Nina Weichert-Leahey | Medical Services
Programs & Services
Languages
- English
- German
Nina Weichert-Leahey | Education
Medical School
Ludwig-Maximilians-Universitaet
2010, Munich, Germany
Medical School
Charité – Universitätsmedizin Berlin
2013, Berlin, Germany
Residency
Boston Combined Residency Program (BCRP)
2019, Boston, MA
Fellowship
Pediatric Hematology/Oncology
Boston Children's Hospital/Dana-Farber Cancer Institute
2022, Boston, MA
Nina Weichert-Leahey | Professional History
Dr. Weichert-Leahey received her medical degree from the Ludwig-Maximilian University in Munich, Germany, in 2010. She subsequently trained in pediatrics at the University Hospital Charité in Berlin, Germany, and completed her residency in Pediatrics at Boston Children's Hospital/Boston Medical Center, followed by a fellowship in Pediatric Hematology/Oncology at Dana-Farber Cancer Institute/Boston Children's Hospital. Her research interests are in pediatric cancer predisposition, cancer genomics, and how to use this knowledge to develop new therapeutics.
Nina Weichert-Leahey | Publications
ANKRD26-related Thrombocytopenia 2 with a Baseline Increase in Blasts: Implications for Clinical Surveillance. Blood. 2025 May 07. View ANKRD26-related Thrombocytopenia 2 with a Baseline Increase in Blasts: Implications for Clinical Surveillance. Abstract
Accurate Measurement of Cell Number-Normalized Differential Gene Expression in Cells Treated With Retinoic Acid. Bio Protoc. 2024 Nov 05; 14(21):e5106. View Accurate Measurement of Cell Number-Normalized Differential Gene Expression in Cells Treated With Retinoic Acid. Abstract
Genetic predisposition to neuroblastoma results from a regulatory polymorphism that promotes the adrenergic cell state. J Clin Invest. 2023 05 15; 133(10). View Genetic predisposition to neuroblastoma results from a regulatory polymorphism that promotes the adrenergic cell state. Abstract
Genetic Predisposition to Neuroblastoma Results from a Regulatory Polymorphism that Promotes the Adrenergic Cell State. bioRxiv. 2023 Mar 01. View Genetic Predisposition to Neuroblastoma Results from a Regulatory Polymorphism that Promotes the Adrenergic Cell State. Abstract
X-linked inhibitor of apoptosis protein represents a promising therapeutic target for relapsed/refractory ALL. EMBO Mol Med. 2023 01 11; 15(1):e14557. View X-linked inhibitor of apoptosis protein represents a promising therapeutic target for relapsed/refractory ALL. Abstract
MEIS2 Is an Adrenergic Core Regulatory Transcription Factor Involved in Early Initiation of TH-MYCN-Driven Neuroblastoma Formation. Cancers (Basel). 2021 Sep 24; 13(19). View MEIS2 Is an Adrenergic Core Regulatory Transcription Factor Involved in Early Initiation of TH-MYCN-Driven Neuroblastoma Formation. Abstract
Alveolar rhabdomyosarcoma presenting as a pleural effusion: An atypical presentation of a malignancy. Pediatr Pulmonol. 2020 12; 55(12):3231-3233. View Alveolar rhabdomyosarcoma presenting as a pleural effusion: An atypical presentation of a malignancy. Abstract
COVID-19 presenting with autoimmune hemolytic anemia in the setting of underlying immune dysregulation. Pediatr Blood Cancer. 2020 09; 67(9):e28382. View COVID-19 presenting with autoimmune hemolytic anemia in the setting of underlying immune dysregulation. Abstract
ASCL1 is a MYCN- and LMO1-dependent member of the adrenergic neuroblastoma core regulatory circuitry. Nat Commun. 2019 12 09; 10(1):5622. View ASCL1 is a MYCN- and LMO1-dependent member of the adrenergic neuroblastoma core regulatory circuitry. Abstract
Selective gene dependencies in MYCN-amplified neuroblastoma include the core transcriptional regulatory circuitry. Nat Genet. 2018 09; 50(9):1240-1246. View Selective gene dependencies in MYCN-amplified neuroblastoma include the core transcriptional regulatory circuitry. Abstract
Cross-Cohort Analysis Identifies a TEAD4-MYCN Positive Feedback Loop as the Core Regulatory Element of High-Risk Neuroblastoma. Cancer Discov. 2018 05; 8(5):582-599. View Cross-Cohort Analysis Identifies a TEAD4-MYCN Positive Feedback Loop as the Core Regulatory Element of High-Risk Neuroblastoma. Abstract
MYC Drives a Subset of High-Risk Pediatric Neuroblastomas and Is Activated through Mechanisms Including Enhancer Hijacking and Focal Enhancer Amplification. Cancer Discov. 2018 03; 8(3):320-335. View MYC Drives a Subset of High-Risk Pediatric Neuroblastomas and Is Activated through Mechanisms Including Enhancer Hijacking and Focal Enhancer Amplification. Abstract
LMO1 Synergizes with MYCN to Promote Neuroblastoma Initiation and Metastasis. Cancer Cell. 2017 09 11; 32(3):310-323.e5. View LMO1 Synergizes with MYCN to Promote Neuroblastoma Initiation and Metastasis. Abstract
Corrigendum: Small genomic insertions form enhancers that misregulate oncogenes. Nat Commun. 2017 06 01; 8:15797. View Corrigendum: Small genomic insertions form enhancers that misregulate oncogenes. Abstract
Small genomic insertions form enhancers that misregulate oncogenes. Nat Commun. 2017 02 09; 8:14385. View Small genomic insertions form enhancers that misregulate oncogenes. Abstract
Genetic predisposition to neuroblastoma mediated by a LMO1 super-enhancer polymorphism. Nature. 2015 Dec 17; 528(7582):418-21. View Genetic predisposition to neuroblastoma mediated by a LMO1 super-enhancer polymorphism. Abstract
Levetiracetam as a possible cause of secondary graft failure after allogenic hematopoietic stem cell transplantation. Eur J Paediatr Neurol. 2015 Jan; 19(1):75-7. View Levetiracetam as a possible cause of secondary graft failure after allogenic hematopoietic stem cell transplantation. Abstract
Evaluation of effectiveness of instruction and study habits in two consecutive clinical semesters of the medical curriculum Munich (MeCuM) reveals the need for more time for self study and higher frequency of assessment. BMC Med Educ. 2011 Aug 26; 11:62. View Evaluation of effectiveness of instruction and study habits in two consecutive clinical semesters of the medical curriculum Munich (MeCuM) reveals the need for more time for self study and higher frequency of assessment. Abstract
Some ABCA3 mutations elevate ER stress and initiate apoptosis of lung epithelial cells. Respir Res. 2011 Jan 07; 12:4. View Some ABCA3 mutations elevate ER stress and initiate apoptosis of lung epithelial cells. Abstract