S. Colla

Clonal evolution of hematopoietic stem cells after cancer chemotherapy

This study examines how chemotherapy affects clonal diversity and mutation patterns in hematopoietic stem cells, finding that melphalan increases mutational burden and promotes clonal aging, potentially leading to therapy-related myeloid neoplasms.

IL-1B-mediated inflammatory signaling drives ineffective erythropoiesis in early-stage myelodysplastic syndromes

This study shows that IL-1B-mediated inflammation drives ineffective erythropoiesis in early-stage MDS and that canakinumab can reduce transfusion dependence in patients with DNMT3A and TET2 mutations.

Hematopoietic Stem Cells Undergo Differentiation State Reprogramming to Overcome Venetoclax Sensitivity in Patients with Myelodysplastic Syndromes

This study shows MDS hematopoietic stem cells reprogram their differentiation state to bypass venetoclax sensitivity through genetic mutations and transcriptional changes.

Targeting MCL1-driven anti-apoptotic pathways to overcome hypomethylating agent resistance in RAS-mutated chronic myelomonocytic leukemia

This study identifies MCL1 as a survival factor in RAS-mutated CMML, explaining resistance to BCL2 inhibitors and suggesting new therapeutic targets.

Targeting DNA2 Overcomes Metabolic Reprogramming in Multiple Myeloma

This study identifies DNA2 as a key factor in mitochondrial metabolism that enables multiple myeloma cells to survive DNA damage, showing that targeting DNA2 overcomes metabolic reprogramming and enhances therapy effectiveness.

STAT3 protects HSCs from intrinsic interferon signaling and loss of long-term blood-forming activity

This study shows that STAT3 is essential for maintaining hematopoietic stem cell function by suppressing interferon signaling and myeloid skewing, and its loss leads to impaired hematopoietic activity.

Telomere dysfunction impairs intestinal differentiation andpredisposes to diet-induced colitis

This study shows that telomere shortening impairs intestinal differentiation, leading to barrier defects and diet-induced colitis through microbiome modulation and nutrient flux.