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1,704 results on '"Relling, Mary V."'

210. Genetic polymorphisms in the carbonyl reductase 3 gene CBR3 and the NAD(P)H: quinone oxidoreductase 1 gene NQO1 in patients who dveloped anthracycline-related congestive heart failure after childhood cancer

Author

Blanco, Javier G., Leisenring, Wendy M., Gonzalez-Covarrubias, Vanessa M., Kawashima, Toana I., Davies, Stella M., Relling, Mary V., Robison, Leslie L., Sklar, Charles A., Stovall, Marilyn, and Bhatia, Smita

Subjects
Cancer in children -- Patient outcomes, Genetic polymorphisms -- Research, Anthracyclines -- Complications and side effects, Congestive heart failure -- Risk factors, Congestive heart failure -- Genetic aspects, Oxidoreductases -- Research, Health
Published
2008

211. Conventional compared with individualized chemotherapy for childhood acute lymphoblastic leukemia

Author

Evans, William E., Relling, Mary V., Rodman, John H., Crom, William R., Boyett, James M., and Pui, Ching-Hon

Subjects
Lymphoblastic leukemia in children, Chemotherapy -- Dosage and administration, Drug metabolism -- Health aspects
Abstract

Tailoring chemotherapy to a child's metabolic rate may improve prognosis in children with certain types of acute lymphoblastic leukemia. Children metabolize drugs differently and those who metabolize drugs quickly may not benefit as well from chemotherapy. Researchers randomly assigned 182 children with acute lymphoblastic leukemia to receive chemotherapy based on their body surface area or on their metabolic rate. Tailoring the drug dosage to the metabolic rate improved prognosis, but only in children with leukemia of the B cell line.

Published
1998

212. Serum ALT elevations in survivors of childhood cancer. A report from the St. Jude Lifetime Cohort Study

Author

Green, Daniel M., Wang, Mingjuan, Krasin, Matthew J., Srivastava, DeoKumar, Relling, Mary V., Howell, Carrie R., Ness, Kirsten K., Kaste, Sue C., Greene, William, Jay, Dennis W., Fernandez-Pineda, Israel, Pui, Ching-Hon, Jeha, Sima, Bishop, Michael W., Furman, Wayne L., Robison, Leslie L., and Hudson, Melissa M.

Subjects
Adult, Male, Adolescent, Infant, Alanine Transaminase, Middle Aged, Risk Assessment, Article, Cohort Studies, Young Adult, Cancer Survivors, Child, Preschool, Prevalence, Humans, Female, Child
Abstract

The purpose of this study was to define the prevalence of and risk factors for elevated serum alanine aminotransferase (ALT) level among adult childhood cancer survivors (CCS). The study cohort comprised 2,751 CCS from the St. Jude Lifetime Cohort Study (10 years postdiagnosis, age ≥18 years). Serum ALT level was graded using the Common Terminology Criteria for Adverse Events v. 4.03. Modified Poisson regression models were used to estimate relative risks and 95% confidence intervals for the association between demographic and clinical factors and grades 1-4 ALT on the selected models. A total of 1,339 (48.7%) CCS were female; 2,271 (82.6%) were non-Hispanic white. Median age at evaluation was 31.4 years (interquartile range [IQR] = 25.8-37.8); median elapsed time from diagnosis to evaluation was 23.2 years (IQR = 17.6-29.7). A total of 1,137 (41.3%) CSS had ALTupper limit of normal (Common Terminology Criteria for Adverse Events v. 4.03 grade 1-1,058 (38.5%); grade 2-56 (2.0%); grade 3-23 (0.8%); grade 4-none). Multivariable models demonstrated non-Hispanic white race/ethnicity, age at evaluation in years, being overweight or obese, presence of the metabolic syndrome, current treatment with atorvastatin or rosuvastatin or simvastatin, hepatitis C virus infection, prior treatment with busulfan or thioguanine, history of hepatic surgery, and the percentage of liver treated with ≥10 Gray, ≥15 Gray, or ≥20 Gray were associated with elevated ALT. Conclusion: Grade 3 or 4 hepatic injury is infrequent in CCS. Mild hepatic injury in this group may be amenable to lifestyle modifications.

Published
2018

213. Pharmacogenomics: Challenges and Opportunities

Author

Roden, Dan M., Altman, Russ B., Benowitz, Neal L., Flockhart, David A., Giacomini, Kathleen M., Johnson, Julie A., Krauss, Ronald M., McLeod, Howard L., Ratain, Mark J., Relling, Mary V., Ring, Huijun Z., Shuldiner, Alan R., Weinshilboum, Richard M., and Weiss, Scott T.

Published
2006

215. Human granulocyte colony-stimulating factor after induction chemotherapy in children with acute lymphoblastic leukemia

Author

Pui, Ching-Hon, Boyett, James M., Hughes, Walter T., Rivera, Gaston K., Hancock, Michael L., Sandlund, John T., Synold, Timothy, Relling, Mary V., Ribeiro, Raul C., Crist, William M., and Evans, William E.

Subjects
Granulocyte colony-stimulating factor -- Evaluation, Neutropenia -- Drug therapy, Chemotherapy -- Adverse and side effects
Abstract

Granulocyte colony-stimulating factor (G-CSF) may reduce the incidence of infection in children with neutropenia but it appears to have few other benefits. Neutropenia is a drop in white blood cells called neutrophils often caused by chemotherapy. Researchers gave daily injections of G-CSF or placebo to 148 children with chemotherapy-induced neutropenia. Children receiving G-CSF had a lower rate of infections, but G-CSF did not reduce hospitalization rates, prolong survival or reduce medical care costs.

Published
1997

217. Improved outcome for children with acute lymphoblastic leukemia: results of Total Therapy Study XIIIB at St Jude Children's Research Hospital

Author

Pui, Ching-Hon, Sandlund, John T., Pei, Deqing, Campana, Dario, Rivera, Gaston K., Ribeiro, Raul C., Rubnitz, Jeffrey E., Razzouk, Bassem I., Howard, Scott C., Hudson, Melissa M., Cheng, Cheng, Kun, Larry E., Raimondi, Susana C., Behm, Frederick G., Downing, James R., Relling, Mary V., and Evans, William E.

Published
2004
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223. Clinical Pharmacogenetics Implementation Consortium Guideline for Thiopurine Dosing Based on TPMT and NUDT15 Genotypes:2018 Update

Author

Relling, Mary V., Schwab, Matthias, Whirl-Carrillo, Michelle, Suarez-Kurtz, Guilherme, Pui, Ching Hon, Stein, Charles M., Moyer, Ann M., Evans, William E., Klein, Teri E., Antillon-Klussmann, Federico Guillermo, Caudle, Kelly E., Kato, Motohiro, Yeoh, Allen E.J., Schmiegelow, Kjeld, Yang, Jun J., Relling, Mary V., Schwab, Matthias, Whirl-Carrillo, Michelle, Suarez-Kurtz, Guilherme, Pui, Ching Hon, Stein, Charles M., Moyer, Ann M., Evans, William E., Klein, Teri E., Antillon-Klussmann, Federico Guillermo, Caudle, Kelly E., Kato, Motohiro, Yeoh, Allen E.J., Schmiegelow, Kjeld, and Yang, Jun J.

Abstract

Thiopurine methyltransferase (TPMT) activity exhibits a monogenic codominant inheritance and catabolizes thiopurines. TPMT variant alleles are associated with low enzyme activity and pronounced pharmacologic effects of thiopurines. Loss-of-function alleles in the NUDT15 gene are common in Asians and Hispanics and reduce the degradation of active thiopurine nucleotide metabolites, also predisposing to myelosuppression. We provide recommendations for adjusting starting doses of azathioprine, mercaptopurine, and thioguanine based on TPMT and NUDT15 genotypes (updates on www.cpicpgx.org).

Published
2019

230. Incorporating G6PDgenotyping to identify patients with G6PD deficiency

Author

Morris, Sarah A., Crews, Kristine R., Hayden, Randall T., Takemoto, Clifford M., Yang, Wenjian, Baker, Donald K., Broeckel, Ulrich, Relling, Mary V., and Haidar, Cyrine E.

Abstract

Supplemental Digital Content is available in the text.Glucose-6-phosphate-dehydrogenase (G6PD) deficiency is a common X-linked enzyme disorder associated with hemolytic anemia after exposure to fava beans or certain medications. Activity testing is the gold standard for detecting G6PD deficiency; however, this test is affected by various hematologic parameters. Clinical G6PDgenotyping is now included in pharmacogenetic arrays and clinical sequencing efforts and may be reconciled with activity results. Patients (n= 1391) enrolled on an institutional pharmacogenetic testing protocol underwent clinical G6PDgenotyping for 164 G6PDvariants. An algorithm accounting for known interferences with the activity assay is proposed. We developed clinical decision support alerts to inform prescribers when high-risk medications were prescribed, warning of gene–drug interactions and recommending therapy alteration. Of 1391 patients with genotype results, 1334 (95.9%) patients were predicted to have normal G6PD activity, 30 (2.1%) were predicted to have variable G6PD activity and 27 (2%) were predicted to have deficient G6PD activity. Of the 417 patients with a normal genotype and an activity result, 415 (99.5%) had a concordant normal G6PD phenotype. Of the 21 patients with a deficient genotype and an activity result, 18 (85.7%) had a concordant deficient activity result. Genotyping reassigned phenotype in five patients with discordant genotype and activity results: three switched from normal to deficient, and two switched from deficient to normal. G6PD activity and genotyping are two independent testing methods that can be used in conjunction to assign a more informed G6PD phenotype than either method alone.

Published
2022
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231. Preponderance of Thiopurine S-Methyltransferase Deficiency and Heterozygosity Among Patients Intolerant to Mercaptopurine or Azathioprine

Author

Evans, William E., Hon, Yuen Yi, Bomgaars, Lisa, Coutre, Steve, Holdsworth, Mark, Janco, Robert, Kalwinsky, David, Keller, Frank, Khatib, Ziad, Margolin, Judy, Murray, Jeffrey, Quinn, John, Ravindranath, Y., Ritchey, Kim, Roberts, William, Rogers, Zora R., Schiff, Deborah, Steuber, Charles, Tucci, Fabio, Kornegay, Nancy, Krynetski, Eugene Y., and Relling, Mary V.

Published
2001

239. Genome-Wide Association Study of Susceptibility Loci for TCF3-PBX1 Acute Lymphoblastic Leukemia in Children.

Author

Lee, Shawn H. R, Qian, Maoxiang, Yang, Wentao, Diedrich, Jonathan D, Raetz, Elizabeth, Yang, Wenjian, Dong, Qian, Devidas, Meenakshi, Pei, Deqing, Yeoh, Allen, Cheng, Cheng, Pui, Ching-Hon, Evans, William E, Mullighan, Charles G, Hunger, Stephen P, Savic, Daniel, Relling, Mary V, Loh, Mignon L, Yang, Jun J, and Lee, Shawn H R

Subjects
GENOME-wide association studies, LYMPHOBLASTIC leukemia, ACUTE leukemia, CHILDHOOD cancer, CELL fusion, SOMATIC mutation, PROTEINS, RESEARCH, SEQUENCE analysis, RESEARCH methodology, EVALUATION research, COMPARATIVE studies, DISEASE susceptibility, RESEARCH funding, ACUTE diseases
Abstract

Acute lymphoblastic leukemia (ALL) is the most common cancer in children. TCF3-PBX1 fusion defines a common molecular subtype of ALL with unique clinical features, but the molecular basis of its inherited susceptibility is unknown. In a genome-wide association study of 1494 ALL cases and 2057 non-ALL controls, we identified a germline risk locus located in an intergenic region between BCL11A and PAPOLG: rs2665658, P = 1.88 × 10-8 for TCF3-PBX1 ALL vs non-ALL, and P = 1.70 × 10-8 for TCF3-PBX1 ALL vs other-ALL. The lead variant was validated in a replication cohort, and conditional analyses pointed to a single causal variant with subtype-specific effect. The risk variant is located in a regulatory DNA element uniquely activated in ALL cells with the TCF3-PBX1 fusion and may distally modulate the transcription of the adjacent gene REL. Our results expand the understanding of subtype-specific ALL susceptibility and highlight plausible interplay between germline variants and somatic genomic abnormalities in ALL pathogenesis. [ABSTRACT FROM AUTHOR]

Published
2021
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242. Changes in body mass index, height, and weight in children during and after therapy for acute lymphoblastic leukemia

Author

Browne, Emily K., Zhou, Yinmei, Chemaitilly, Wassim, Panetta, John C., Ness, Kirsten K., Kaste, Sue C., Cheng, Cheng, Relling, Mary V., Pui, Ching-Hon, and Inaba, Hiroto

Subjects
Male, Pediatric Obesity, Adolescent, Body Weight, Overweight, Precursor Cell Lymphoblastic Leukemia-Lymphoma, Article, Body Height, Dexamethasone, Drug Administration Schedule, Body Mass Index, Child Development, Child, Preschool, Antineoplastic Combined Chemotherapy Protocols, Humans, Prednisone, Female, Longitudinal Studies, Child
Abstract

BACKGROUND: Children with acute lymphoblastic leukemia (ALL) have increased risk for obesity and short stature. Data on patients treated on contemporary protocols without cranial irradiation are limited. METHODS: Changes in body mass index (BMI), height, and weight Z-scores from diagnosis to 5 years off therapy were evaluated with multivariable analysis in 372 children with ALL (aged 2–18 years at diagnosis) enrolled on the St. Jude Total XV protocol in 2000–2007. RESULTS: The percentage of overweight/obese patients increased from 25.5% at diagnosis to approximately 50% during the off-therapy period. Median BMI Z-scores increased significantly during glucocorticoid therapy (induction [Δ0.56; P

Published
2018

243. Clinical Pharmacogenetics Implementation Consortium Guideline for Thiopurine Dosing Based on TPMT and NUDT15 Genotypes: 2018 Update

Author

Relling, Mary V., Schwab, Matthias, Whirl-Carrillo, Michelle, Suarez-Kurtz, Guilherme, Pui, Ching-Hon, Stein, Charles M., Moyer, Ann M., Evans, William E., Klein, Teri E., Antillon-Klussmann, Federico Guillermo, Caudle, Kelly E., Kato, Motohiro, Yeoh, Allen EJ, Schmiegelow, Kjeld, and Yang, Jun J.

Subjects
Antimetabolites, Antineoplastic, Dose-Response Relationship, Drug, Mercaptopurine, Pharmacogenetics, Azathioprine, Inactivation, Metabolic, Humans, Drug Dosage Calculations, Methyltransferases, Pyrophosphatases, Thioguanine, Article, Pharmacogenomic Testing
Abstract

Thiopurine methyltransferase (TPMT) activity exhibits a monogenic codominant inheritance and catabolizes thiopurines. TPMT variant alleles are associated with low enzyme activity and pronounced pharmacologic effects of thiopurines. Loss-of-function alleles in the NUDT15 gene are common in Asians and Hispanics and reduce the degradation of active thiopurine nucleotide metabolites, also predisposing to myelosuppression. We provide recommendations for adjusting starting doses of azathioprine, mercaptopurine, and thioguanine based on TPMT and NUDT15 genotypes (updates on www.cpicpgx.org).

Published
2018

244. Excellent Outcomes with Reduced Frequency of Vincristine and Dexamethasone Pulses in Children with National Cancer Institute (NCI) Standard-Risk B Acute Lymphoblastic Leukemia (SR B-ALL): A Report from Children's Oncology Group (COG) Study AALL0932

Author

Angiolillo, Anne, primary, Schore, Reuven J., primary, Kairalla, John, primary, Devidas, Meenakshi, primary, Rabin, Karen R., primary, Zweidler-McKay, Patrick A., primary, Borowitz, Michael J., primary, Wood, Brent L, primary, Carroll, Andrew J., primary, Heerema, Nyla A., primary, Relling, Mary V., primary, Lane, Ashley, primary, Maloney, Kelly, primary, Wang, Cindy, primary, Carroll, William L., primary, Winick, Naomi, primary, Raetz, Elizabeth A., primary, Loh, Mignon L., primary, and Hunger, Stephen P., primary

Published
2019
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245. Germline RUNX1 Variation and Predisposition to T-Cell Acute Lymphoblastic Leukemia in Children

Author

Li, Yizhen, primary, Qian, Maoxiang, primary, Devidas, Meenakshi, primary, Yang, Wentao, primary, Winter, Stuart S., primary, Dunsmore, Kimberly P., primary, Smith, Colton A, primary, Lin, Ting-Nien, primary, Zhao, Xuijie, primary, Zhang, Ranran, primary, Gastier Foster, Julie M., primary, Raetz, Elizabeth A., primary, Carroll, William L., primary, Rabin, Karen R., primary, Yang, Wenjian, primary, Zweidler-McKay, Patrick A., primary, Pui, Ching-Hon, primary, Evans, William E., primary, Mullighan, Charles G., primary, Hunger, Stephen P., primary, Relling, Mary V., primary, Loh, Mignon L., primary, and Yang, Jun J., primary

Published
2019
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246. Identification of New Risk Loci and Regulatory Mechanisms Influencing Genetic Susceptibility to Acute Lymphoblastic Leukaemia

Author

Vijayakrishnan, Jayaram, primary, Qian, Maoxiang, primary, Studd, James B, primary, Yang, Wenjian, primary, Kinnersley, Ben, primary, Law, Philip, primary, Broderick, Peter, primary, Raetz, Elizabeth A., primary, Allan, James M., primary, Pui, Ching-Hon, primary, Vora, Ajay, primary, Evans, William E., primary, Moorman, Anthony V., primary, Yeoh, Allen Eng Juh, primary, Li, Chunliang, primary, Bartram, Claus, primary, Mullighan, Charles G., primary, Zimmermann, Martin, primary, Hunger, Stephen P., primary, Schrappe, Martin, primary, Relling, Mary V., primary, Stanulla, Martin, primary, Loh, Mignon L., primary, Houlston, Richard S., primary, and Yang, Jun J., primary

Published
2019
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247. The Genomic Landscape of Childhood Acute Lymphoblastic Leukemia

Author

Roberts, Kathryn G., primary, Brady, Samuel W., primary, Gu, Zhaohui, primary, Shi, Lei, primary, Pounds, Stanley, primary, Pei, Deqing, primary, Cheng, Cheng, primary, Dai, Yunfeng, primary, Devidas, Meenakshi, primary, Qu, Chunxu, primary, Hill, Ashley, primary, Ma, Xiaotu, primary, Wei, Lei, primary, Arunachalam, Sasi, primary, Hagiwara, Kohei, primary, Liu, Yangling, primary, Flasch, Diane, primary, Liu, Yu, primary, Parker, Matthew, primary, Chen, Xiaolong, primary, Li, Yongjin, primary, Fan, Yiping, primary, Michael, Robert, primary, Rusch, Michael, primary, Wilkinson, Mark, primary, Foy, Scott, primary, Hedges, Dale, primary, Newman, Scott, primary, Zhou, Xin, primary, Wang, Jian, primary, Reshmi, Shalini C., primary, Gastier-Foster, Julie M., primary, Gesuwan, Patee, primary, Smith, Malcolm A, primary, Gerhard, Daniela S., primary, Winick, Naomi, primary, Carroll, Andrew J., primary, Heerema, Nyla A., primary, Harvey, Richard C., primary, Willman, Cheryl L., primary, Larsen, Eric, primary, Raetz, Elizabeth A., primary, Borowitz, Michael J., primary, Wood, Brent L, primary, Carroll, William L., primary, Zweidler-McKay, Patrick A., primary, Rabin, Karen R., primary, Mattano, Leonard A., primary, Maloney, Kelly, primary, Winter, Stuart S., primary, Burke, Michael J., primary, Salzer, Wanda L., primary, Dunsmore, Kimberly P., primary, Angiolillo, Anne, primary, Crews, Kristine R, primary, Downing, James R., primary, Jeha, Sima, primary, Evans, William E., primary, Pui, Ching-Hon, primary, Yang, Jun J., primary, Relling, Mary V., primary, Hunger, Stephen P., primary, Loh, Mignon L., primary, Zhang, Jinghui, primary, and Mullighan, Charles G., primary

Published
2019
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250. StandardizingCYP 2D6Genotype to Phenotype Translation: Consensus Recommendations from the Clinical Pharmacogenetics Implementation Consortium and Dutch Pharmacogenetics Working Group

Author

Caudle, Kelly E., primary, Sangkuhl, Katrin, additional, Whirl‐Carrillo, Michelle, additional, Swen, Jesse J., additional, Haidar, Cyrine E., additional, Klein, Teri E., additional, Gammal, Roseann S., additional, Relling, Mary V., additional, Scott, Stuart A., additional, Hertz, Daniel L., additional, Guchelaar, Henk‐Jan, additional, and Gaedigk, Andrea, additional

Published
2019
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