Search

Your search keyword '"Heatley, Susan L"' showing total 8 results
Start Over Author "Heatley, Susan L" Publisher springer science and business media llc
8 results on '"Heatley, Susan L"'

1. Measurable residual disease analysis in paediatric acute lymphoblastic leukaemia patients with ABL-class fusions

Author

Venn, Nicola C., primary, Huang, Libby, additional, Hovorková, Lenka, additional, Muskovic, Walter, additional, Wong, Marie, additional, Law, Tamara, additional, Heatley, Susan L., additional, Khaw, Seong Lin, additional, Revesz, Tom, additional, Dalla Pozza, Luciano, additional, Shaw, Peter J., additional, Fraser, Chris, additional, Moore, Andrew S., additional, Cross, Siobhan, additional, Bendak, Katerina, additional, Norris, Murray D., additional, Henderson, Michelle J., additional, White, Deborah L., additional, Cowley, Mark J., additional, Trahair, Toby N., additional, Zuna, Jan, additional, and Sutton, Rosemary, additional

Published
2022
Full Text
View/download PDF

6. The genomic landscape of hypodiploid acute lymphoblastic leukemia

Author

Holmfeldt, Linda, primary, Wei, Lei, additional, Diaz-Flores, Ernesto, additional, Walsh, Michael, additional, Zhang, Jinghui, additional, Ding, Li, additional, Payne-Turner, Debbie, additional, Churchman, Michelle, additional, Andersson, Anna, additional, Chen, Shann-Ching, additional, McCastlain, Kelly, additional, Becksfort, Jared, additional, Ma, Jing, additional, Wu, Gang, additional, Patel, Samir N, additional, Heatley, Susan L, additional, Phillips, Letha A, additional, Song, Guangchun, additional, Easton, John, additional, Parker, Matthew, additional, Chen, Xiang, additional, Rusch, Michael, additional, Boggs, Kristy, additional, Vadodaria, Bhavin, additional, Hedlund, Erin, additional, Drenberg, Christina, additional, Baker, Sharyn, additional, Pei, Deqing, additional, Cheng, Cheng, additional, Huether, Robert, additional, Lu, Charles, additional, Fulton, Robert S, additional, Fulton, Lucinda L, additional, Tabib, Yashodhan, additional, Dooling, David J, additional, Ochoa, Kerri, additional, Minden, Mark, additional, Lewis, Ian D, additional, To, L Bik, additional, Marlton, Paula, additional, Roberts, Andrew W, additional, Raca, Gordana, additional, Stock, Wendy, additional, Neale, Geoffrey, additional, Drexler, Hans G, additional, Dickins, Ross A, additional, Ellison, David W, additional, Shurtleff, Sheila A, additional, Pui, Ching-Hon, additional, Ribeiro, Raul C, additional, Devidas, Meenakshi, additional, Carroll, Andrew J, additional, Heerema, Nyla A, additional, Wood, Brent, additional, Borowitz, Michael J, additional, Gastier-Foster, Julie M, additional, Raimondi, Susana C, additional, Mardis, Elaine R, additional, Wilson, Richard K, additional, Downing, James R, additional, Hunger, Stephen P, additional, Loh, Mignon L, additional, and Mullighan, Charles G, additional

Published
2013
Full Text
View/download PDF

8. HMGN1 plays a significant role in CRLF2 driven Down Syndrome leukemia and provides a potential therapeutic target in this high-risk cohort

Author

David T Yeung, Timothy P. Hughes, Deborah L. White, Sofia Omari, Paul Q. Thomas, Elyse C. Page, Susan L. Heatley, Charles E. de Bock, Laura N Eadie, Barbara J. McClure, Page, Elyse C, Heatley, Susan L, Eadie, Laura N, McClure, Barbara J, de Bock, Charles E, Omari, Sofia, Yeung, David T, Hughes, Timothy P, Thomas, Paul Q, and White, Deborah L

Subjects
CRLF2r, Cancer Research, Down syndrome, medicine.medical_treatment, leukemia, Hepatosplenomegaly, acute lymphoblastic leukemia, Biology, medicine.disease, Haematopoiesis, Leukemia, Cytokine, Downregulation and upregulation, HMGN1, high-mobility group nucleosome-binding protein 1, Genetics, medicine, Cancer research, cytokine receptor-like factor 2 rearranged, Down Syndrome, medicine.symptom, Stem cell, Chromosome 21, Molecular Biology, HMGN1 Protein
Abstract

Refereed/Peer-reviewed The genetic basis of the predisposition for Down Syndrome (DS) patients to develop cytokine receptor-like factor 2 rearranged (CRLF2r) acute lymphoblastic leukemia (ALL) is currently unknown. Genes located on chromosome 21 and expressed in hematopoietic cells are likely candidates for investigation of CRLF2r DS-ALL pathogenesis. We explored the high-mobility group nucleosome-binding protein 1 (HMGN1), located in the DS critical region, in an inducible CRISPR/Cas9 knockout (KO) xenograft model to assess the effect of HMGN1 loss of function on the leukemic burden. We demonstrated HMGN1 KO-mitigated leukemic phenotypes including hepatosplenomegaly, thrombocytopenia, and anemia, commonly observed in leukemia patients, and significantly increased survival in vivo. HMGN1 overexpression in murine stem cells and Ba/F3 cells in vitro, in combination with P2RY8-CRLF2, resulted in cytokine-independent transformation and upregulation of cell signaling pathways associated with leukemic development. Finally, in vitro screening demonstrated successful targeting of P2RY8-CRLF2 and HMGN1 co-expressing cell lines and patient samples with fedratinib (JAK2 inhibitor), and GSK-J4 (demethylase inhibitor) in combination. Together, these data provide critical insight into the development and persistence of CRLF2r DS-ALL and identify HMGN1 as a potential therapeutic target to improve outcomes and reduce toxicity in this high-risk cohort of young patients.

Published
2021
Full Text
View/download PDF

Catalog

Books, media, physical & digital resources
See catalog results