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1. Association of leukemic molecular profile with efficacy of inotuzumab ozogamicin in adults with relapsed/refractory ALL.

Author

Zhao, Yaqi, Laird, A, Roberts, Kathryn, Yafawi, Rolla, Kantarjian, Hagop, DeAngelo, Daniel, Stelljes, Matthias, Liedtke, Michaela, Stock, Wendy, Gökbuget, Nicola, OBrien, Susan, Jabbour, Elias, Cassaday, Ryan, Loyd, Melanie, Olsen, Scott, Neale, Geoffrey, Liu, Xueli, Vandendries, Erik, Advani, Anjali, and Mullighan, Charles

Subjects
Humans, Inotuzumab Ozogamicin, Precursor Cell Lymphoblastic Leukemia-Lymphoma, Adult, Female, Male, Middle Aged, Treatment Outcome, Aged, Recurrence, Antineoplastic Agents, Immunological, Young Adult, Drug Resistance, Neoplasm, Adolescent
Abstract

The phase 3 INO-VATE trial demonstrated higher rates of remission, measurable residual disease negativity, and improved overall survival for patients with relapsed/refractory (R/R) acute lymphoblastic leukemia (ALL) who received inotuzumab ozogamicin (InO) vs standard-of-care chemotherapy (SC). Here, we examined associations between genomic alterations and the efficacy of InO. Of 326 randomized patients, 91 (InO, n = 43; SC, n = 48) had samples evaluable for genomic analysis. The spectrum of gene fusions and other genomic alterations observed was comparable with prior studies of adult ALL. Responses to InO were observed in all leukemic subtypes, genomic alterations, and risk groups. Significantly higher rates of complete remission (CR)/CR with incomplete count recovery were observed with InO vs SC in patients with BCR::ABL1-like ALL (85.7% [6/7] vs 0% [0/5]; P = .0076), with TP53 alterations (100% [5/5] vs 12.5% [1/8]; P = .0047), and in the high-risk BCR::ABL1- (BCR::ABL1-like, low-hypodiploid, KMT2A-rearranged) group (83.3% [10/12] vs 10.5% [2/19]; P < .0001). This retrospective, exploratory analysis of the INO-VATE trial demonstrated potential for benefit with InO for patients with R/R ALL across leukemic subtypes, including BCR::ABL1-like ALL, and for those bearing diverse genomic alterations. Further confirmation of the efficacy of InO in patients with R/R ALL exhibiting the BCR::ABL1-like subtype or harboring TP53 alterations is warranted. This trial was registered at www.ClinicalTrials.gov as #NCT01564784.

Published
2024

2. Diagnostic utility of DNA methylation analysis in genetically unsolved pediatric epilepsies and CHD2 episignature refinement

Author

LaFlamme, Christy W., Rastin, Cassandra, Sengupta, Soham, Pennington, Helen E., Russ-Hall, Sophie J., Schneider, Amy L., Bonkowski, Emily S., Almanza Fuerte, Edith P., Allan, Talia J., Zalusky, Miranda Perez-Galey, Goffena, Joy, Gibson, Sophia B., Nyaga, Denis M., Lieffering, Nico, Hebbar, Malavika, Walker, Emily V., Darnell, Daniel, Olsen, Scott R., Kolekar, Pandurang, Djekidel, Mohamed Nadhir, Rosikiewicz, Wojciech, McConkey, Haley, Kerkhof, Jennifer, Levy, Michael A., Relator, Raissa, Lev, Dorit, Lerman-Sagie, Tally, Park, Kristen L., Alders, Marielle, Cappuccio, Gerarda, Chatron, Nicolas, Demain, Leigh, Genevieve, David, Lesca, Gaetan, Roscioli, Tony, Sanlaville, Damien, Tedder, Matthew L., Gupta, Sachin, Jones, Elizabeth A., Weisz-Hubshman, Monika, Ketkar, Shamika, Dai, Hongzheng, Worley, Kim C., Rosenfeld, Jill A., Chao, Hsiao-Tuan, Neale, Geoffrey, Carvill, Gemma L., Wang, Zhaoming, Berkovic, Samuel F., Sadleir, Lynette G., Miller, Danny E., Scheffer, Ingrid E., Sadikovic, Bekim, and Mefford, Heather C.

Published
2024
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3. Molecular classification and outcome of children with rare CNS embryonal tumors: results from St. Jude Childrens Research Hospital including the multi-center SJYC07 and SJMB03 clinical trials.

Author

Liu, Anthony, Dhanda, Sandeep, Lin, Tong, Sioson, Edgar, Vasilyeva, Aksana, Gudenas, Brian, Tatevossian, Ruth, Jia, Sujuan, Neale, Geoffrey, Bowers, Daniel, Hassall, Tim, Partap, Sonia, Crawford, John, Chintagumpala, Murali, Bouffet, Eric, McCowage, Geoff, Broniscer, Alberto, Qaddoumi, Ibrahim, Armstrong, Greg, Wright, Karen, Upadhyaya, Santhosh, Vinitsky, Anna, Tinkle, Christopher, Lucas, John, Chiang, Jason, Indelicato, Daniel, Sanders, Robert, Klimo, Paul, Boop, Frederick, Merchant, Thomas, Ellison, David, Northcott, Paul, Orr, Brent, Zhou, Xin, Onar-Thomas, Arzu, Gajjar, Amar, and Robinson, Giles

Subjects
Brain Neoplasms, Central Nervous System Neoplasms, Child, Forkhead Transcription Factors, Glioblastoma, Hospitals, Humans, Neoplasms, Germ Cell and Embryonal, Neuroectodermal Tumors, Primitive
Abstract

Methylation profiling has radically transformed our understanding of tumors previously called central nervous system primitive neuro-ectodermal tumors (CNS-PNET). While this marks a momentous step toward defining key differences, reclassification has thrown treatment into disarray. To shed light on response to therapy and guide clinical decision-making, we report outcomes and molecular features of children with CNS-PNETs from two multi-center risk-adapted studies (SJMB03 for patients ≥ 3 years; SJYC07 for patients

Published
2022

5. Distinct DNA methylation signatures associated with blood lipids as exposures or outcomes among survivors of childhood cancer: a report from the St. Jude lifetime cohort

Author

Dong, Qian, Chen, Cheng, Song, Nan, Qin, Na, Plonski, Noel-Marie, Finch, Emily R., Shelton, Kyla, Easton, John, Mulder, Heather, Plyer, Emily, Neale, Geoffrey, Walker, Emily, Li, Qian, Huang, I-Chan, Zhang, Jinghui, Wang, Hui, Hudson, Melissa M., Robison, Leslie L., Ness, Kirsten K., and Wang, Zhaoming

Published
2023
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6. Three-dimensional woven composites

Author

Dahale, Monali, primary, Archer, Edward, additional, McIlhagger, Alistair, additional, Ralph, Calvin, additional, Neale, Geoffrey, additional, and Dempsey, Cody, additional

Published
2023
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7. Contributors

Author

Akkerman, Remko, primary, Aravand, Ali, additional, Archer, Edward, additional, Barasinski, Anais, additional, Bogdanor, Michael, additional, Broughton, James, additional, Chen, Shuai, additional, Chinesta, Francisco, additional, Clifford, Mike, additional, Dahale, Monali, additional, Dempsey, Cody, additional, Dumont, Pierre, additional, Endruweit, Andreas, additional, Favaloro, Anthony, additional, Frommel, Christoph, additional, Ghnatios, Chady, additional, Goodsell, Johnathan, additional, Haanappel, Sebastiaan, additional, Haase, Tobias, additional, Hancock, Steven, additional, Harper, Lee, additional, Hubert, Pascal, additional, Hughes, David, additional, Larsen, Lars, additional, Luca, Patrick de, additional, Martoïa, Florian, additional, McIlhagger, Alistair, additional, Neale, Geoffrey, additional, Orgéas, Laurent, additional, Parsons, Andrew, additional, Pérez-Martín, Helena, additional, Pickering, Steve, additional, Potluri, Prasad, additional, Potter, Kevin, additional, Ralph, Calvin, additional, Ray, Dipa, additional, Roy, Sree Shankhachur, additional, Turner, Thomas, additional, Vistein, Michael, additional, Willmeroth, Mark, additional, and Yu, Fei, additional

Published
2023
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9. Germline Elongator mutations in Sonic Hedgehog medulloblastoma.

Author

Robinson, Giles, Gudenas, Brian, Smith, Kyle, Forget, Antoine, Kojic, Marija, Garcia-Lopez, Jesus, Hadley, Jennifer, Hamilton, Kayla, Indersie, Emilie, Buchhalter, Ivo, Kerssemakers, Jules, Jäger, Natalie, Sharma, Tanvi, Rausch, Tobias, Kool, Marcel, Sturm, Dominik, Jones, David, Vasilyeva, Aksana, Tatevossian, Ruth, Neale, Geoffrey, Lombard, Bérangère, Loew, Damarys, Nakitandwe, Joy, Rusch, Michael, Bowers, Daniel, Bendel, Anne, Partap, Sonia, Chintagumpala, Murali, Crawford, John, Gottardo, Nicholas, Smith, Amy, Dufour, Christelle, Rutkowski, Stefan, Eggen, Tone, Wesenberg, Finn, Kjaerheim, Kristina, Feychting, Maria, Lannering, Birgitta, Schüz, Joachim, Johansen, Christoffer, Andersen, Tina, Röösli, Martin, Kuehni, Claudia, Grotzer, Michael, Remke, Marc, Puget, Stéphanie, Pajtler, Kristian, Milde, Till, Witt, Olaf, Ryzhova, Marina, Korshunov, Andrey, Orr, Brent, Ellison, David, Brugieres, Laurence, Lichter, Peter, Nichols, Kim, Gajjar, Amar, Wainwright, Brandon, Ayrault, Olivier, Korbel, Jan, Northcott, Paul, Pfister, Stefan, and Waszak, Sebastian

Subjects
Cerebellar Neoplasms, Child, Female, Germ-Line Mutation, Humans, Male, Medulloblastoma, Pedigree, RNA, Transfer, Transcriptional Elongation Factors
Abstract

Cancer genomics has revealed many genes and core molecular processes that contribute to human malignancies, but the genetic and molecular bases of many rare cancers remains unclear. Genetic predisposition accounts for 5 to 10% of cancer diagnoses in children1,2, and genetic events that cooperate with known somatic driver events are poorly understood. Pathogenic germline variants in established cancer predisposition genes have been recently identified in 5% of patients with the malignant brain tumour medulloblastoma3. Here, by analysing all protein-coding genes, we identify and replicate rare germline loss-of-function variants across ELP1 in 14% of paediatric patients with the medulloblastoma subgroup Sonic Hedgehog (MBSHH). ELP1 was the most common medulloblastoma predisposition gene and increased the prevalence of genetic predisposition to 40% among paediatric patients with MBSHH. Parent-offspring and pedigree analyses identified two families with a history of paediatric medulloblastoma. ELP1-associated medulloblastomas were restricted to the molecular SHHα subtype4 and characterized by universal biallelic inactivation of ELP1 owing to somatic loss of chromosome arm 9q. Most ELP1-associated medulloblastomas also exhibited somatic alterations in PTCH1, which suggests that germline ELP1 loss-of-function variants predispose individuals to tumour development in combination with constitutive activation of SHH signalling. ELP1 is the largest subunit of the evolutionarily conserved Elongator complex, which catalyses translational elongation through tRNA modifications at the wobble (U34) position5,6. Tumours from patients with ELP1-associated MBSHH were characterized by a destabilized Elongator complex, loss of Elongator-dependent tRNA modifications, codon-dependent translational reprogramming, and induction of the unfolded protein response, consistent with loss of protein homeostasis due to Elongator deficiency in model systems7-9. Thus, genetic predisposition to proteome instability may be a determinant in the pathogenesis of paediatric brain cancers. These results support investigation of the role of protein homeostasis in other cancer types and potential for therapeutic interference.

Published
2020

13. Health-related quality of life and DNA methylation-based aging biomarkers among survivors of childhood cancer.

Author

Plonski, Noel-Marie, Pan, Yue, Chen, Cheng, Dong, Qian, Zhang, Xijun, Song, Nan, Shelton, Kyla, Easton, John, Mulder, Heather, Zhang, Jinghui, Neale, Geoffrey, Walker, Emily, Wang, Hui, Webster, Rachel, Brinkman, Tara, Krull, Kevin R, Armstrong, Gregory T, Ness, Kirsten K, Hudson, Melissa M, and Li, Qian

Subjects
QUALITY of life, CHILDHOOD cancer, CANCER survivors, BIOMARKERS, AGING
Abstract

Background Childhood cancer survivors are at high risk for morbidity and mortality and poor patient-reported outcomes, typically health-related quality of life (HRQOL). However, associations between DNA methylation–based aging biomarkers and HRQOL have not been evaluated. Methods DNA methylation was generated with Infinium EPIC BeadChip on blood-derived DNA (median for age at blood draw = 34.5 years, range = 18.5-66.6 years), and HRQOL was assessed with age at survey (mean = 32.3 years, range = 18.4-64.5 years) from 2206 survivors in the St Jude Lifetime Cohort. DNA methylation–based aging biomarkers, including epigenetic age using multiple clocks (eg, GrimAge) and others (eg, DNAmB2M: beta-2-microglobulin; DNAmADM: adrenomedullin), were derived from the DNAm Age Calculator (https://dnamage.genetics.ucla.edu). HRQOL was assessed using the Medical Outcomes Study 36-Item Short-Form Health Survey to capture 8 domains and physical and mental component summaries. General linear models evaluated associations between HRQOL and epigenetic age acceleration (EAA; eg, EAA_GrimAge) or other age-adjusted DNA methylation–based biomarkers (eg, ageadj_DNAmB2M) after adjusting for age at blood draw, sex, cancer treatments, and DNA methylation–based surrogate for smoking pack-years. All P values were 2-sided. Results Worse HRQOL was associated with greater EAA_GrimAge (physical component summaries: β = -0.18 years, 95% confidence interval [CI] = -0.251 to -0.11 years; P  = 1.85 × 10−5; and 4 individual HRQOL domains), followed by ageadj_DNAmB2M (physical component summaries: β = -0.08 years, 95% CI = -0.124 to -0.037 years; P  = .003; and 3 individual HRQOL domains) and ageadj_DNAmADM (physical component summaries: β = -0.082 years, 95% CI = -0.125 to -0.039 years; P  = .002; and 2 HRQOL domains). EAA_Hannum (Hannum clock) was not associated with any HRQOL. Conclusions Overall and domain-specific measures of HRQOL are associated with DNA methylation measures of biological aging. Future longitudinal studies should test biological aging as a potential mechanism underlying the association between poor HRQOL and increased risk of clinically assessed adverse health outcomes. [ABSTRACT FROM AUTHOR]

Published
2024
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15. Energy absorption mechanisms in layer-to-layer 3D woven composites

Author

International Conference on Composite Materials (22nd : 2019 : Melboune, VIC.), Neale, Geoffrey, Dahale, Monali, Yoo, Sanghyun, Toso, Nathalie, Kelly, John, McGarrigle, Cormac, Archer, Edward, McIlhagger, Alistair, and Harkin-Jones, Eileen

Published
2019

17. Persistent variations of blood DNA methylation associated with treatment exposures and risk for cardiometabolic outcomes in long-term survivors of childhood cancer in the St. Jude Lifetime Cohort

Author

Song, Nan, Hsu, Chia-Wei, Pan, Haitao, Zheng, Yinan, Hou, Lifang, Sim, Jin-ah, Li, Zhenghong, Mulder, Heather, Easton, John, Walker, Emily, Neale, Geoffrey, Wilson, Carmen L., Ness, Kirsten K., Krull, Kevin R., Srivastava, Deo Kumar, Yasui, Yutaka, Zhang, Jinghui, Hudson, Melissa M., Robison, Leslie L., Huang, I-Chan, and Wang, Zhaoming

Published
2021
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18. Germline Elongator mutations in Sonic Hedgehog medulloblastoma

Author

Waszak, Sebastian M., Robinson, Giles W,, Gudenas, Brian L., Smith, Kyle S., Forget, Antoine, Kojic, Marija, Garcia-Lopez, Jesus, Hadley, Jennifer, Hamilton, Kayla V., Indersie, Emilie, Buchhalter, Ivo, Kerssemakers, Jules, Jäger, Natalie, Sharma, Tanvi, Rausch, Tobias, Kool, Marcel, Sturm, Dominik, Jones, David T. W., Vasilyeva, Aksana, Tatevossian, Ruth G., Neale, Geoffrey, Lombard, Bérangère, Loew, Damarys, Nakitandwe, Joy, Rusch, Michael, Bowers, Daniel C., Bendel, Anne, Partap, Sonia, Chintagumpala, Murali, Crawford, John, Gottardo, Nicholas G., Smith, Amy, Dufour, Christelle, Rutkowski, Stefan, Eggen, Tone, Wesenberg, Finn, Kjaerheim, Kristina, Feychting, Maria, Lannering, Birgitta, Schüz, Joachim, Johansen, Christoffer, Andersen, Tina V., Röösli, Martin, Kuehni, Claudia E., Grotzer, Michael, Remke, Marc, Puget, Stéphanie, Pajtler, Kristian W., Milde, Till, Witt, Olaf, Ryzhova, Marina, Korshunov, Andrey, Orr, Brent A., Ellison, David W., Brugieres, Laurence, Lichter, Peter, Nichols, Kim E., Gajjar, Amar, Wainwright, Brandon J., Ayrault, Olivier, Korbel, Jan O., Northcott, Paul A., and Pfister, Stefan M.

Published
2020
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22. Inherited GATA3 variants are associated with Ph-like childhood acute lymphoblastic leukemia and risk of relapse.

Author

Perez-Andreu, Virginia, Roberts, Kathryn G, Harvey, Richard C, Yang, Wenjian, Cheng, Cheng, Pei, Deqing, Xu, Heng, Gastier-Foster, Julie, E, Shuyu, Lim, Joshua Yew-Suang, Chen, I-Ming, Fan, Yiping, Devidas, Meenakshi, Borowitz, Michael J, Smith, Colton, Neale, Geoffrey, Burchard, Esteban G, Torgerson, Dara G, Klussmann, Federico Antillon, Villagran, Cesar Rolando Najera, Winick, Naomi J, Camitta, Bruce M, Raetz, Elizabeth, Wood, Brent, Yue, Feng, Carroll, William L, Larsen, Eric, Bowman, W Paul, Loh, Mignon L, Dean, Michael, Bhojwani, Deepa, Pui, Ching-Hon, Evans, William E, Relling, Mary V, Hunger, Stephen P, Willman, Cheryl L, Mullighan, Charles G, and Yang, Jun J

Subjects
Humans, Genetic Predisposition to Disease, Recurrence, Risk, Case-Control Studies, Gene Frequency, Genotype, Inheritance Patterns, Polymorphism, Single Nucleotide, Child, GATA3 Transcription Factor, Precursor Cell Lymphoblastic Leukemia-Lymphoma, Genome-Wide Association Study, Cancer, Childhood Leukemia, Rare Diseases, Pediatric, Hematology, Orphan Drug, Pediatric Research Initiative, Pediatric Cancer, Genetics, Aetiology, 2.1 Biological and endogenous factors, Biological Sciences, Medical and Health Sciences, Developmental Biology
Abstract

Recent genomic profiling of childhood acute lymphoblastic leukemia (ALL) identified a high-risk subtype with an expression signature resembling that of Philadelphia chromosome-positive ALL and poor prognosis (Ph-like ALL). However, the role of inherited genetic variation in Ph-like ALL pathogenesis remains unknown. In a genome-wide association study (GWAS) of 511 ALL cases and 6,661 non-ALL controls, we identified a susceptibility locus for Ph-like ALL (GATA3, rs3824662; P = 2.17 × 10(-14), odds ratio (OR) = 3.85 for Ph-like ALL versus non-ALL; P = 1.05 × 10(-8), OR = 3.25 for Ph-like ALL versus non-Ph-like ALL), with independent validation. The rs3824662 risk allele was associated with somatic lesions underlying Ph-like ALL (CRLF2 rearrangement, JAK gene mutation and IKZF1 deletion) and with variation in GATA3 expression. Finally, genotype at the GATA3 SNP was also associated with early treatment response and risk of ALL relapse. Our results provide insights into interactions between inherited and somatic variants and their role in ALL pathogenesis and prognosis.

Published
2013

23. Cross-species genomic and epigenomic landscape of retinoblastoma

Author

Benavente, Claudia A, McEvoy, Justina D, Finkelstein, David, Wei, Lei, Kang, Guolian, Wang, Yong-Dong, Neale, Geoffrey, Ragsdale, Susan, Valentine, Virginia, Bahrami, Armita, Temirov, Jamshid, Pounds, Stanley, Zhang, Jinghui, and Dyer, Michael A

Subjects
Rare Diseases, Genetics, Cancer, Pediatric, Pediatric Research Initiative, Human Genome, Eye Disease and Disorders of Vision, Pediatric Cancer, Aetiology, 2.1 Biological and endogenous factors, Animals, Disease Models, Animal, Epigenomics, Gene Expression Regulation, Neoplastic, Genetic Engineering, Genomics, Humans, Mice, Mice, Knockout, Retinoblastoma, Retinoblastoma Protein, Species Specificity, retinoblastoma, RB1, epigenetics, Oncology and Carcinogenesis
Abstract

Genetically engineered mouse models (GEMMs) of human cancer are important for advancing our understanding of tumor initiation and progression as well as for testing novel therapeutics. Retinoblastoma is a childhood cancer of the developing retina that initiates with biallelic inactivation of the RB1 gene. GEMMs faithfully recapitulate the histopathology, molecular, cellular, morphometric, neuroanatomical and neurochemical features of human retinoblastoma. In this study, we analyzed the genomic and epigenomic landscape of murine retinoblastoma and compared them to human retinoblastomas to gain insight into shared mechanisms of tumor progression across species. Similar to human retinoblastoma, mouse tumors have low rates of single nucleotide variations. However, mouse retinoblastomas have higher rates of aneuploidy and regional and focal copy number changes that vary depending on the genetic lesions that initiate tumorigenesis in the developing murine retina. Furthermore, the epigenetic landscape in mouse retinoblastoma was significantly different from human tumors and some pathways that are candidates for molecular targeted therapy for human retinoblastoma such as SYK or MCL1 are not deregulated in GEMMs. Taken together, these data suggest there are important differences between mouse and human retinoblastomas with respect to the mechanism of tumor progression and those differences can have significant implications for translational research to test the efficacy of novel therapies for this devastating childhood cancer.

Published
2013

27. Epigenetic Age in Peripheral Blood Among Children, Adolescent, and Adult Survivors of Childhood Cancer

Author

Plonski, Noel-Marie, primary, Chen, Cheng, additional, Dong, Qian, additional, Qin, Na, additional, Song, Nan, additional, Parikh, Hemang M., additional, Shelton, Kyla, additional, Finch, Emily R., additional, Easton, John, additional, Mulder, Heather, additional, Zhang, Jinghui, additional, Neale, Geoffrey, additional, Walker, Emily, additional, Wang, Hui, additional, Krull, Kevin, additional, Ness, Kirsten K., additional, Hudson, Melissa M., additional, Robison, Leslie L., additional, Li, Qian, additional, Williams, AnnaLynn, additional, and Wang, Zhaoming, additional

Published
2023
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28. Abstract 4363: Monocyte-specific epigenetic age acceleration and cardiomyopathy risk among survivors of childhood cancer

Author

Chen, Cheng, primary, Dong, Qian, additional, Na, Qin, additional, Song, Nan, additional, Easton, John, additional, Mulder, Heather L., additional, Walker, Emily, additional, Neale, Geoffrey, additional, Finch, Emily R., additional, Li, Qian, additional, Yasui, Yutaka, additional, Mulrooney, Daniel A., additional, Hudson, Melissa M., additional, Ness, Kirsten K., additional, Zhang, Jinghui, additional, Chen, Xiang, additional, Wang, Hui, additional, Robison, Leslie L., additional, and Wang, Zhaoming, additional

Published
2023
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29. Abstract 4514: Variations of blood DNA methylation associated with cancer treatment exposures among childhood cancer survivors of African ancestry

Author

Dong, Qian, primary, Das, Sarmistha, additional, Chen, Cheng, additional, Easton, John, additional, Mulder, Heather L., additional, Walker, Emily, additional, Neale, Geoffrey, additional, Srivastava, Deo Kumar, additional, Huang, I-Chan, additional, Zhang, Jinghui, additional, Hudson, Melissa M., additional, Robison, Leslie L., additional, Ness, Kirsten K., additional, Song, Nan, additional, and Wang, Zhaoming, additional

Published
2023
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30. Abstract 3503: Racial disparity and roles of social determinants of health in epigenetic age acceleration among survivors of childhood cancer

Author

Plonski, Noel-Marie, primary, Chen, Cheng, additional, Dong, Qian, additional, Qin, Na, additional, Song, Nan, additional, Easton, John, additional, Mulder, Heather, additional, Walker, Emily, additional, Neale, Geoffrey, additional, Zhang, Jinghui, additional, Krull, Kevin, additional, Ness, Kirsten K., additional, Hudson, Melissa M., additional, Robison, Leslie L., additional, Huang, I-Chan, additional, and Wang, Zhaoming, additional

Published
2023
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31. Supplementary Table S6 from Relapse-Fated Latent Diagnosis Subclones in Acute B Lineage Leukemia Are Drug Tolerant and Possess Distinct Metabolic Programs

Author

Dobson, Stephanie M., primary, García-Prat, Laura, primary, Vanner, Robert J., primary, Wintersinger, Jeffrey, primary, Waanders, Esmé, primary, Gu, Zhaohui, primary, McLeod, Jessica, primary, Gan, Olga I., primary, Grandal, Ildiko, primary, Payne-Turner, Debbie, primary, Edmonson, Michael N., primary, Ma, Xiaotu, primary, Fan, Yiping, primary, Voisin, Veronique, primary, Chan-Seng-Yue, Michelle, primary, Xie, Stephanie Z., primary, Hosseini, Mohsen, primary, Abelson, Sagi, primary, Gupta, Pankaj, primary, Rusch, Michael, primary, Shao, Ying, primary, Olsen, Scott R., primary, Neale, Geoffrey, primary, Chan, Steven M., primary, Bader, Gary, primary, Easton, John, primary, Guidos, Cynthia J., primary, Danska, Jayne S., primary, Zhang, Jinghui, primary, Minden, Mark D., primary, Morris, Quaid, primary, Mullighan, Charles G., primary, and Dick, John E., primary

Published
2023
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32. Data from Relapse-Fated Latent Diagnosis Subclones in Acute B Lineage Leukemia Are Drug Tolerant and Possess Distinct Metabolic Programs

Author

Dobson, Stephanie M., primary, García-Prat, Laura, primary, Vanner, Robert J., primary, Wintersinger, Jeffrey, primary, Waanders, Esmé, primary, Gu, Zhaohui, primary, McLeod, Jessica, primary, Gan, Olga I., primary, Grandal, Ildiko, primary, Payne-Turner, Debbie, primary, Edmonson, Michael N., primary, Ma, Xiaotu, primary, Fan, Yiping, primary, Voisin, Veronique, primary, Chan-Seng-Yue, Michelle, primary, Xie, Stephanie Z., primary, Hosseini, Mohsen, primary, Abelson, Sagi, primary, Gupta, Pankaj, primary, Rusch, Michael, primary, Shao, Ying, primary, Olsen, Scott R., primary, Neale, Geoffrey, primary, Chan, Steven M., primary, Bader, Gary, primary, Easton, John, primary, Guidos, Cynthia J., primary, Danska, Jayne S., primary, Zhang, Jinghui, primary, Minden, Mark D., primary, Morris, Quaid, primary, Mullighan, Charles G., primary, and Dick, John E., primary

Published
2023
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33. Supplementary Table S4 from SLFN11 is Widely Expressed in Pediatric Sarcoma and Induces Variable Sensitization to Replicative Stress Caused By DNA-Damaging Agents

Author

Gartrell, Jessica, primary, Mellado-Largarde, Marcia, primary, Clay, Michael R., primary, Bahrami, Armita, primary, Sahr, Natasha A., primary, Sykes, April, primary, Blankenship, Kaley, primary, Hoffmann, Lauren, primary, Xie, Jia, primary, Cho, Hyekyung P., primary, Twarog, Nathaniel, primary, Connelly, Michele, primary, Yan, Koon-Kiu, primary, Yu, Jiyang, primary, Porter, Shaina N., primary, Pruett-Miller, Shondra M., primary, Neale, Geoffrey, primary, Tinkle, Christopher L., primary, Federico, Sara M., primary, Stewart, Elizabeth A., primary, and Shelat, Anang A., primary

Published
2023
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34. Supplementary Data from SLFN11 is Widely Expressed in Pediatric Sarcoma and Induces Variable Sensitization to Replicative Stress Caused By DNA-Damaging Agents

Author

Gartrell, Jessica, primary, Mellado-Largarde, Marcia, primary, Clay, Michael R., primary, Bahrami, Armita, primary, Sahr, Natasha A., primary, Sykes, April, primary, Blankenship, Kaley, primary, Hoffmann, Lauren, primary, Xie, Jia, primary, Cho, Hyekyung P., primary, Twarog, Nathaniel, primary, Connelly, Michele, primary, Yan, Koon-Kiu, primary, Yu, Jiyang, primary, Porter, Shaina N., primary, Pruett-Miller, Shondra M., primary, Neale, Geoffrey, primary, Tinkle, Christopher L., primary, Federico, Sara M., primary, Stewart, Elizabeth A., primary, and Shelat, Anang A., primary

Published
2023
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35. Supplementary Figures S1-S11 from Relapse-Fated Latent Diagnosis Subclones in Acute B Lineage Leukemia Are Drug Tolerant and Possess Distinct Metabolic Programs

Author

Dobson, Stephanie M., primary, García-Prat, Laura, primary, Vanner, Robert J., primary, Wintersinger, Jeffrey, primary, Waanders, Esmé, primary, Gu, Zhaohui, primary, McLeod, Jessica, primary, Gan, Olga I., primary, Grandal, Ildiko, primary, Payne-Turner, Debbie, primary, Edmonson, Michael N., primary, Ma, Xiaotu, primary, Fan, Yiping, primary, Voisin, Veronique, primary, Chan-Seng-Yue, Michelle, primary, Xie, Stephanie Z., primary, Hosseini, Mohsen, primary, Abelson, Sagi, primary, Gupta, Pankaj, primary, Rusch, Michael, primary, Shao, Ying, primary, Olsen, Scott R., primary, Neale, Geoffrey, primary, Chan, Steven M., primary, Bader, Gary, primary, Easton, John, primary, Guidos, Cynthia J., primary, Danska, Jayne S., primary, Zhang, Jinghui, primary, Minden, Mark D., primary, Morris, Quaid, primary, Mullighan, Charles G., primary, and Dick, John E., primary

Published
2023
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37. Forty-five patient-derived xenografts capture the clinical and biological heterogeneity of Wilms tumor

Author

Murphy, Andrew J., Chen, Xiang, Pinto, Emilia M., Williams, Justin S., Clay, Michael R., Pounds, Stanley B., Cao, Xueyuan, Shi, Lei, Lin, Tong, Neale, Geoffrey, Morton, Christopher L., Woolard, Mary A., Mulder, Heather L., Gil, Hyea Jin, Rehg, Jerold E., Billups, Catherine A., Harlow, Matthew L., Dome, Jeffrey S., Houghton, Peter J., Easton, John, Zhang, Jinghui, George, Rani E., Zambetti, Gerard P., and Davidoff, Andrew M.

Published
2019
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39. Supplementary Table S2 from The Common Germline TP53-R337H Mutation Is Hypomorphic and Confers Incomplete Penetrance and Late Tumor Onset in a Mouse Model

Author

Jeffers, John R., primary, Pinto, Emilia M., primary, Rehg, Jerold E., primary, Clay, Michael R., primary, Wang, Jinling, primary, Neale, Geoffrey, primary, Heath, Richard J., primary, Lozano, Guillermina, primary, Lalli, Enzo, primary, Figueiredo, Bonald C., primary, Pappo, Alberto S., primary, Rodriguez-Galindo, Carlos, primary, Chen, Wenan, primary, Pounds, Stanley, primary, Ribeiro, Raul C., primary, and Zambetti, Gerard P., primary

Published
2023
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40. Supplementary Figure S1 from The Common Germline TP53-R337H Mutation Is Hypomorphic and Confers Incomplete Penetrance and Late Tumor Onset in a Mouse Model

Author

Jeffers, John R., primary, Pinto, Emilia M., primary, Rehg, Jerold E., primary, Clay, Michael R., primary, Wang, Jinling, primary, Neale, Geoffrey, primary, Heath, Richard J., primary, Lozano, Guillermina, primary, Lalli, Enzo, primary, Figueiredo, Bonald C., primary, Pappo, Alberto S., primary, Rodriguez-Galindo, Carlos, primary, Chen, Wenan, primary, Pounds, Stanley, primary, Ribeiro, Raul C., primary, and Zambetti, Gerard P., primary

Published
2023
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41. Supplementary Table 6 from Prognostic Significance of Major Histocompatibility Complex Class II Expression in Pediatric Adrenocortical Tumors: A St. Jude and Children's Oncology Group Study

Author

Pinto, Emilia Modolo, primary, Rodriguez-Galindo, Carlos, primary, Choi, John Kim, primary, Pounds, Stanley, primary, Liu, Zhifa, primary, Neale, Geoffrey, primary, Finkelstein, David, primary, Hicks, John M., primary, Pappo, Alberto S., primary, Figueiredo, Bonald C., primary, Ribeiro, Raul C., primary, and Zambetti, Gerard P., primary

Published
2023
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42. Data from Bromodomain-Selective BET Inhibitors Are Potent Antitumor Agents against MYC-Driven Pediatric Cancer

Author

Slavish, P. Jake, primary, Chi, Liying, primary, Yun, Mi-Kyung, primary, Tsurkan, Lyudmila, primary, Martinez, Nancy E., primary, Jonchere, Barbara, primary, Chai, Sergio C., primary, Connelly, Michele, primary, Waddell, M. Brett, primary, Das, Sourav, primary, Neale, Geoffrey, primary, Li, Zhenmei, primary, Shadrick, William R., primary, Olsen, Rachelle R., primary, Freeman, Kevin W., primary, Low, Jonathan A., primary, Price, Jeanine E., primary, Young, Brandon M., primary, Bharatham, Nagakumar, primary, Boyd, Vincent A., primary, Yang, Jun, primary, Lee, Richard E., primary, Morfouace, Marie, primary, Roussel, Martine F., primary, Chen, Taosheng, primary, Savic, Daniel, primary, Guy, R. Kiplin, primary, White, Stephen W., primary, Shelat, Anang A., primary, and Potter, Philip M., primary

Published
2023
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43. Supplementary Data from Bromodomain-Selective BET Inhibitors Are Potent Antitumor Agents against MYC-Driven Pediatric Cancer

Author

Slavish, P. Jake, primary, Chi, Liying, primary, Yun, Mi-Kyung, primary, Tsurkan, Lyudmila, primary, Martinez, Nancy E., primary, Jonchere, Barbara, primary, Chai, Sergio C., primary, Connelly, Michele, primary, Waddell, M. Brett, primary, Das, Sourav, primary, Neale, Geoffrey, primary, Li, Zhenmei, primary, Shadrick, William R., primary, Olsen, Rachelle R., primary, Freeman, Kevin W., primary, Low, Jonathan A., primary, Price, Jeanine E., primary, Young, Brandon M., primary, Bharatham, Nagakumar, primary, Boyd, Vincent A., primary, Yang, Jun, primary, Lee, Richard E., primary, Morfouace, Marie, primary, Roussel, Martine F., primary, Chen, Taosheng, primary, Savic, Daniel, primary, Guy, R. Kiplin, primary, White, Stephen W., primary, Shelat, Anang A., primary, and Potter, Philip M., primary

Published
2023
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44. Supplementary Data from The Common Germline TP53-R337H Mutation Is Hypomorphic and Confers Incomplete Penetrance and Late Tumor Onset in a Mouse Model

Author

Jeffers, John R., primary, Pinto, Emilia M., primary, Rehg, Jerold E., primary, Clay, Michael R., primary, Wang, Jinling, primary, Neale, Geoffrey, primary, Heath, Richard J., primary, Lozano, Guillermina, primary, Lalli, Enzo, primary, Figueiredo, Bonald C., primary, Pappo, Alberto S., primary, Rodriguez-Galindo, Carlos, primary, Chen, Wenan, primary, Pounds, Stanley, primary, Ribeiro, Raul C., primary, and Zambetti, Gerard P., primary

Published
2023
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45. Supplementary Figure 2 from Emergence of Polyclonal FLT3 Tyrosine Kinase Domain Mutations during Sequential Therapy with Sorafenib and Sunitinib in FLT3-ITD–Positive Acute Myeloid Leukemia

Author

Baker, Sharyn D., primary, Zimmerman, Eric I., primary, Wang, Yong-Dong, primary, Orwick, Shelley, primary, Zatechka, Douglas S., primary, Buaboonnam, Jassada, primary, Neale, Geoffrey A., primary, Olsen, Scott R., primary, Enemark, Eric J., primary, Shurtleff, Sheila, primary, Rubnitz, Jeffrey E., primary, Mullighan, Charles G., primary, and Inaba, Hiroto, primary

Published
2023
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46. Supplementary Table 4 from Molecular Characterization of the Pediatric Preclinical Testing Panel

Author

Neale, Geoffrey, primary, Su, Xiaoping, primary, Morton, Christopher L., primary, Phelps, Doris, primary, Gorlick, Richard, primary, Lock, Richard B., primary, Reynolds, C. Patrick, primary, Maris, John M., primary, Friedman, Henry S., primary, Dome, Jeffrey, primary, Khoury, Joseph, primary, Triche, Timothy J., primary, Seeger, Robert C., primary, Gilbertson, Richard, primary, Khan, Javed, primary, Smith, Malcolm A., primary, and Houghton, Peter J., primary

Published
2023
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47. Data from The Common Germline TP53-R337H Mutation Is Hypomorphic and Confers Incomplete Penetrance and Late Tumor Onset in a Mouse Model

Author

Jeffers, John R., primary, Pinto, Emilia M., primary, Rehg, Jerold E., primary, Clay, Michael R., primary, Wang, Jinling, primary, Neale, Geoffrey, primary, Heath, Richard J., primary, Lozano, Guillermina, primary, Lalli, Enzo, primary, Figueiredo, Bonald C., primary, Pappo, Alberto S., primary, Rodriguez-Galindo, Carlos, primary, Chen, Wenan, primary, Pounds, Stanley, primary, Ribeiro, Raul C., primary, and Zambetti, Gerard P., primary

Published
2023
Full Text
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49. Supplementary Table 6 from Molecular Characterization of the Pediatric Preclinical Testing Panel

Author

Neale, Geoffrey, primary, Su, Xiaoping, primary, Morton, Christopher L., primary, Phelps, Doris, primary, Gorlick, Richard, primary, Lock, Richard B., primary, Reynolds, C. Patrick, primary, Maris, John M., primary, Friedman, Henry S., primary, Dome, Jeffrey, primary, Khoury, Joseph, primary, Triche, Timothy J., primary, Seeger, Robert C., primary, Gilbertson, Richard, primary, Khan, Javed, primary, Smith, Malcolm A., primary, and Houghton, Peter J., primary

Published
2023
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50. Supplementary Table 3 from Emergence of Polyclonal FLT3 Tyrosine Kinase Domain Mutations during Sequential Therapy with Sorafenib and Sunitinib in FLT3-ITD–Positive Acute Myeloid Leukemia

Author

Baker, Sharyn D., primary, Zimmerman, Eric I., primary, Wang, Yong-Dong, primary, Orwick, Shelley, primary, Zatechka, Douglas S., primary, Buaboonnam, Jassada, primary, Neale, Geoffrey A., primary, Olsen, Scott R., primary, Enemark, Eric J., primary, Shurtleff, Sheila, primary, Rubnitz, Jeffrey E., primary, Mullighan, Charles G., primary, and Inaba, Hiroto, primary

Published
2023
Full Text
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