Vera Adema

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.

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.

Aug 21, 2024 | digitalcommons.library.tmc.edu | Juan José Rodríguez-Sevilla |Vera Adema |Guillermo Garcia-Manero |Simona Colla

Home > UTHealth > GSBS > Journal Articles > 518 Cell Reports Medicine myelodysplastic syndromes, hypomethylating agents, secondary acute myeloid leukemia, novel therapeutic agents DOWNLOADS Included in Bioinformatics Commons, Biological Phenomena, Cell Phenomena, and Immunity Commons, Biomedical Informatics Commons, Medical Cell Biology Commons, Oncology Commons COinS...

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.

Feb 7, 2024 | nature.com | Feiyang Ma |Natalia Baran |Jintan Liu |Ken Furudate |Paola Storti |Irene Ganan-Gomez | +10 more

AbstractDNA damage resistance is a major barrier to effective DNA-damaging therapy in multiple myeloma (MM). To discover mechanisms through which MM cells overcome DNA damage, we investigate how MM cells become resistant to antisense oligonucleotide (ASO) therapy targeting Interleukin enhancer binding factor 2 (ILF2), a DNA damage regulator that is overexpressed in 70% of MM patients whose disease has progressed after standard therapies have failed.