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1,070 results on '"Goldstein, Alisa M."'

1. Genomic profiles and clinical presentation of chordoma

Author

Koka, Hela, Zhou, Weiyin, McMaster, Mary L., Bai, Jiwei, Luo, Wen, Klein, Alyssa, Zhang, Tongwu, Hua, Xing, Li, Xin, Wang, Difei, Xiong, Yujia, Jones, Kristine, Vogt, Aurelie, Hicks, Belynda, Parry, Dilys, Goldstein, Alisa M., and Yang, Xiaohong R.

Published
2024
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2. Genome-wide analyses characterize shared heritability among cancers and identify novel cancer susceptibility regions

Author

Lindström, Sara, Wang, Lu, Feng, Helian, Majumdar, Arunabha, Huo, Sijia, Macdonald, James, Harrison, Tabitha, Turman, Constance, Chen, Hongjie, Mancuso, Nicholas, Bammler, Theo, Consortium, Breast Cancer Association, Gallinger, Steve, Gruber, Stephen B, Gunter, Marc J, Le Marchand, Loic, Moreno, Victor, Offit, Kenneth, Study, Genetics And Epidemiology Of Colorectal Cancer Consortium Colorectal Transdisciplinary Study Colon Cancer Family Registry, De Vivo, Immaculata, O’Mara, Tracy A, Spurdle, Amanda B, Tomlinson, Ian, Consortium, Endometrial Cancer Association, Fitzgerald, Rebecca, Gharahkhani, Puya, Gockel, Ines, Jankowski, Janusz, Macgregor, Stuart, Schumacher, Johannes, Barnholtz-Sloan, Jill, Bondy, Melissa L, Houlston, Richard S, Jenkins, Robert B, Melin, Beatrice, Wrensch, Margaret, Brennan, Paul, Christiani, David C, Johansson, Mattias, Mckay, James, Aldrich, Melinda C, Amos, Christopher I, Landi, Maria Teresa, Tardon, Adonina, Consortium, International Lung Cancer, Bishop, D Timothy, Demenais, Florence, Goldstein, Alisa M, Iles, Mark M, Kanetsky, Peter A, Law, Matthew H, Consortium, Ovarian Cancer Association, Amundadottir, Laufey T, Stolzenberg-Solomon, Rachael, Wolpin, Brian M, Consortium, Pancreatic Cancer Cohort, Klein, Alison, Petersen, Gloria, Risch, Harvey, Consortium, The PRACTICAL Consortium Pancreatic Cancer Case-Control, Chanock, Stephen J, Purdue, Mark P, Scelo, Ghislaine, Pharoah, Paul, Kar, Siddhartha, Hung, Rayjean J, Pasaniuc, Bogdan, and Kraft, Peter

Subjects
Biomedical and Clinical Sciences, Oncology and Carcinogenesis, Human Genome, Genetics, Digestive Diseases, Prevention, Clinical Research, Urologic Diseases, Cancer, Rare Diseases, Aetiology, 2.1 Biological and endogenous factors, Male, Humans, Genome-Wide Association Study, Genetic Predisposition to Disease, Neoplasms, Risk Factors, Transcriptome, Polymorphism, Single Nucleotide, Breast Cancer Association Consortium, Colorectal Transdisciplinary Study (CORECT), Colon Cancer Family Registry Study (CCFR), Genetics And Epidemiology Of Colorectal Cancer Consortium, Endometrial Cancer Association Consortium, International Lung Cancer Consortium, Ovarian Cancer Association Consortium, Pancreatic Cancer Cohort Consortium, Pancreatic Cancer Case-Control Consortium (Panc4), The PRACTICAL Consortium, Oncology & Carcinogenesis, Oncology and carcinogenesis
Abstract

BackgroundThe shared inherited genetic contribution to risk of different cancers is not fully known. In this study, we leverage results from 12 cancer genome-wide association studies (GWAS) to quantify pairwise genome-wide genetic correlations across cancers and identify novel cancer susceptibility loci.MethodsWe collected GWAS summary statistics for 12 solid cancers based on 376 759 participants with cancer and 532 864 participants without cancer of European ancestry. The included cancer types were breast, colorectal, endometrial, esophageal, glioma, head and neck, lung, melanoma, ovarian, pancreatic, prostate, and renal cancers. We conducted cross-cancer GWAS and transcriptome-wide association studies to discover novel cancer susceptibility loci. Finally, we assessed the extent of variant-specific pleiotropy among cancers at known and newly identified cancer susceptibility loci.ResultsWe observed widespread but modest genome-wide genetic correlations across cancers. In cross-cancer GWAS and transcriptome-wide association studies, we identified 15 novel cancer susceptibility loci. Additionally, we identified multiple variants at 77 distinct loci with strong evidence of being associated with at least 2 cancer types by testing for pleiotropy at known cancer susceptibility loci.ConclusionsOverall, these results suggest that some genetic risk variants are shared among cancers, though much of cancer heritability is cancer-specific and thus tissue-specific. The increase in statistical power associated with larger sample sizes in cross-disease analysis allows for the identification of novel susceptibility regions. Future studies incorporating data on multiple cancer types are likely to identify additional regions associated with the risk of multiple cancer types.

Published
2023

3. Inflated expectations: Rare-variant association analysis using public controls

Author

Kim, Jung, Karyadi, Danielle M, Hartley, Stephen W, Zhu, Bin, Wang, Mingyi, Wu, Dongjing, Song, Lei, Armstrong, Gregory T, Bhatia, Smita, Robison, Leslie L, Yasui, Yutaka, Carter, Brian, Sampson, Joshua N, Freedman, Neal D, Goldstein, Alisa M, Mirabello, Lisa, Chanock, Stephen J, Morton, Lindsay M, Savage, Sharon A, and Stewart, Douglas R

Subjects
Epidemiology, Biological Sciences, Health Sciences, Genetics, Motivation, High-Throughput Nucleotide Sequencing, Polymorphism, Single Nucleotide, Software, General Science & Technology
Abstract

The use of publicly available sequencing datasets as controls (hereafter, "public controls") in studies of rare variant disease associations has great promise but can increase the risk of false-positive discovery. The specific factors that could contribute to inflated distribution of test statistics have not been systematically examined. Here, we leveraged both public controls, gnomAD v2.1 and several datasets sequenced in our laboratory to systematically investigate factors that could contribute to the false-positive discovery, as measured by λΔ95, a measure to quantify the degree of inflation in statistical significance. Analyses of datasets in this investigation found that 1) the significantly inflated distribution of test statistics decreased substantially when the same variant caller and filtering pipelines were employed, 2) differences in library prep kits and sequencers did not affect the false-positive discovery rate and, 3) joint vs. separate variant-calling of cases and controls did not contribute to the inflation of test statistics. Currently available methods do not adequately adjust for the high false-positive discovery. These results, especially if replicated, emphasize the risks of using public controls for rare-variant association tests in which individual-level data and the computational pipeline are not readily accessible, which prevents the use of the same variant-calling and filtering pipelines on both cases and controls. A plausible solution exists with the emergence of cloud-based computing, which can make it possible to bring containerized analytical pipelines to the data (rather than the data to the pipeline) and could avert or minimize these issues. It is suggested that future reports account for this issue and provide this as a limitation in reporting new findings based on studies that cannot practically analyze all data on a single pipeline.

Published
2023

4. Impact of Transcript (p16/p14ARF) Alteration on Cancer Risk in CDKN2A Germline Pathogenic Variant Carriers.

Author

Sargen, Michael R, Helgadottir, Hildur, Yang, Xiaohong R, Harland, Mark, Hatton, Jessica N, Jones, Kristine, Hicks, Belynda D, Hutchinson, Amy, Curry, Michael, Tucker, Margaret A, Goldstein, Alisa M, and Pfeiffer, Ruth M

Subjects
Biomedical and Clinical Sciences, Oncology and Carcinogenesis, Rare Diseases, Digestive Diseases, Lung, Cancer, Prevention, Clinical Research, Humans, United States, Aged, Tumor Suppressor Protein p14ARF, Squamous Cell Carcinoma of Head and Neck, Cyclin-Dependent Kinase Inhibitor p16, Melanoma, Risk Factors, Head and Neck Neoplasms, Oncology and carcinogenesis
Abstract

Few studies have evaluated the relationship between CDKN2A germline pathogenic variants (GPV), transcript (p16/p14ARF) alteration, and cancer risk. Standardized incidence ratios (SIRs) comparing cancer risk with the general population were calculated for 385 CDKN2A GPV carriers from 2 large cohorts (259 United States and 126 Swedish individuals) using Poisson regression; statistical significance was defined as P less than .002 (Bonferroni correction). Cumulative incidence is reported for melanoma and nonmelanoma cancer. Incidence was increased for melanoma (SIR = 159.8, 95% confidence interval [CI] = 132.1 to 193.2), pancreatic cancer (SIR = 24.1, 95% CI = 14.7 to 39.4), head and neck squamous cell carcinoma (SIR = 16.2, 95% CI = 9.5 to 27.6), and lung cancer (SIR = 5.6, 95% CI = 3.4 to 9.1) in GPV carriers. Similar associations were observed with p16 alteration. Combined p16 and p14ARF alteration was associated with increased incidence of esophageal cancer (SIR = 16.7, 95% CI = 5.7 to 48.9) and malignant peripheral nerve sheath tumor (SIR = 113.0, 95% CI = 16.4 to 780.9), although cancer events were limited (n

Published
2022

5. CSMD1 Shows Complex Patterns of Somatic Copy Number Alterations and Expressions of mRNAs and Target Micro RNAs in Esophageal Squamous Cell Carcinoma

Author

Hu, Nan, Wang, Chaoyu, Zhang, Tongwu, Su, Hua, Liu, Huaitian, Yang, Howard H, Giffen, Carol, Hu, Ying, Taylor, Philip R, and Goldstein, Alisa M

Subjects
Biomedical and Clinical Sciences, Oncology and Carcinogenesis, Biotechnology, Genetics, Cancer, Digestive Diseases, CSMD1, allelic imbalance, esophageal squamous cell carcinoma, gene expression, miRNA, somatic copy number alternation, Oncology and carcinogenesis
Abstract

BackgroundHuman Cub and Sushi Multiple Domains 1 (CSMD1) is a novel candidate tumor-suppressor gene that codes for multiple domains, including complement regulatory and adhesion proteins, and has recently been shown to have alterations in multiple cancers. We investigated CSMD1 in esophageal squamous cell carcinoma (ESCC) by performing an integrated analysis on somatic copy number alterations (CNAs), including copy-number gain or loss, allelic imbalance (AI), loss of heterozygosity (LOH), and the expressions of mRNA and its target miRNAs on specimens from the same patients with ESCC.Results(i) Two-thirds of ESCC patients had all three types of alterations studied-somatic DNA alterations in 70%, and abnormal expressions of CSMD1 RNA in 69% and in target miRNAs in 66%; patterns among these alterations were complex. (ii) In total, 97% of 888 CSMD1 SNPs studied showed somatic DNA alterations, with most located near exons 4-11, 24-25, 39-40, 55-56, and 69-70. (iii) In total, 68% of SNPs with a CNA were correlated with expression of CSMD1. (iv) A total of 33 correlations between non-coding SNPs and expression of CSMD1 target miRs were found.ConclusionsOur results indicate that the CSMD1 gene may play a role in ESCC through complex patterns of DNA alterations and RNA and miRNA expressions. Alterations in some somatic SNPs in non-coding regions of CSMD1 appear to influence expression of this gene and its target miRNAs.

Published
2022

6. The Mutographs biorepository: A unique genomic resource to study cancer around the world

Author

Perdomo, Sandra, Abedi-Ardekani, Behnoush, de Carvalho, Ana Carolina, Ferreiro-Iglesias, Aida, Gaborieau, Valérie, Cattiaux, Thomas, Renard, Hélène, Chopard, Priscilia, Carreira, Christine, Spanu, Andreea, Nikmanesh, Arash, Cardoso Penha, Ricardo Cortez, Antwi, Samuel O., Ashton-Prolla, Patricia, Canova, Cristina, Chitapanarux, Taned, Cox, Riley, Curado, Maria Paula, de Oliveira, José Carlos, Dzamalala, Charles, Fabianova, Elenora, Ferri, Lorenzo, Fitzgerald, Rebecca, Foretova, Lenka, Gallinger, Steven, Goldstein, Alisa M., Holcatova, Ivana, Huertas, Antonio, Janout, Vladimir, Jarmalaite, Sonata, Kaneva, Radka, Kowalski, Luiz Paulo, Kulis, Tomislav, Lagiou, Pagona, Lissowska, Jolanta, Malekzadeh, Reza, Mates, Dana, McCorrmack, Valerie, Menya, Diana, Mhatre, Sharayu, Mmbaga, Blandina Theophil, de Moricz, André, Nyirády, Péter, Ognjanovic, Miodrag, Papadopoulou, Kyriaki, Polesel, Jerry, Purdue, Mark P., Rascu, Stefan, Rebolho Batista, Lidia Maria, Reis, Rui Manuel, Ribeiro Pinto, Luis Felipe, Rodríguez-Urrego, Paula A., Sangkhathat, Surasak, Sangrajrang, Suleeporn, Shibata, Tatsuhiro, Stakhovsky, Eduard, Świątkowska, Beata, Vaccaro, Carlos, Vasconcelos de Podesta, Jose Roberto, Vasudev, Naveen S., Vilensky, Marta, Yeung, Jonathan, Zaridze, David, Zendehdel, Kazem, Scelo, Ghislaine, Chanudet, Estelle, Wang, Jingwei, Fitzgerald, Stephen, Latimer, Calli, Moody, Sarah, Humphreys, Laura, Alexandrov, Ludmil B., Stratton, Michael R., and Brennan, Paul

Published
2024
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7. Novel MAPK/AKT-impairing germline NRAS variant identified in a melanoma-prone family

Author

Brown, Kevin M., Xu, Mai, Sargen, Michael, Jang, Hyunbum, Zhang, Mingzhen, Zhang, Tongwu, Zhu, Bin, Jones, Kristie, Kim, Jung, Mendoza, Laura, Hayward, Nicholas K., Tucker, Margaret A., Goldstein, Alisa M., Yang, Xiaohong Rose, Stewart, Douglas R., Hicks, Belynda, Consonni, Dario, Pesatori, Angela C., Fargnoli, Maria Concetta, Peris, Ketty, Stratigos, Alex, Menin, Chiara, Ghiorzo, Paola, Puig, Susana, Nagore, Eduardo, Andresson, Thorkell, Nussinov, Ruth, Calista, Donato, and Landi, Maria Teresa

Published
2022
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8. First international workshop of the ATM and cancer risk group (4-5 December 2019)

Author

Lesueur, Fabienne, Easton, Douglas F., Renault, Anne-Laure, Tavtigian, Sean V., Bernstein, Jonine L., Kote-Jarai, Zsofia, Eeles, Rosalind A., Plaseska-Karanfia, Dijana, Feliubadaló, Lidia, Arun, Banu, Herold, Natalie, Versmold, Beatrix, Schmutzler, Rita Katharina, Nguyen-Dumont, Tú, Southey, Melissa C., Dorling, Leila, Dunning, Alison M., Ghiorzo, Paola, Dalmasso, Bruna Samia, Cavaciuti, Eve, Le Gal, Dorothée, Roberts, Nicholas J., Dominguez-Valentin, Mev, Rookus, Matti, Taylor, Alexander M. R., Goldstein, Alisa M., Goldgar, David E., Stoppa-Lyonnet, Dominique, and Andrieu, Nadine

Published
2022
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10. Mutational signatures in esophageal squamous cell carcinoma from eight countries with varying incidence

Author

Moody, Sarah, Senkin, Sergey, Islam, S. M. Ashiqul, Wang, Jingwei, Nasrollahzadeh, Dariush, Cortez Cardoso Penha, Ricardo, Fitzgerald, Stephen, Bergstrom, Erik N., Atkins, Joshua, He, Yudou, Khandekar, Azhar, Smith-Byrne, Karl, Carreira, Christine, Gaborieau, Valerie, Latimer, Calli, Thomas, Emily, Abnizova, Irina, Bucciarelli, Pauline E., Jones, David, Teague, Jon W., Abedi-Ardekani, Behnoush, Serra, Stefano, Scoazec, Jean-Yves, Saffar, Hiva, Azmoudeh-Ardalan, Farid, Sotoudeh, Masoud, Nikmanesh, Arash, Poustchi, Hossein, Niavarani, Ahmadreza, Gharavi, Samad, Eden, Michael, Richman, Paul, Campos, Lia S., Fitzgerald, Rebecca C., Ribeiro, Luis Felipe, Soares-Lima, Sheila Coelho, Dzamalala, Charles, Mmbaga, Blandina Theophil, Shibata, Tatsuhiro, Menya, Diana, Goldstein, Alisa M., Hu, Nan, Malekzadeh, Reza, Fazel, Abdolreza, McCormack, Valerie, McKay, James, Perdomo, Sandra, Scelo, Ghislaine, Chanudet, Estelle, Humphreys, Laura, Alexandrov, Ludmil B., Brennan, Paul, and Stratton, Michael R.

Published
2021
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12. Germline Mutations in PALB2, BRCA1, and RAD51C, Which Regulate DNA Recombination Repair, in Patients With Gastric Cancer

Author

Sahasrabudhe, Ruta, Lott, Paul, Bohorquez, Mabel, Toal, Ted, Estrada, Ana P, Suarez, John J, Brea-Fernández, Alejandro, Cameselle-Teijeiro, José, Pinto, Carla, Ramos, Irma, Mantilla, Alejandra, Prieto, Rodrigo, Corvalan, Alejandro, Norero, Enrique, Alvarez, Carolina, Tapia, Teresa, Carvallo, Pilar, Gonzalez, Luz M, Cock-Rada, Alicia, Solano, Angela, Neffa, Florencia, Della Valle, Adriana, Yau, Chris, Soares, Gabriela, Borowsky, Alexander, Hu, Nan, He, Li-Ji, Han, Xiao-You, Group, Latin American Gastric Cancer Genetics Collaborative, Echeverry, Magdalena, Suarez, John, Mateus, Gilbert, Bravo, Maria Mercedes, Bolaños, Fernando, Vélez, Alejandro, Torres, Javier, Carvajal-Carmona, Luis, Taylor, Philip R, Goldstein, Alisa M, Ruiz-Ponte, Clara, Teixeira, Manuel R, and Carvajal-Carmona, Luis G

Subjects
Biomedical and Clinical Sciences, Oncology and Carcinogenesis, Genetic Testing, Clinical Research, Orphan Drug, Genetics, Cancer, Digestive Diseases, Rare Diseases, 2.1 Biological and endogenous factors, Aetiology, Aged, Aged, 80 and over, BRCA1 Protein, DNA-Binding Proteins, Fanconi Anemia Complementation Group N Protein, Female, Genetic Predisposition to Disease, Germ-Line Mutation, Humans, Male, Middle Aged, Mutation, Nuclear Proteins, Recombinational DNA Repair, Stomach Neoplasms, Tumor Suppressor Proteins, Stomach, Tumor, WES, Interaction, Latin American Gastric Cancer Genetics Collaborative Group, Clinical Sciences, Neurosciences, Paediatrics and Reproductive Medicine, Gastroenterology & Hepatology, Clinical sciences, Nutrition and dietetics
Abstract

Up to 10% of cases of gastric cancer are familial, but so far, only mutations in CDH1 have been associated with gastric cancer risk. To identify genetic variants that affect risk for gastric cancer, we collected blood samples from 28 patients with hereditary diffuse gastric cancer (HDGC) not associated with mutations in CDH1 and performed whole-exome sequence analysis. We then analyzed sequences of candidate genes in 333 independent HDGC and non-HDGC cases. We identified 11 cases with mutations in PALB2, BRCA1, or RAD51C genes, which regulate homologous DNA recombination. We found these mutations in 2 of 31 patients with HDGC (6.5%) and 9 of 331 patients with sporadic gastric cancer (2.8%). Most of these mutations had been previously associated with other types of tumors and partially co-segregated with gastric cancer in our study. Tumors that developed in patients with these mutations had a mutation signature associated with somatic homologous recombination deficiency. Our findings indicate that defects in homologous recombination increase risk for gastric cancer.

Published
2017

13. Molecular Characterization of the Human Stomach Microbiota in Gastric Cancer Patients

Author

Yu, Guoqin, Torres, Javier, Hu, Nan, Medrano-Guzman, Rafael, Herrera-Goepfert, Roberto, Humphrys, Michael S, Wang, Lemin, Wang, Chaoyu, Ding, Ti, Ravel, Jacques, Taylor, Philip R, Abnet, Christian C, and Goldstein, Alisa M

Subjects
Microbiology, Biological Sciences, Genetics, Nutrition, Infectious Diseases, Digestive Diseases - (Peptic Ulcer), Rare Diseases, Cancer, Prevention, Emerging Infectious Diseases, Digestive Diseases, Adult, Aged, Bacteria, China, Female, Gastrointestinal Microbiome, Helicobacter pylori, Humans, Male, Mexico, Middle Aged, Stomach, Stomach Neoplasms, Young Adult, 16S rRNA, KEGG modules, gastric cancer, microbiome, Biochemistry and Cell Biology, Medical microbiology
Abstract

Helicobacter pylori (Hp) is the primary cause of gastric cancer but we know little of its relative abundance and other microbes in the stomach, especially at the time of gastric cancer diagnosis. Here we characterized the taxonomic and derived functional profiles of gastric microbiota in two different sets of gastric cancer patients, and compared them with microbial profiles in other body sites. Paired non-malignant and tumor tissues were sampled from 160 gastric cancer patients with 80 from China and 80 from Mexico. The 16S rRNA gene V3-V4 region was sequenced using MiSeq platform for taxonomic profiles. PICRUSt was used to predict functional profiles. Human Microbiome Project was used for comparison. We showed that Hp is the most abundant member of gastric microbiota in both Chinese and Mexican samples (51 and 24%, respectively), followed by oral-associated bacteria. Taxonomic (phylum-level) profiles of stomach microbiota resembled oral microbiota, especially when the Helicobacter reads were removed. The functional profiles of stomach microbiota, however, were distinct from those found in other body sites and had higher inter-subject dissimilarity. Gastric microbiota composition did not differ by Hp colonization status or stomach anatomic sites, but did differ between paired non-malignant and tumor tissues in either Chinese or Mexican samples. Our study showed that Hp is the dominant member of the non-malignant gastric tissue microbiota in many gastric cancer patients. Our results provide insights on the gastric microbiota composition and function in gastric cancer patients, which may have important clinical implications.

Published
2017

15. Kinetics of EBV antibody‐based NPC risk scores in Taiwan NPC multiplex families.

Author

Hsu, Wan‐Lun, Tao, Jun, Fu, Sheng, Yu, Kelly J., Simon, Julia, Chen, Tseng‐Cheng, Chen, Chien‐Jen, Goldstein, Alisa M., Yu, Kai, Hildesheim, Allan, Waterboer, Tim, Wang, Cheng‐Ping, and Liu, Zhiwei

Subjects
DISEASE risk factors, VIRAL antibodies, NASOPHARYNX cancer, EARLY detection of cancer, ANTIBODY formation
Abstract

Nasopharyngeal carcinoma (NPC) risk prediction models based on Epstein–Barr virus (EBV)‐antibody testing have shown potential for screening of NPC; however, the long‐term stability is unclear. Here, we investigated the kinetics of two EBV‐antibody NPC risk scores within the Taiwan NPC Multiplex Family Study. Among 545 participants with multiple blood samples, we evaluated the stability of a 2‐marker enzyme‐linked immunosorbent assay score and 13‐marker multiplex serology score using the intra‐class correlation coefficient (ICC) by fitting a linear mixed model that accounted for the clustering effect of multiple measurements per subject and age. We also estimated the clustering of positive tests using Fleiss's kappa statistic. Over an average 20‐year follow‐up, the 2‐marker score showed high stability over time, whereas the 13‐marker score was more variable (p <.05). Case–control status is associated with the kinetics of the antibody response, with higher ICCs among cases. Positive tests were more likely to cluster within the same individual for the 2‐marker score than the 13‐marker score (p <.05). The 2‐marker score had an increase in specificity from ~90% for single measurement to ~96% with repeat testing. The 13‐marker score had a specificity of ~73% for a single measurement that increased to ~92% with repeat testing. Among individuals who developed NPC, none experienced score reversion. Our findings suggest that repeated testing could improve the specificity of NPC screening in high‐risk NPC multiplex families. Further studies are required to determine the impact on sensitivity, establish optimal screening intervals, and generalize these findings to general population settings in high‐risk regions. [ABSTRACT FROM AUTHOR]

Published
2024
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17. Female chromosome X mosaicism is age-related and preferentially affects the inactivated X chromosome

Author

Machiela, Mitchell J, Zhou, Weiyin, Karlins, Eric, Sampson, Joshua N, Freedman, Neal D, Yang, Qi, Hicks, Belynda, Dagnall, Casey, Hautman, Christopher, Jacobs, Kevin B, Abnet, Christian C, Aldrich, Melinda C, Amos, Christopher, Amundadottir, Laufey T, Arslan, Alan A, Beane-Freeman, Laura E, Berndt, Sonja I, Black, Amanda, Blot, William J, Bock, Cathryn H, Bracci, Paige M, Brinton, Louise A, Bueno-de-Mesquita, H Bas, Burdett, Laurie, Buring, Julie E, Butler, Mary A, Canzian, Federico, Carreon, Tania, Chaffee, Kari G, Chang, I-Shou, Chatterjee, Nilanjan, Chen, Chu, Chen, Constance, Chen, Kexin, Chung, Charles C, Cook, Linda S, Bou, Marta Crous, Cullen, Michael, Davis, Faith G, De Vivo, Immaculata, Ding, Ti, Doherty, Jennifer, Duell, Eric J, Epstein, Caroline G, Fan, Jin-Hu, Figueroa, Jonine D, Fraumeni, Joseph F, Friedenreich, Christine M, Fuchs, Charles S, Gallinger, Steven, Gao, Yu-Tang, Gapstur, Susan M, Garcia-Closas, Montserrat, Gaudet, Mia M, Gaziano, J Michael, Giles, Graham G, Gillanders, Elizabeth M, Giovannucci, Edward L, Goldin, Lynn, Goldstein, Alisa M, Haiman, Christopher A, Hallmans, Goran, Hankinson, Susan E, Harris, Curtis C, Henriksson, Roger, Holly, Elizabeth A, Hong, Yun-Chul, Hoover, Robert N, Hsiung, Chao A, Hu, Nan, Hu, Wei, Hunter, David J, Hutchinson, Amy, Jenab, Mazda, Johansen, Christoffer, Khaw, Kay-Tee, Kim, Hee Nam, Kim, Yeul Hong, Kim, Young Tae, Klein, Alison P, Klein, Robert, Koh, Woon-Puay, Kolonel, Laurence N, Kooperberg, Charles, Kraft, Peter, Krogh, Vittorio, Kurtz, Robert C, LaCroix, Andrea, Lan, Qing, Landi, Maria Teresa, Le Marchand, Loic, Li, Donghui, Liang, Xiaolin, Liao, Linda M, Lin, Dongxin, Liu, Jianjun, Lissowska, Jolanta, Lu, Lingeng, Magliocco, Anthony M, and Malats, Nuria

Published
2016

18. Estimated Prevalence, Tumor Spectrum, and Neurofibromatosis Type 1–Like Phenotype of CDKN2A-Related Melanoma-Astrocytoma Syndrome

Author

Sargen, Michael R., primary, Kim, Jung, additional, Potjer, Thomas P., additional, Velthuizen, Mary E., additional, Martir-Negron, Arelis E., additional, Odia, Yazmin, additional, Helgadottir, Hildur, additional, Hatton, Jessica N., additional, Haley, Jeremy S., additional, Thone, Gretchen, additional, Widemann, Brigitte C., additional, Gross, Andrea M., additional, Yohe, Marielle E., additional, Kaplan, Rosandra N., additional, Shern, Jack F., additional, Sundby, R. Taylor, additional, Astiazaran-Symonds, Esteban, additional, Yang, Xiaohong R., additional, Carey, David J., additional, Tucker, Margaret A., additional, Stewart, Douglas R., additional, and Goldstein, Alisa M., additional

Published
2023
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20. Whole genome sequencing of skull-base chordoma reveals genomic alterations associated with recurrence and chordoma-specific survival

Author

Bai, Jiwei, Shi, Jianxin, Li, Chuzhong, Wang, Shuai, Zhang, Tongwu, Hua, Xing, Zhu, Bin, Koka, Hela, Wu, Ho-Hsiang, Song, Lei, Wang, Difei, Wang, Mingyi, Zhou, Weiyin, Ballew, Bari J., Zhu, Bin, Hicks, Belynda, Mirabello, Lisa, Parry, Dilys M., Zhai, Yixuan, Li, Mingxuan, Du, Jiang, Wang, Junmei, Zhang, Shuheng, Liu, Qian, Zhao, Peng, Gui, Songbai, Goldstein, Alisa M., Zhang, Yazhuo, and Yang, Xiaohong R.

Published
2021
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21. Gene-Level Associations in Patients With and Without Pathogenic Germline Variants in CDKN2A and Pancreatic Cancer

Author

Astiazaran-Symonds, Esteban, Graham, Cole, Kim, Jung, Tucker, Margaret A., Ingvar, Christian, Helgadottir, Hildur, Pastorino, Lorenza, van Doorn, Remco, Sampson, Joshua N., Zhu, Bin, Bruno, William, Queirolo, Paola, Fornarini, Giuseppe, Sciallero, Stefania, Carter, Brian, Hicks, Belynda, Hutchinson, Amy, Jones, Kristine, Stewart, Douglas R., Chanock, Stephen J., Freedman, Neal D., Landi, Maria Teresa, Höiom, Veronica, Puig, Susana, Gruis, Nelleke, Yang, Xiaohong R., Ghiorzo, Paola, and Goldstein, Alisa M.

Published
2022
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22. Genome-wide association meta-analyses combining multiple risk phenotypes provide insights into the genetic architecture of cutaneous melanoma susceptibility

Author

Landi, Maria Teresa, Bishop, D. Timothy, MacGregor, Stuart, Machiela, Mitchell J., Stratigos, Alexander J., Ghiorzo, Paola, Brossard, Myriam, Calista, Donato, Choi, Jiyeon, Fargnoli, Maria Concetta, Zhang, Tongwu, Rodolfo, Monica, Trower, Adam J., Menin, Chiara, Martinez, Jacobo, Hadjisavvas, Andreas, Song, Lei, Stefanaki, Irene, Scolyer, Richard, Yang, Rose, Goldstein, Alisa M., Potrony, Miriam, Kypreou, Katerina P., Pastorino, Lorenza, Queirolo, Paola, Pellegrini, Cristina, Cattaneo, Laura, Zawistowski, Matthew, Gimenez-Xavier, Pol, Rodriguez, Arantxa, Elefanti, Lisa, Manoukian, Siranoush, Rivoltini, Licia, Smith, Blair H., Loizidou, Maria A., Del Regno, Laura, Massi, Daniela, Mandala, Mario, Khosrotehrani, Kiarash, Akslen, Lars A., Amos, Christopher I., Andresen, Per A., Avril, Marie-Françoise, Azizi, Esther, Soyer, H. Peter, Bataille, Veronique, Dalmasso, Bruna, Bowdler, Lisa M., Burdon, Kathryn P., Chen, Wei V., Codd, Veryan, Craig, Jamie E., Dębniak, Tadeusz, Falchi, Mario, Fang, Shenying, Friedman, Eitan, Simi, Sarah, Galan, Pilar, Garcia-Casado, Zaida, Gillanders, Elizabeth M., Gordon, Scott, Green, Adele, Gruis, Nelleke A., Hansson, Johan, Harland, Mark, Harris, Jessica, Helsing, Per, Henders, Anjali, Hočevar, Marko, Höiom, Veronica, Hunter, David, Ingvar, Christian, Kumar, Rajiv, Lang, Julie, Lathrop, G. Mark, Lee, Jeffrey E., Li, Xin, Lubiński, Jan, Mackie, Rona M., Malt, Maryrose, Malvehy, Josep, McAloney, Kerrie, Mohamdi, Hamida, Molven, Anders, Moses, Eric K., Neale, Rachel E., Novaković, Srdjan, Nyholt, Dale R., Olsson, Håkan, Orr, Nicholas, Fritsche, Lars G., Puig-Butille, Joan Anton, Qureshi, Abrar A., Radford-Smith, Graham L., Randerson-Moor, Juliette, Requena, Celia, Rowe, Casey, Samani, Nilesh J., Sanna, Marianna, Schadendorf, Dirk, Schulze, Hans-Joachim, Simms, Lisa A., Smithers, Mark, Song, Fengju, Swerdlow, Anthony J., van der Stoep, Nienke, Kukutsch, Nicole A., Visconti, Alessia, Wallace, Leanne, Ward, Sarah V., Wheeler, Lawrie, Sturm, Richard A., Hutchinson, Amy, Jones, Kristine, Malasky, Michael, Vogt, Aurelie, Zhou, Weiyin, Pooley, Karen A., Elder, David E., Han, Jiali, Hicks, Belynda, Hayward, Nicholas K., Kanetsky, Peter A., Brummett, Chad, Montgomery, Grant W., Olsen, Catherine M., Hayward, Caroline, Dunning, Alison M., Martin, Nicholas G., Evangelou, Evangelos, Mann, Graham J., Long, Georgina, Pharoah, Paul D. P., Easton, Douglas F., Barrett, Jennifer H., Cust, Anne E., Abecasis, Goncalo, Duffy, David L., Whiteman, David C., Gogas, Helen, De Nicolo, Arcangela, Tucker, Margaret A., Newton-Bishop, Julia A., Peris, Ketty, Chanock, Stephen J., Demenais, Florence, Brown, Kevin M., Puig, Susana, Nagore, Eduardo, Shi, Jianxin, Iles, Mark M., and Law, Matthew H.

Published
2020
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23. Assessing the Incremental Contribution of Common Genomic Variants to Melanoma Risk Prediction in Two Population-Based Studies

Author

Mann, Graham J., Cust, Anne E., Schmid, Helen, Hopper, John L., Aitken, Joanne F., Armstrong, Bruce K., Giles, Graham G., Holland, Elizabeth, Kefford, Richard F., Jenkins, Mark A., Newton Bishop, Julia A., Affleck, Paul, Barrett, Jennifer H., Bishop, D. Timothy, Harrison, Jane, Iles, Mark M., Randerson-Moor, Juliette, Harland, Mark, Taylor, John C., Whittaker, Linda, Kukalizch, Kairen, Leake, Susan, Karpavicius, Birute, Haynes, Sue, Mack, Tricia, Chan, May, Taylor, Yvonne, Davies, John, King, Paul, Drummond, Martin, Kanetsky, Peter A., Goldstein, Alisa M., MacGregor, Stuart, Law, Matthew H., Bui, Minh, Brossard, Myriam, Demenais, Florence, Hoggart, Clive, Brown, Kevin M., Landi, Maria Teresa, and Newton-Bishop, Julia A.

Published
2018
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24. Atypical Spitz tumor with SQSTM1::NTRK2 fusion: Report of a case with unique spindled cell features.

Author

Phillips, Gregory S., Mengden‐Koon, Stephanie, Dhossche, Julie, LeBoit, Philip E., Goldstein, Alisa M., Lee, Ina, Raffeld, Mark, Papanicolau‐Sengos, Antonios, Sargen, Michael R., and Chung, Jina

Abstract

A host of signature genetic alterations have been demonstrated in Spitz neoplasms, most notably fusions of kinase genes (including BRAF, ALK, ROS1, NTRK1, NTRK3, RET, MET, MAP3K8) or variants in HRAS. While there are multiple reports of rearrangements involving NTRK1 and NTRK3 in Spitz tumors, there are very few reports of NTRK2‐rearranged Spitz nevi in the literature. This report presents an NTRK2‐rearranged atypical Spitz tumor with spindled cell features. The patient was a 6‐year‐old female with a growing pigmented papule on the back. Histopathological evaluation revealed an asymmetric, biphasic, compound proliferation of melanocytes featuring an epithelioid cell population arranged as variably sized nests and single cells along the basal layer with extension down adnexa, as well as a population of spindled melanocytes with desmoplastic features and loss of Melan‐A expression in the dermis. There was partial loss of p16 expression in the epidermal component and diffuse loss in the dermal component. Immunohistochemistry for PRAME, ALK, NTRK1, HRAS Q61R, p53, and BRAF V600E were negative. A SQSTM1::NTRK2 fusion was identified by RNA sequencing. No TERT promoter hotspot variants were detected. This case report expands the known histopathologic spectrum of genetic alterations in Spitz neoplasms. [ABSTRACT FROM AUTHOR]

Published
2024
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27. Germline Variation at CDKN2A and Associations with Nevus Phenotypes among Members of Melanoma Families

Author

Taylor, Nicholas J., Mitra, Nandita, Goldstein, Alisa M., Tucker, Margaret A., Avril, Marie-Françoise, Azizi, Esther, Bergman, Wilma, Bishop, D. Timothy, Bressac-de Paillerets, Brigitte, Bruno, William, Calista, Donato, Cannon-Albright, Lisa A., Cuellar, Francisco, Cust, Anne E., Demenais, Florence, Elder, David E., Gerdes, Anne-Marie, Ghiorzo, Paola, Grazziotin, Thais C., Hansson, Johan, Harland, Mark, Hayward, Nicholas K., Hocevar, Marko, Höiom, Veronica, Ingvar, Christian, Landi, Maria Teresa, Landman, Gilles, Larre-Borges, Alejandra, Leachman, Sancy A., Mann, Graham J., Nagore, Eduardo, Olsson, Håkan, Palmer, Jane M., Perić, Barbara, Pjanova, Dace, Pritchard, Antonia, Puig, Susana, van der Stoep, Nienke, Wadt, Karin A.W., Whitaker, Linda, Yang, Xiaohong R., Newton Bishop, Julia A., Gruis, Nelleke A., and Kanetsky, Peter A.

Published
2017
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28. Supplementary Material 2 from A Gene Expression Signature from Peripheral Whole Blood for Stage I Lung Adenocarcinoma

Author

Rotunno, Melissa, primary, Hu, Nan, primary, Su, Hua, primary, Wang, Chaoyu, primary, Goldstein, Alisa M., primary, Bergen, Andrew W., primary, Consonni, Dario, primary, Pesatori, Angela C., primary, Bertazzi, Pier Alberto, primary, Wacholder, Sholom, primary, Shih, Joanna, primary, Caporaso, Neil E., primary, Taylor, Phil R., primary, and Landi, Maria Teresa, primary

Published
2023
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29. Data from A Gene Expression Signature from Peripheral Whole Blood for Stage I Lung Adenocarcinoma

Author

Rotunno, Melissa, primary, Hu, Nan, primary, Su, Hua, primary, Wang, Chaoyu, primary, Goldstein, Alisa M., primary, Bergen, Andrew W., primary, Consonni, Dario, primary, Pesatori, Angela C., primary, Bertazzi, Pier Alberto, primary, Wacholder, Sholom, primary, Shih, Joanna, primary, Caporaso, Neil E., primary, Taylor, Phil R., primary, and Landi, Maria Teresa, primary

Published
2023
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30. Supplementary Material 1 from A Gene Expression Signature from Peripheral Whole Blood for Stage I Lung Adenocarcinoma

Author

Rotunno, Melissa, primary, Hu, Nan, primary, Su, Hua, primary, Wang, Chaoyu, primary, Goldstein, Alisa M., primary, Bergen, Andrew W., primary, Consonni, Dario, primary, Pesatori, Angela C., primary, Bertazzi, Pier Alberto, primary, Wacholder, Sholom, primary, Shih, Joanna, primary, Caporaso, Neil E., primary, Taylor, Phil R., primary, and Landi, Maria Teresa, primary

Published
2023
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31. Data from Gene Expression Profiling Identifies Two Chordoma Subtypes Associated with Distinct Molecular Mechanisms and Clinical Outcomes

Author

Bai, Jiwei, primary, Shi, Jianxin, primary, Zhang, Yazhuo, primary, Li, Chuzhong, primary, Xiong, Yujia, primary, Koka, Hela, primary, Wang, Difei, primary, Zhang, Tongwu, primary, Song, Lei, primary, Luo, Wen, primary, Zhu, Bin, primary, Hicks, Belynda, primary, Hutchinson, Amy, primary, Kirk, Erin, primary, Troester, Melissa A., primary, Li, Mingxuan, primary, Shen, Yutao, primary, Ma, Tianshun, primary, Wang, Junmei, primary, Liu, Xing, primary, Wang, Shuai, primary, Gui, Songbai, primary, McMaster, Mary L., primary, Chanock, Stephen J., primary, Parry, Dilys M., primary, Goldstein, Alisa M., primary, and Yang, Xiaohong R., primary

Published
2023
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32. Supplementary fig 2 from Gene Expression Profiling Identifies Two Chordoma Subtypes Associated with Distinct Molecular Mechanisms and Clinical Outcomes

Author

Bai, Jiwei, primary, Shi, Jianxin, primary, Zhang, Yazhuo, primary, Li, Chuzhong, primary, Xiong, Yujia, primary, Koka, Hela, primary, Wang, Difei, primary, Zhang, Tongwu, primary, Song, Lei, primary, Luo, Wen, primary, Zhu, Bin, primary, Hicks, Belynda, primary, Hutchinson, Amy, primary, Kirk, Erin, primary, Troester, Melissa A., primary, Li, Mingxuan, primary, Shen, Yutao, primary, Ma, Tianshun, primary, Wang, Junmei, primary, Liu, Xing, primary, Wang, Shuai, primary, Gui, Songbai, primary, McMaster, Mary L., primary, Chanock, Stephen J., primary, Parry, Dilys M., primary, Goldstein, Alisa M., primary, and Yang, Xiaohong R., primary

Published
2023
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33. Supplementary fig 4 from Gene Expression Profiling Identifies Two Chordoma Subtypes Associated with Distinct Molecular Mechanisms and Clinical Outcomes

Author

Bai, Jiwei, primary, Shi, Jianxin, primary, Zhang, Yazhuo, primary, Li, Chuzhong, primary, Xiong, Yujia, primary, Koka, Hela, primary, Wang, Difei, primary, Zhang, Tongwu, primary, Song, Lei, primary, Luo, Wen, primary, Zhu, Bin, primary, Hicks, Belynda, primary, Hutchinson, Amy, primary, Kirk, Erin, primary, Troester, Melissa A., primary, Li, Mingxuan, primary, Shen, Yutao, primary, Ma, Tianshun, primary, Wang, Junmei, primary, Liu, Xing, primary, Wang, Shuai, primary, Gui, Songbai, primary, McMaster, Mary L., primary, Chanock, Stephen J., primary, Parry, Dilys M., primary, Goldstein, Alisa M., primary, and Yang, Xiaohong R., primary

Published
2023
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34. Supplementary Legend 1 from Gene Expression Profiling Identifies Two Chordoma Subtypes Associated with Distinct Molecular Mechanisms and Clinical Outcomes

Author

Bai, Jiwei, primary, Shi, Jianxin, primary, Zhang, Yazhuo, primary, Li, Chuzhong, primary, Xiong, Yujia, primary, Koka, Hela, primary, Wang, Difei, primary, Zhang, Tongwu, primary, Song, Lei, primary, Luo, Wen, primary, Zhu, Bin, primary, Hicks, Belynda, primary, Hutchinson, Amy, primary, Kirk, Erin, primary, Troester, Melissa A., primary, Li, Mingxuan, primary, Shen, Yutao, primary, Ma, Tianshun, primary, Wang, Junmei, primary, Liu, Xing, primary, Wang, Shuai, primary, Gui, Songbai, primary, McMaster, Mary L., primary, Chanock, Stephen J., primary, Parry, Dilys M., primary, Goldstein, Alisa M., primary, and Yang, Xiaohong R., primary

Published
2023
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35. Supplementary fig 3 from Gene Expression Profiling Identifies Two Chordoma Subtypes Associated with Distinct Molecular Mechanisms and Clinical Outcomes

Author

Bai, Jiwei, primary, Shi, Jianxin, primary, Zhang, Yazhuo, primary, Li, Chuzhong, primary, Xiong, Yujia, primary, Koka, Hela, primary, Wang, Difei, primary, Zhang, Tongwu, primary, Song, Lei, primary, Luo, Wen, primary, Zhu, Bin, primary, Hicks, Belynda, primary, Hutchinson, Amy, primary, Kirk, Erin, primary, Troester, Melissa A., primary, Li, Mingxuan, primary, Shen, Yutao, primary, Ma, Tianshun, primary, Wang, Junmei, primary, Liu, Xing, primary, Wang, Shuai, primary, Gui, Songbai, primary, McMaster, Mary L., primary, Chanock, Stephen J., primary, Parry, Dilys M., primary, Goldstein, Alisa M., primary, and Yang, Xiaohong R., primary

Published
2023
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36. Supplementary fig 1 from Gene Expression Profiling Identifies Two Chordoma Subtypes Associated with Distinct Molecular Mechanisms and Clinical Outcomes

Author

Bai, Jiwei, primary, Shi, Jianxin, primary, Zhang, Yazhuo, primary, Li, Chuzhong, primary, Xiong, Yujia, primary, Koka, Hela, primary, Wang, Difei, primary, Zhang, Tongwu, primary, Song, Lei, primary, Luo, Wen, primary, Zhu, Bin, primary, Hicks, Belynda, primary, Hutchinson, Amy, primary, Kirk, Erin, primary, Troester, Melissa A., primary, Li, Mingxuan, primary, Shen, Yutao, primary, Ma, Tianshun, primary, Wang, Junmei, primary, Liu, Xing, primary, Wang, Shuai, primary, Gui, Songbai, primary, McMaster, Mary L., primary, Chanock, Stephen J., primary, Parry, Dilys M., primary, Goldstein, Alisa M., primary, and Yang, Xiaohong R., primary

Published
2023
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37. Supplementary fig 5 from Gene Expression Profiling Identifies Two Chordoma Subtypes Associated with Distinct Molecular Mechanisms and Clinical Outcomes

Author

Bai, Jiwei, primary, Shi, Jianxin, primary, Zhang, Yazhuo, primary, Li, Chuzhong, primary, Xiong, Yujia, primary, Koka, Hela, primary, Wang, Difei, primary, Zhang, Tongwu, primary, Song, Lei, primary, Luo, Wen, primary, Zhu, Bin, primary, Hicks, Belynda, primary, Hutchinson, Amy, primary, Kirk, Erin, primary, Troester, Melissa A., primary, Li, Mingxuan, primary, Shen, Yutao, primary, Ma, Tianshun, primary, Wang, Junmei, primary, Liu, Xing, primary, Wang, Shuai, primary, Gui, Songbai, primary, McMaster, Mary L., primary, Chanock, Stephen J., primary, Parry, Dilys M., primary, Goldstein, Alisa M., primary, and Yang, Xiaohong R., primary

Published
2023
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38. Table S1-S5 from Gene Expression Profiling Identifies Two Chordoma Subtypes Associated with Distinct Molecular Mechanisms and Clinical Outcomes

Author

Bai, Jiwei, primary, Shi, Jianxin, primary, Zhang, Yazhuo, primary, Li, Chuzhong, primary, Xiong, Yujia, primary, Koka, Hela, primary, Wang, Difei, primary, Zhang, Tongwu, primary, Song, Lei, primary, Luo, Wen, primary, Zhu, Bin, primary, Hicks, Belynda, primary, Hutchinson, Amy, primary, Kirk, Erin, primary, Troester, Melissa A., primary, Li, Mingxuan, primary, Shen, Yutao, primary, Ma, Tianshun, primary, Wang, Junmei, primary, Liu, Xing, primary, Wang, Shuai, primary, Gui, Songbai, primary, McMaster, Mary L., primary, Chanock, Stephen J., primary, Parry, Dilys M., primary, Goldstein, Alisa M., primary, and Yang, Xiaohong R., primary

Published
2023
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43. Data from MicroRNA Expression Differentiates Histology and Predicts Survival of Lung Cancer

Author

Landi, Maria Teresa, primary, Zhao, Yingdong, primary, Rotunno, Melissa, primary, Koshiol, Jill, primary, Liu, Hui, primary, Bergen, Andrew W., primary, Rubagotti, Maurizia, primary, Goldstein, Alisa M., primary, Linnoila, Ilona, primary, Marincola, Francesco M., primary, Tucker, Margaret A., primary, Bertazzi, Pier Alberto, primary, Pesatori, Angela C., primary, Caporaso, Neil E., primary, McShane, Lisa M., primary, and Wang, Ena, primary

Published
2023
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44. Data from Genomic Landscape of Somatic Alterations in Esophageal Squamous Cell Carcinoma and Gastric Cancer

Author

Hu, Nan, primary, Kadota, Mitsutaka, primary, Liu, Huaitian, primary, Abnet, Christian C., primary, Su, Hua, primary, Wu, Hailong, primary, Freedman, Neal D., primary, Yang, Howard H., primary, Wang, Chaoyu, primary, Yan, Chunhua, primary, Wang, Lemin, primary, Gere, Sheryl, primary, Hutchinson, Amy, primary, Song, Guohong, primary, Wang, Yuan, primary, Ding, Ti, primary, Qiao, You-Lin, primary, Koshiol, Jill, primary, Dawsey, Sanford M., primary, Giffen, Carol, primary, Goldstein, Alisa M., primary, Taylor, Philip R., primary, and Lee, Maxwell P., primary

Published
2023
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45. Supplementary table 8 from Genomic Landscape of Somatic Alterations in Esophageal Squamous Cell Carcinoma and Gastric Cancer

Author

Hu, Nan, primary, Kadota, Mitsutaka, primary, Liu, Huaitian, primary, Abnet, Christian C., primary, Su, Hua, primary, Wu, Hailong, primary, Freedman, Neal D., primary, Yang, Howard H., primary, Wang, Chaoyu, primary, Yan, Chunhua, primary, Wang, Lemin, primary, Gere, Sheryl, primary, Hutchinson, Amy, primary, Song, Guohong, primary, Wang, Yuan, primary, Ding, Ti, primary, Qiao, You-Lin, primary, Koshiol, Jill, primary, Dawsey, Sanford M., primary, Giffen, Carol, primary, Goldstein, Alisa M., primary, Taylor, Philip R., primary, and Lee, Maxwell P., primary

Published
2023
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46. Supplementary table 6 from Genomic Landscape of Somatic Alterations in Esophageal Squamous Cell Carcinoma and Gastric Cancer

Author

Hu, Nan, primary, Kadota, Mitsutaka, primary, Liu, Huaitian, primary, Abnet, Christian C., primary, Su, Hua, primary, Wu, Hailong, primary, Freedman, Neal D., primary, Yang, Howard H., primary, Wang, Chaoyu, primary, Yan, Chunhua, primary, Wang, Lemin, primary, Gere, Sheryl, primary, Hutchinson, Amy, primary, Song, Guohong, primary, Wang, Yuan, primary, Ding, Ti, primary, Qiao, You-Lin, primary, Koshiol, Jill, primary, Dawsey, Sanford M., primary, Giffen, Carol, primary, Goldstein, Alisa M., primary, Taylor, Philip R., primary, and Lee, Maxwell P., primary

Published
2023
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47. Supplementary table 2 from Genomic Landscape of Somatic Alterations in Esophageal Squamous Cell Carcinoma and Gastric Cancer

Author

Hu, Nan, primary, Kadota, Mitsutaka, primary, Liu, Huaitian, primary, Abnet, Christian C., primary, Su, Hua, primary, Wu, Hailong, primary, Freedman, Neal D., primary, Yang, Howard H., primary, Wang, Chaoyu, primary, Yan, Chunhua, primary, Wang, Lemin, primary, Gere, Sheryl, primary, Hutchinson, Amy, primary, Song, Guohong, primary, Wang, Yuan, primary, Ding, Ti, primary, Qiao, You-Lin, primary, Koshiol, Jill, primary, Dawsey, Sanford M., primary, Giffen, Carol, primary, Goldstein, Alisa M., primary, Taylor, Philip R., primary, and Lee, Maxwell P., primary

Published
2023
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48. Supplementary table 4 from Genomic Landscape of Somatic Alterations in Esophageal Squamous Cell Carcinoma and Gastric Cancer

Author

Hu, Nan, primary, Kadota, Mitsutaka, primary, Liu, Huaitian, primary, Abnet, Christian C., primary, Su, Hua, primary, Wu, Hailong, primary, Freedman, Neal D., primary, Yang, Howard H., primary, Wang, Chaoyu, primary, Yan, Chunhua, primary, Wang, Lemin, primary, Gere, Sheryl, primary, Hutchinson, Amy, primary, Song, Guohong, primary, Wang, Yuan, primary, Ding, Ti, primary, Qiao, You-Lin, primary, Koshiol, Jill, primary, Dawsey, Sanford M., primary, Giffen, Carol, primary, Goldstein, Alisa M., primary, Taylor, Philip R., primary, and Lee, Maxwell P., primary

Published
2023
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49. Table Legend from Genomic Landscape of Somatic Alterations in Esophageal Squamous Cell Carcinoma and Gastric Cancer

Author

Hu, Nan, primary, Kadota, Mitsutaka, primary, Liu, Huaitian, primary, Abnet, Christian C., primary, Su, Hua, primary, Wu, Hailong, primary, Freedman, Neal D., primary, Yang, Howard H., primary, Wang, Chaoyu, primary, Yan, Chunhua, primary, Wang, Lemin, primary, Gere, Sheryl, primary, Hutchinson, Amy, primary, Song, Guohong, primary, Wang, Yuan, primary, Ding, Ti, primary, Qiao, You-Lin, primary, Koshiol, Jill, primary, Dawsey, Sanford M., primary, Giffen, Carol, primary, Goldstein, Alisa M., primary, Taylor, Philip R., primary, and Lee, Maxwell P., primary

Published
2023
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50. Supplementary table 3 from Genomic Landscape of Somatic Alterations in Esophageal Squamous Cell Carcinoma and Gastric Cancer

Author

Hu, Nan, primary, Kadota, Mitsutaka, primary, Liu, Huaitian, primary, Abnet, Christian C., primary, Su, Hua, primary, Wu, Hailong, primary, Freedman, Neal D., primary, Yang, Howard H., primary, Wang, Chaoyu, primary, Yan, Chunhua, primary, Wang, Lemin, primary, Gere, Sheryl, primary, Hutchinson, Amy, primary, Song, Guohong, primary, Wang, Yuan, primary, Ding, Ti, primary, Qiao, You-Lin, primary, Koshiol, Jill, primary, Dawsey, Sanford M., primary, Giffen, Carol, primary, Goldstein, Alisa M., primary, Taylor, Philip R., primary, and Lee, Maxwell P., primary

Published
2023
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