
Feiyang Ma
Articles
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Nov 13, 2024 |
nature.com | Vera Adema |Kelly S. Chien |Sanam Loghavi |Feiyang Ma |Guillermo Montalban-Bravo |Xuelin Huang | +1 more
AbstractIn myelodysplastic syndromes (MDS), the IL-1β pathway is upregulated, and previous studies using mouse models of founder MDS mutations demonstrated that it enhances hematopoietic stem and progenitor cells’ (HSPCs’) aberrant differentiation towards the myeloid lineage at the expense of erythropoiesis.
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Nov 13, 2024 |
nature.com | Vera Adema |Kelly S. Chien |Sanam Loghavi |Feiyang Ma |Guillermo Montalban-Bravo |Xuelin Huang | +1 more
AbstractIn myelodysplastic syndromes (MDS), the IL-1β pathway is upregulated, and previous studies using mouse models of founder MDS mutations demonstrated that it enhances hematopoietic stem and progenitor cells’ (HSPCs’) aberrant differentiation towards the myeloid lineage at the expense of erythropoiesis.
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Sep 23, 2024 |
nature.com | Enbo Zhu |Jiaji Yu |Yan-Ruide Li |Feiyang Ma |Yang Liu |James Brown | +2 more
AbstractChimeric antigen receptor (CAR)-engineered T cells represent a front-line therapy for cancers. However, the current CAR T cell manufacturing protocols do not adequately reproduce immunological synapse formation. Here, in response to this limitation, we have developed a flexible graphene oxide antigen-presenting platform (GO-APP) that anchors antibodies onto graphene oxide.
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Aug 21, 2024 |
digitalcommons.library.tmc.edu | Juan José Rodríguez-Sevilla |Irene Ganan-Gomez |Feiyang Ma |Kelly S. Chien
The molecular mechanisms of venetoclax-based therapy failure in patients with acute myeloid leukemia were recently clarified, but the mechanisms by which patients with myelodysplastic syndromes (MDS) acquire secondary resistance to venetoclax after an initial response remain to be elucidated.
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Mar 18, 2024 |
nature.com | Feiyang Ma |Kelly S. Chien |Sanam Loghavi |Guillermo Montalban-Bravo |Vera Adema |Rashmi Kanagal-Shamanna | +2 more
AbstractThe molecular mechanisms of venetoclax-based therapy failure in patients with acute myeloid leukemia were recently clarified, but the mechanisms by which patients with myelodysplastic syndromes (MDS) acquire secondary resistance to venetoclax after an initial response remain to be elucidated.
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