Rafael Pharmaceuticals Crosses Enrollment of 150 Patients in Pivotal Phase III Trial (ARMADA 2000) of CPI-613® (Devimistat) for Relapsed or Refractory Acute Myeloid Leukemia (AML)

Rafael Pharmaceuticals, Inc. announced that it has crossed the enrollment of 150 patients in its Phase III clinical trial for patients with relapsed or refractory AML.
[Rafael Pharmaceuticals, Inc. (GlobeNewswire, Inc.)]
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WPD Pharmaceuticals Announces Amended Sublicense Agreement with Moleculin Biotech for WP1066, WP1122 and Annamycin Drug Candidates

WPD Pharmaceuticals Inc. announced that is has entered into an amended and restated sublicense agreement with Moleculin Biotech, Inc.
[WPD Pharmaceuticals, Inc.]
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HOXBLINC Long Non-Coding RNA Activation Promotes Leukemogenesis in NPM1-Mutant Acute Myeloid Leukemia

Scientists showed that the activation of HOXBLINC, a HOXB locus-associated long non-coding RNA, was a critical downstream mediator of NPM1c+-associated leukemic transcription program and leukemogenesis.
[Nature Communications]
Zhu, G., Luo, H., Feng, Y., Guryanova, O. A., Xu, J., Chen, S., Lai, Q., Sharma, A., Xu, B., Zhao, Z., Feng, R., Ni, H., Claxton, D., Guo, Y., Mesa, R. A., Qiu, Y., Yang, F.-C., Li, W., Nimer, S. D., … Xu, M. (2021). HOXBLINC long non-coding RNA activation promotes leukemogenesis in NPM1-mutant acute myeloid leukemia. Nature Communications, 12(1), 1956. https://doi.org/10.1038/s41467-021-22095-2 Cite
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YBX1 Is Required for Maintaining Myeloid Leukemia Cell Survival by Regulating BCL2 Stability in an m6A-Dependent Manner

Investigators showed that YBX1 was specifically required for maintaining myeloid leukemia cell survival in an m6A-dependent manner.
[Blood]
Feng, M., Xie, X., Han, G., Zhang, T., Li, Y., Li, Y., Yin, R., Wang, Q., Zhang, T., Wang, P., Hu, J., Cheng, Y., Gao, Z., Wang, J., Chang, J., Cui, M., Gao, K., Chai, J., Liu, W., … Zhang, H. (2021). YBX1 is required for maintaining myeloid leukemia cell survival by regulating BCL2 stability in an m6A-dependent manner. Blood, blood.2020009676. https://doi.org/10.1182/blood.2020009676 Cite
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Ddx41 Inhibition of DNA Damage Signaling Permits Erythroid Progenitor Expansion in Zebrafish

Researchers demonstrated that loss of DEAD-box Helicase 41 (ddx41) led to anemia caused by diminished proliferation and defective differentiation of erythroid progenitors.
[Haematologica]
Weinreb, J. T., Gupta, V., Sharvit, E., Weil, R., & Bowman, T. V. (2020). Ddx41 inhibition of DNA damage signaling permits erythroid progenitor expansion in zebrafish. Haematologica. https://doi.org/10.3324/haematol.2020.257246 Cite
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Endothelial Jak3 Expression Enhances Pro-Hematopoietic Angiocrine Function in Mice

Scientists showed that Jak3 was expressed in endothelial cells across hematopoietic and non-hematopoietic organs, with heightened expression in the bone marrow.
[Communications Biology]
Barcia Durán, J. G., Lu, T., Houghton, S., Geng, F., Schreiner, R., Xiang, J., Rafii, S., Redmond, D., & Lis, R. (2021). Endothelial Jak3 expression enhances pro-hematopoietic angiocrine function in mice. Communications Biology, 4(1), 1–14. https://doi.org/10.1038/s42003-021-01846-3 Cite
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Targeting the AnxA1/Fpr2/ALX Pathway Regulates Neutrophil Function, Promoting Thromboinflammation Resolution in Sickle Cell Disease

Administration of annexin A1 mimetic peptide AnxA1Ac2-26 ameliorated cerebral thrombotic responses in sickle transgenic mice via regulation of the FPR2/ALX pathway.
[Blood]
Ansari, J., Senchenkova, E. Y., Vital, S. A., Al-Yafeai, Z., Kaur, G., Sparkenbaugh, E. M., Orr, A. W., Pawlinski, R., Hebbel, R. P., Granger, D. N., Kubes, P., & Gavins, F. N. E. (2021). Targeting the AnxA1/Fpr2/ALX pathway regulates neutrophil function, promoting thromboinflammation resolution in sickle cell disease. Blood, 137(11), 1538–1549. https://doi.org/10.1182/blood.2020009166 Cite
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New ASH Research Restart Award to Help Ensure Research Continuity and Workforce Stability during Pandemic

The American Society of Hematology announced the names of 19 talented early-career investigators who will receive critical funding to support their resumption of research that was paused amid pandemic-related shutdowns and uncertainty.
[Amercian Society of Hematology]
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Chronic Infection Drives Dnmt3a-Loss-of-Function Clonal Hematopoiesis via IFNγ Signaling

Scientists created Dnmt3a-mosaic mice by transplanting Dnmt3a−/− and WT HSCs into WT mice and observed the substantial expansion of Dnmt3a−/− HSCs during chronic mycobacterial infection.
[Cell Stem Cell]
Hormaechea-Agulla, D., Matatall, K. A., Le, D. T., Kain, B., Long, X., Kus, P., Jaksik, R., Challen, G. A., Kimmel, M., & King, K. Y. (2021). Chronic infection drives Dnmt3a-loss-of-function clonal hematopoiesis via IFNγ signaling. Cell Stem Cell, 0(0). https://doi.org/10.1016/j.stem.2021.03.002 Cite
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Multistage Feedback Driven Compartmental Dynamics of Hematopoiesis

To characterize the dynamics following different types of perturbations, researchers investigated a model representing hematopoiesis as a sequence of compartments covering all maturation stages- from stem to mature cells- where feedback regulated cell production to ongoing necessities.
[iScience]
Père, N. V. M., Lenaerts, T., Pacheco, J. M. dos S., & Dingli, D. (2021). Multistage feedback driven compartmental dynamics of hematopoiesis. IScience, 0(0). https://doi.org/10.1016/j.isci.2021.102326 Cite
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CCR5 Maintains Macrophages in the Bone Marrow and Drives Hematopoietic Failure in a Mouse Model of Severe Aplastic Anemia

IFNγ was required for increased expression of the chemokine receptor CCR5 on MΦs. CCR5 antagonism in murine SAA improved survival, correlating with increased platelets and significantly increased platelet-biased CD41hi HSCs.
[Leukemia]
Seyfried, A. N., McCabe, A., Smith, J. N. P., Calvi, L. M., & MacNamara, K. C. (2021). CCR5 maintains macrophages in the bone marrow and drives hematopoietic failure in a mouse model of severe aplastic anemia. Leukemia, 1–13. https://doi.org/10.1038/s41375-021-01219-z Cite
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