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2. Hematologic DNMT3A reduction and high-fat diet synergize to promote weight gain and tissue inflammation

Author

Reyes, Jaime M., Tovy, Ayala, Zhang, Linda, Bortoletto, Angelina S., Rosas, Carina, Chen, Chun-Wei, Waldvogel, Sarah M., Guzman, Anna G., Aguilar, Rogelio, Gupta, Sinjini, Liu, Ling, Buckley, Matthew T., Patel, Kalyani R., Marcogliese, Andrea N., Li, Yumei, Curry, Choladda V., Rando, Thomas A., Brunet, Anne, Parchem, Ronald J., Rau, Rachel E., and Goodell, Margaret A.

Published
2024
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3. DNMT3A-coordinated splicing governs the stem state switch towards differentiation in embryonic and haematopoietic stem cells

Author

Ramabadran, Raghav, Wang, Jarey H., Reyes, Jaime M., Guzman, Anna G., Gupta, Sinjini, Rosas, Carina, Brunetti, Lorenzo, Gundry, Michael C., Tovy, Ayala, Long, Hali, Gu, Tianpeng, Cullen, Sean M., Tyagi, Siddhartha, Rux, Danielle, Kim, Jean J., Kornblau, Steven M., Kyba, Michael, Stossi, Fabio, Rau, Rachel E., Takahashi, Koichi, Westbrook, Thomas F., and Goodell, Margaret A.

Published
2023
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6. Observation and Management of Juvenile Myelomonocytic Leukemia and Noonan Syndrome-Associated Myeloproliferative Disorder: A Real-World Experience †.

Author

Lucas, Bryony J., Connors, Jeremy S., Wang, Heping, Conneely, Shannon, Cuglievan, Branko, Garcia, Miriam B., and Rau, Rachel E.

Subjects
THERAPEUTIC use of antineoplastic agents, THERAPEUTIC use of antimetabolites, MYELOID leukemia genetics, CYTOGENETICS, NOONAN syndrome, GERM cells, AZACITIDINE, MYELOPROLIFERATIVE neoplasms, TREATMENT effectiveness, RETROSPECTIVE studies, CANCER chemotherapy, MEDICAL records, ACQUISITION of data, MYELOID leukemia, GENETIC mutation, GENETICS, ALLELES, DISEASE complications, CHILDREN
Abstract

Simple Summary: Juvenile Myelomonocytic Leukemia (JMML) is a rare and clonal hematopoietic disorder of infancy and early childhood with myeloproliferative/myelodysplastic features resulting from germline or somatic mutations in the RAS pathway. Given its rarity, management is not standardized and varies widely, ranging from observation to bone marrow transplant depending on genomic and clinical features. We describe the course of JMML or Noonan Syndrome-associated Myeloproliferative Disorder in 22 pediatric patients treated at three institutions to provide guidance for monitoring versus intervention, including transplant, supported by patient outcomes. We provide additional insight into the expected time to spontaneous resolution in those with germline PTPN11 mutations and treatment approaches for patients with germline CBL mutations where no standard exists. Juvenile Myelomonocytic Leukemia (JMML) is a rare and clonal hematopoietic disorder of infancy and early childhood with myeloproliferative/myelodysplastic features resulting from germline or somatic mutations in the RAS pathway. Treatment is not uniform, with management varying from observation to stem cell transplant. The aim of our retrospective review is to describe the treatment and outcomes of a cohort of patients with JMML or Noonan Syndrome-associated Myeloproliferative Disorder (NS-MPD) to provide management guidance for this rare and heterogeneous disease. We report on 22 patients with JMML or NS-MPD managed at three institutions in the Texas Medical Center. Of patients with known genetic mutations and cytogenetics, 6 harbored germline mutations, 12 had somatic mutations, and 9 showed cytogenetic abnormalities. Overall, 14/22 patients are alive. Spontaneous clinical remission occurred in one patient with somatic NRAS mutation, as well as two with germline PTPN11 mutations with NS-MPD, and two others with germline PTPN11 mutations and NS-MPD remain under surveillance. Patients with NS-MPD were excluded from treatment analysis as none required chemotherapeutic intervention. All patients (5/5) treated with 5-azacitidine alone and one of the four treated with 6-mercaptopurine monotherapy had a reduction in mutant variant allele frequency. Transformation to acute myeloid leukemia was seen in two patients who both died. Among patients who received transplants, 7/13 are alive, and relapse post-transplant occurred in 3/13 with a median time to relapse of 3.55 months. This report provides insight into therapy responses and long-term outcomes across different genetic subsets of JMML and lends insight into the expected time to spontaneous resolution in patients with NS-MPD with germline PTPN11 mutations. [ABSTRACT FROM AUTHOR]

Published
2024
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14. SARS‐CoV‐2 infections in patients enrolled on the Children's Oncology Group standard‐risk B‐cell acute lymphoblastic leukemia trial, AALL1731

Author

Elgarten, Caitlin W., primary, Kairalla, John A., additional, Thompson, Joel C., additional, Miller, Tamara P., additional, Wang, Cindy, additional, Conway, Susan, additional, Loh, Mignon L., additional, Raetz, Elizabeth A., additional, Gupta, Sumit, additional, Rau, Rachel E., additional, Angiolillo, Anne, additional, Rabin, Karen R., additional, and Alexander, Sarah, additional

Published
2023
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15. Data from SWI/SNF Blockade Disrupts PU.1-Directed Enhancer Programs in Normal Hematopoietic Cells and Acute Myeloid Leukemia

Author

Chambers, Courtney, primary, Cermakova, Katerina, primary, Chan, Yuen San, primary, Kurtz, Kristen, primary, Wohlan, Katharina, primary, Lewis, Andrew Henry, primary, Wang, Christiana, primary, Pham, Anh, primary, Dejmek, Milan, primary, Sala, Michal, primary, Loeza Cabrera, Mario, primary, Aguilar, Rogelio, primary, Nencka, Radim, primary, Lacorazza, H. Daniel, primary, Rau, Rachel E., primary, and Hodges, H. Courtney, primary

Published
2023
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16. Supplementary Dataset 1 from SWI/SNF Blockade Disrupts PU.1-Directed Enhancer Programs in Normal Hematopoietic Cells and Acute Myeloid Leukemia

Author

Chambers, Courtney, primary, Cermakova, Katerina, primary, Chan, Yuen San, primary, Kurtz, Kristen, primary, Wohlan, Katharina, primary, Lewis, Andrew Henry, primary, Wang, Christiana, primary, Pham, Anh, primary, Dejmek, Milan, primary, Sala, Michal, primary, Loeza Cabrera, Mario, primary, Aguilar, Rogelio, primary, Nencka, Radim, primary, Lacorazza, H. Daniel, primary, Rau, Rachel E., primary, and Hodges, H. Courtney, primary

Published
2023
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17. Supplementary Data from SWI/SNF Blockade Disrupts PU.1-Directed Enhancer Programs in Normal Hematopoietic Cells and Acute Myeloid Leukemia

Author

Chambers, Courtney, primary, Cermakova, Katerina, primary, Chan, Yuen San, primary, Kurtz, Kristen, primary, Wohlan, Katharina, primary, Lewis, Andrew Henry, primary, Wang, Christiana, primary, Pham, Anh, primary, Dejmek, Milan, primary, Sala, Michal, primary, Loeza Cabrera, Mario, primary, Aguilar, Rogelio, primary, Nencka, Radim, primary, Lacorazza, H. Daniel, primary, Rau, Rachel E., primary, and Hodges, H. Courtney, primary

Published
2023
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18. Supplementary Dataset 2 from SWI/SNF Blockade Disrupts PU.1-Directed Enhancer Programs in Normal Hematopoietic Cells and Acute Myeloid Leukemia

Author

Chambers, Courtney, primary, Cermakova, Katerina, primary, Chan, Yuen San, primary, Kurtz, Kristen, primary, Wohlan, Katharina, primary, Lewis, Andrew Henry, primary, Wang, Christiana, primary, Pham, Anh, primary, Dejmek, Milan, primary, Sala, Michal, primary, Loeza Cabrera, Mario, primary, Aguilar, Rogelio, primary, Nencka, Radim, primary, Lacorazza, H. Daniel, primary, Rau, Rachel E., primary, and Hodges, H. Courtney, primary

Published
2023
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19. Supplementary Dataset 4 from SWI/SNF Blockade Disrupts PU.1-Directed Enhancer Programs in Normal Hematopoietic Cells and Acute Myeloid Leukemia

Author

Chambers, Courtney, primary, Cermakova, Katerina, primary, Chan, Yuen San, primary, Kurtz, Kristen, primary, Wohlan, Katharina, primary, Lewis, Andrew Henry, primary, Wang, Christiana, primary, Pham, Anh, primary, Dejmek, Milan, primary, Sala, Michal, primary, Loeza Cabrera, Mario, primary, Aguilar, Rogelio, primary, Nencka, Radim, primary, Lacorazza, H. Daniel, primary, Rau, Rachel E., primary, and Hodges, H. Courtney, primary

Published
2023
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20. Supplementary Dataset 3 from SWI/SNF Blockade Disrupts PU.1-Directed Enhancer Programs in Normal Hematopoietic Cells and Acute Myeloid Leukemia

Author

Chambers, Courtney, primary, Cermakova, Katerina, primary, Chan, Yuen San, primary, Kurtz, Kristen, primary, Wohlan, Katharina, primary, Lewis, Andrew Henry, primary, Wang, Christiana, primary, Pham, Anh, primary, Dejmek, Milan, primary, Sala, Michal, primary, Loeza Cabrera, Mario, primary, Aguilar, Rogelio, primary, Nencka, Radim, primary, Lacorazza, H. Daniel, primary, Rau, Rachel E., primary, and Hodges, H. Courtney, primary

Published
2023
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22. RecombinantErwiniaasparaginase (JZP458) in acute lymphoblastic leukemia: results from the phase 2/3 AALL1931 study

Author

Maese, Luke, primary, Loh, Mignon L., additional, Choi, Mi Rim, additional, Lin, Tong, additional, Aoki, Etsuko, additional, Zanette, Michelle, additional, Agarwal, Shirali, additional, Iannone, Robert, additional, Silverman, Jeffrey A., additional, Silverman, Lewis B., additional, Raetz, Elizabeth A., additional, and Rau, Rachel E., additional

Published
2023
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24. RNA sequestration in P-bodies sustains myeloid leukaemia

Author

Kodali, Srikanth, Proietti, Ludovica, Valcarcel, Gemma, López-Rubio, Anna V., Pessina, Patrizia, Eder, Thomas, Shi, Junchao, Jen, Annie, Lupión-Garcia, Núria, Starner, Anne C., Bartels, Mason D., Cui, Yingzhi, Sands, Caroline M., Planas-Riverola, Ainoa, Martínez, Alba, Velasco-Hernandez, Talia, Tomás-Daza, Laureano, Alber, Bernhard, Manhart, Gabriele, Mayer, Isabella Maria, Kollmann, Karoline, Fatica, Alessandro, Menendez, Pablo, Shishkova, Evgenia, Rau, Rachel E., Javierre, Biola M., Coon, Joshua, Chen, Qi, Van Nostrand, Eric L., Sardina, Jose L., Grebien, Florian, and Di Stefano, Bruno

Abstract

Post-transcriptional mechanisms are fundamental safeguards of progenitor cell identity and are often dysregulated in cancer. Here, we identified regulators of P-bodies as crucial vulnerabilities in acute myeloid leukaemia (AML) through genome-wide CRISPR screens in normal and malignant haematopoietic progenitors. We found that leukaemia cells harbour aberrantly elevated numbers of P-bodies and show that P-body assembly is crucial for initiation and maintenance of AML. Notably, P-body loss had little effect upon homoeostatic haematopoiesis but impacted regenerative haematopoiesis. Molecular characterization of P-bodies purified from human AML cells unveiled their critical role in sequestering messenger RNAs encoding potent tumour suppressors from the translational machinery. P-body dissolution promoted translation of these mRNAs, which in turn rewired gene expression and chromatin architecture in leukaemia cells. Collectively, our findings highlight the contrasting and unique roles of RNA sequestration in P-bodies during tissue homoeostasis and oncogenesis. These insights open potential avenues for understanding myeloid leukaemia and future therapeutic interventions.

Published
2024
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25. SWI/SNF blockade disrupts PU.1-directed enhancer programs in normal hematopoietic cells and acute myeloid leukemia

Author

Chambers, Courtney, primary, Cermakova, Katerina, additional, Chan, Yuen San, additional, Kurtz, Kristen, additional, Wohlan, Katharina, additional, Lewis, Andrew Henry., additional, Wang, Christiana, additional, Pham, Anh, additional, Dejmek, Milan, additional, Sala, Michal, additional, Loeza Cabrera, Mario, additional, Aguilar, Rogelio, additional, Nencka, Radim, additional, Lacorazza, Daniel, additional, Rau, Rachel E., additional, and Hodges, H. Courtney, additional

Published
2023
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28. Efficacy, Safety, and Population Pharmacokinetic Modeling of Intravenous Recombinant Erwinia Asparaginase (JZP458) in Acute Lymphoblastic Leukemia/Lymphoblastic Lymphoma: Results from Study AALL1931

Author

Maese, Luke, primary, Loh, Mignon L., additional, Choi, Mi Rim, additional, Lin, Tong, additional, Aoki, Etsuko, additional, Agarwal, Shirali, additional, Wu, Xiaotian, additional, Iannone, Robert, additional, Silverman, Jeffrey A., additional, Silverman, Lewis B., additional, Raetz, Elizabeth A., additional, and Rau, Rachel E., additional

Published
2022
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29. Relocalization of PU.1 Underlies the On- and Off-Tumor Effects of SWI/SNF Blockade in AML

Author

Chambers, Courtney, primary, Kurtz, Kristen, additional, Lewis, Andrew Henry, additional, Wohlan, Katharina, additional, Chan, Yuen San, additional, Cermakova, Katerina, additional, Dejmek, Milan, additional, Sala, Michal, additional, Aguilar, Rogelio, additional, Loeza Cabrera, Mario, additional, Nencka, Radim, additional, Lacorazza, H. Daniel, additional, Rau, Rachel E., additional, and Hodges, H. Courtney, additional

Published
2022
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32. Improving infectious adverse event reporting for children and adolescents enrolled in clinical trials for acute lymphoblastic leukemia: A report from the Children's Oncology Group

Author

Elgarten, Caitlin W., primary, Thompson, Joel C., additional, Angiolillo, Anne, additional, Chen, Zhiguo, additional, Conway, Susan, additional, Devidas, Meenakshi, additional, Gupta, Sumit, additional, Kairalla, John A., additional, McNeer, Jennifer L., additional, O'Brien, Maureen M., additional, Rabin, Karen R., additional, Rau, Rachel E., additional, Rheingold, Susan R., additional, Wang, Cindy, additional, Wood, Charlotte, additional, Raetz, Elizabeth A., additional, Loh, Mignon L., additional, Alexander, Sarah, additional, and Miller, Tamara P., additional

Published
2022
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37. Murine Models of Acute Myeloid Leukemia

Author

Kurtz, Kristen J., Conneely, Shannon E., O’Keefe, Madeleine, Wohlan, Katharina, and Rau, Rachel E.

Subjects
Cancer Research, Oncology
Abstract

Acute myeloid leukemia (AML) is a phenotypically and genetically heterogeneous hematologic malignancy. Extensive sequencing efforts have mapped the genomic landscape of adult and pediatric AML revealing a number of biologically and prognostically relevant driver lesions. Beyond identifying recurrent genetic aberrations, it is of critical importance to fully delineate the complex mechanisms by which they contribute to the initiation and evolution of disease to ultimately facilitate the development of targeted therapies. Towards these aims, murine models of AML are indispensable research tools. The rapid evolution of genetic engineering techniques over the past 20 years has greatly advanced the use of murine models to mirror specific genetic subtypes of human AML, define cell-intrinsic and extrinsic disease mechanisms, study the interaction between co-occurring genetic lesions, and test novel therapeutic approaches. This review summarizes the mouse model systems that have been developed to recapitulate the most common genomic subtypes of AML. We will discuss the strengths and weaknesses of varying modeling strategies, highlight major discoveries emanating from these model systems, and outline future opportunities to leverage emerging technologies for mechanistic and preclinical investigations.

Published
2022

40. Effects of age, obesity, and body surface area on asparaginase-associated toxicities during acute lymphoblastic leukemia induction therapy: A report from the Children’s Oncology Group.

Author

Orgel, Etan, primary, Militano, Olga, additional, Chen, Zhiguo, additional, Devidas, Meenakshi, additional, Maese, Luke Devon, additional, Rau, Rachel E., additional, Angiolillo, Anne L., additional, McNeer, Jennifer Lynn, additional, Schore, Reuven J., additional, Raetz, Elizabeth A., additional, Silverman, Lewis B., additional, Winick, Naomi J., additional, Larsen, Eric, additional, Carroll, William L., additional, Winter, Stuart S, additional, Dunsmore, Kimberley, additional, Hunger, Stephen, additional, and Loh, Mignon L., additional

Published
2022
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42. Efficacy and safety of intramuscular (IM) recombinant Erwinia asparaginase in acute lymphoblastic leukemia (ALL) or lymphoblastic lymphoma (LBL): The Children’s Oncology Group (COG) AALL1931 study.

Author

Maese, Luke Devon, primary, Loh, Mignon L., additional, Choi, L. Mi Rim, additional, Lin, Tong, additional, Aoki, Etsuko, additional, Zanette, Michelle, additional, Agarwal, Shirali, additional, Silverman, Jeffrey Alan, additional, Silverman, Lewis B., additional, Raetz, Elizabeth A., additional, and Rau, Rachel E., additional

Published
2022
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43. Constitutive loss of DNMT3A causes morbid obesity through misregulation of adipogenesis

Author

Tovy, Ayala, primary, Reyes, Jaime M, additional, Zhang, Linda, additional, Huang, Yung-Hsin, additional, Rosas, Carina, additional, Daquinag, Alexes C, additional, Guzman, Anna, additional, Ramabadran, Raghav, additional, Chen, Chun-Wei, additional, Gu, Tianpeng, additional, Gupta, Sinjini, additional, Ortinau, Laura, additional, Park, Dongsu, additional, Cox, Aaron R, additional, Rau, Rachel E, additional, Hartig, Sean M, additional, Kolonin, Mikhail G, additional, and Goodell, Margaret A, additional

Published
2022
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44. Author response: Constitutive loss of DNMT3A causes morbid obesity through misregulation of adipogenesis

Author

Tovy, Ayala, primary, Reyes, Jaime M, additional, Zhang, Linda, additional, Huang, Yung-Hsin, additional, Rosas, Carina, additional, Daquinag, Alexes C, additional, Guzman, Anna, additional, Ramabadran, Raghav, additional, Chen, Chun-Wei, additional, Gu, Tianpeng, additional, Gupta, Sinjini, additional, Ortinau, Laura, additional, Park, Dongsu, additional, Cox, Aaron R, additional, Rau, Rachel E, additional, Hartig, Sean M, additional, Kolonin, Mikhail G, additional, and Goodell, Margaret A, additional

Published
2022
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47. Blinatumomab Associated Seizure Risk in Patients with Down Syndrome and B-Lymphoblastic Leukemia: An Interim Report from Children's Oncology Group (COG) Study AALL1731

Author

Li, Amanda M., primary, Rabin, Karen R, additional, Kairalla, John, additional, Wang, Cindy, additional, Devidas, Meenakshi, additional, Militano, Olga, additional, Okada, Maki, additional, Hitzler, Johann K, additional, Angiolillo, Anne L, additional, Raetz, Elizabeth A., additional, Loh, Mignon L., additional, Gupta, Sumit, additional, and Rau, Rachel E., additional

Published
2021
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48. Initial Results from a Phase 2/3 Study of Recombinant Erwinia Asparaginase (JZP458) in Patients with Acute Lymphoblastic Leukemia (ALL)/Lymphoblastic Lymphoma (LBL) Who Are Allergic/Hypersensitive to E. coli-Derived Asparaginases

Author

Maese, Luke, primary, Loh, Mignon L., additional, Lin, Tong, additional, Aoki, Etsuko, additional, Zanette, Michelle, additional, Agarwal, Shirali, additional, Silverman, Jeffrey A., additional, Choi, Mi Rim, additional, Silverman, Lewis B., additional, Raetz, Elizabeth A., additional, and Rau, Rachel E., additional

Published
2021
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50. Constitutive loss of DNMT3A causes morbid obesity through misregulation of adipogenesis

Author

Tovy, Ayala, primary, Reyes, Jaime M., additional, Zhang, Linda, additional, Huang, Yung-Hsin, additional, Rosas, Carina, additional, Daquinag, Alexes C., additional, Guzman, Anna G., additional, Ramabadran, Raghav, additional, Chen, Chun-Wei, additional, Gu, Tianpeng, additional, Gupta, Sinjini, additional, Ortinau, Laura, additional, Park, Dongsu, additional, Cox, Aaron R., additional, Rau, Rachel E, additional, Hartig, Sean M., additional, Kolonin, Mikhail G, additional, and Goodell, Margaret A., additional

Published
2021
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