiologists routinely conduct centralized single pathology reviews to minimize interobserver diagnostic variability, but this practice does not facilitate the combination of studies across geographic regions and institutions where diagnostic practices differ. A meeting of neuropathologists and epidemiologists focused on brain tumor classification issues in the context of protocol needs for consortial studies (http://epi.grants.cancer.gov/btec/). It resulted in recommendations relevant to brain tumors and possibly other rare disease studies. Two categories of brain tumors have enough general agreement over time, across regions, and between individual pathologists that one can consider using existing diagnostic data without further review: glioblastomas and meningiomas (as long as uniform guidelines such as those provided by the WHO are used). Prospective studies of these tumors benefit from collection of pathology reports, at a minimum recording the pathology department and classification system used in the diagnosis. Other brain tumors, such as oligodendroglioma, are less distinct and require careful histopathologic review for consistent classification across study centers. Epidemiologic study protocols must consider the study specific aims, diagnostic changes that have taken place over time, and other issues unique to the type(s) of tumor being studied. As diagnostic changes are being made rapidly, there are no readily available answers on disease classification issues. It is essential that epidemiologists and neuropathologists collaborate to develop appropriate study designs and protocols for specific hypothesis and populations.

Published
2008
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31. Brain tumor epidemiology : consensus from the Brain Tumor Epidemiology Consortium.

Author

Bondy, Melissa L, Scheurer, Michael E, Malmer, Beatrice, Barnholtz-Sloan, Jill S, Davis, Faith G, Il'yasova, Dora, Kruchko, Carol, McCarthy, Bridget J, Rajaraman, Preetha, Schwartzbaum, Judith A, Sadetzki, Siegal, Schlehofer, Brigitte, Tihan, Tarik, Wiemels, Joseph L, Wrensch, Margaret, Buffler, Patricia A, Bondy, Melissa L, Scheurer, Michael E, Malmer, Beatrice, Barnholtz-Sloan, Jill S, Davis, Faith G, Il'yasova, Dora, Kruchko, Carol, McCarthy, Bridget J, Rajaraman, Preetha, Schwartzbaum, Judith A, Sadetzki, Siegal, Schlehofer, Brigitte, Tihan, Tarik, Wiemels, Joseph L, Wrensch, Margaret, and Buffler, Patricia A

Abstract

Epidemiologists in the Brain Tumor Epidemiology Consortium (BTEC) have prioritized areas for further research. Although many risk factors have been examined over the past several decades, there are few consistent findings, possibly because of small sample sizes in individual studies and differences between studies in patients, tumor types, and methods of classification. Individual studies generally have lacked samples of sufficient size to examine interactions. A major priority based on available evidence and technologies includes expanding research in genetics and molecular epidemiology of brain tumors. BTEC has taken an active role in promoting understudied groups, such as pediatric brain tumors; the etiology of rare glioma subtypes, such as oligodendroglioma; and meningioma, which, although it is not uncommon, has only recently been registered systematically in the United States. There also is a pressing need for more researchers, especially junior investigators, to study brain tumor epidemiology. However, relatively poor funding for brain tumor research has made it difficult to encourage careers in this area. In this report, BTEC epidemiologists reviewed the group's consensus on the current state of scientific findings, and they present a consensus on research priorities to identify which important areas the science should move to address.

Published
2008
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39. Environmental Exposures and Adult Brain Cancers

Author

Davis, Faith G., primary, Il’yasova, Dora, additional, Rankin, Kristin M., additional, McCarthy, Bridget J., additional, Erdal, Serap, additional, Lewis, Juliana F. M., additional, Al-Alem, Umaima, additional, and Bigner, Darell, additional

Published
2009
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40. Human Exposure to Selected Animal Neurocarcinogens: A Biomarker-Based Assessment and Implications for Brain Tumor Epidemiology

Author

Il'yasova, Dora, primary, McCarthy, Bridget J., additional, Erdal, Serap, additional, Shimek, Joanna, additional, Goldstein, Jennifer, additional, Doerge, Daniel R., additional, Myers, Steven R., additional, Vineis, Paolo, additional, Wishnok, John S., additional, Swenberg, James A., additional, Bigner, Darell D., additional, and Davis, Faith G., additional

Published
2009
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43. Issues of Diagnostic Review in Brain Tumor Studies: From the Brain Tumor Epidemiology Consortium

Author

Davis, Faith G., primary, Malmer, Beatrice S., additional, Aldape, Ken, additional, Barnholtz-Sloan, Jill S., additional, Bondy, Melissa L., additional, Brännström, Thomas, additional, Bruner, Janet M., additional, Burger, Peter C., additional, Collins, V. Peter, additional, Inskip, Peter D., additional, Kruchko, Carol, additional, McCarthy, Bridget J., additional, McLendon, Roger E., additional, Sadetzki, Siegal, additional, Tihan, Tarik, additional, Wrensch, Margaret R., additional, and Buffler, Patricia A., additional

Published
2008
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