ANGPTL2-Containing Small Extracellular Vesicles from Vascular Endothelial Cells Accelerate Leukemia Progression

The authors used seven cell-type specific mouse Cre lines to conditionally knockout Vps33b in Cdh5+ or Tie2+ endothelial cells, Lepr+ bone marrow perivascular cells, Osx+ osteo-progenitor cells, Pf4+ megakaryocytes and Tcf21+ spleen stromal cells.
[Journal of Clinical Investigation]
Huang, D., Sun, G., Hao, X., He, X., Zheng, Z., Chen, C., Yu, Z., Xie, L., Ma, S., Liu, L., Zhou, B. O., Cheng, H., Zheng, J., & Cheng, T. (2020). ANGPTL2-containing small extracellular vesicles from vascular endothelial cells accelerate leukemia progression. The Journal of Clinical Investigation. https://doi.org/10.1172/JCI138986 Cite
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Extinguishing the Embers: Targeting AML Metabolism

The authors detail the metabolic features of leukemic stem cells (LSCs) and how these characteristics promote resistance to traditional chemotherapy. They also discuss new therapeutic approaches that target metabolic vulnerabilities of LSC to selectively eradicate them.
[Trends in Molecular Medicine]
Culp-Hill, R., D’Alessandro, A., & Pietras, E. M. (2020). Extinguishing the Embers: Targeting AML Metabolism. Trends in Molecular Medicine, 0(0). https://doi.org/10.1016/j.molmed.2020.10.001 Cite
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Sumitomo Dainippon Pharma Oncology Announces First Patient Dosed in the Dubermatinib Arm of The Leukemia & Lymphoma Society’s Beat AML Master Clinical Trial in Patients with Acute Myeloid Leukemia

Sumitomo Dainippon Pharma Oncology, Inc. announced the first patient has been dosed in a Phase Ib/II study evaluating the oral investigational agent, dubermatinib, an AXL kinase inhibitor, in combination with decitabine, in patients 60 years or older with newly diagnosed acute myeloid leukemia who have TP53 mutations and/or complex karyotype.
[Sumitomo Dainippon Pharma Oncology, Inc.]
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Fatty Acid Metabolism Underlies Venetoclax Resistance in Acute Myeloid Leukemia Stem Cells

Scientists demonstrated that resistance to venetoclax with azacitidine occurs via upregulation of fatty acid oxidation, which occurs either due to RAS pathway mutations or as a compensatory adaptation in relapsed disease.
[Nature Cancer]
Stevens, B. M., Jones, C. L., Pollyea, D. A., Culp-Hill, R., D’Alessandro, A., Winters, A., Krug, A., Abbott, D., Goosman, M., Pei, S., Ye, H., Gillen, A. E., Becker, M. W., Savona, M. R., Smith, C., & Jordan, C. T. (2020). Fatty acid metabolism underlies venetoclax resistance in acute myeloid leukemia stem cells. Nature Cancer, 1–12. https://doi.org/10.1038/s43018-020-00126-z Cite
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A Trispecific Killer Engager Molecule Against CLEC12A Effectively Induces NK-Cell Mediated Killing of AML Cells

To target acute myeloid leukemia blasts and leukemic stem cells using natural killer (NK) cells, scientists developed a trispecific killer engager molecule containing a humanized anti-CD16 heavy chain camelid single-domain antibody that activates NK cells.
[Leukemia]
Arvindam, U. S., van Hauten, P. M. M., Schirm, D., Schaap, N., Hobo, W., Blazar, B. R., Vallera, D. A., Dolstra, H., Felices, M., & Miller, J. S. (2020). A trispecific killer engager molecule against CLEC12A effectively induces NK-cell mediated killing of AML cells. Leukemia, 1–11. https://doi.org/10.1038/s41375-020-01065-5 Cite
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Antileukemic Activity of the VPS34-IN1 Inhibitor in Acute Myeloid Leukemia

Using a recently developed specific inhibitor, the authors found that vacuolar protein sorting 34 inhibition induces apoptosis in acute myeloid leukemia cells but not in normal CD34+ hematopoietic cells.
[Oncogenesis]
Meunier, G., Birsen, R., Cazelles, C., Belhadj, M., Cantero-Aguilar, L., Kosmider, O., Fontenay, M., Azar, N., Mayeux, P., Chapuis, N., Tamburini, J., & Bouscary, D. (2020). Antileukemic activity of the VPS34-IN1 inhibitor in acute myeloid leukemia. Oncogenesis, 9(10), 1–14. https://doi.org/10.1038/s41389-020-00278-8 Cite
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HTLV-1 Targets Human Placental Trophoblasts in Seropositive Pregnant Women

Investigators found that human T cell leukemia virus type 1 proviral DNA was present in the placental villous tissues of the fetuses of nearly half of pregnant carriers and in a small number of cord blood samples.
[Journal of Clinical Investigation]
Tezuka, K., Fuchi, N., Okuma, K., Tsukiyama, T., Miura, S., Hasegawa, Y., Nagata, A., Komatsu, N., Hasegawa, H., Sasaki, D., Sasaki, E., Mizukami, T., Kuramitsu, M., Matsuoka, S., Yanagihara, K., Miura, K., & Hamaguchi, I. (2020). HTLV-1 targets human placental trophoblasts in seropositive pregnant women. The Journal of Clinical Investigation, 130(11). https://doi.org/10.1172/JCI135525 Cite
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BCL11B Suppresses Tumor Progression and Stem Cell Traits in Hepatocellular Carcinoma by Restoring p53 Signaling Activity

In vitro and in vivo experiments confirmed BCL11B as a tumor suppressor in hepatocellular carcinoma with inhibitory effects on proliferation, cell cycle progression, apoptosis, and mobility.
[Cell Death & Disease]
Yang, W.-J., Sun, Y.-F., Jin, A.-L., Lv, L.-H., Zhu, J., Wang, B.-L., Zhou, Y., Zhang, C.-Y., Wang, H., Hu, B., Wang, P.-X., Te, L., Pan, B.-S., Zhou, J., Fan, J., Yang, X.-R., & Guo, W. (2020). BCL11B suppresses tumor progression and stem cell traits in hepatocellular carcinoma by restoring p53 signaling activity. Cell Death & Disease, 11(10), 1–13. https://doi.org/10.1038/s41419-020-03115-3 Cite
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Agios Announces Withdrawal of European Marketing Authorization Application for TIBSOVO® as a Treatment for Relapsed or Refractory IDH1-mutant Acute Myeloid Leukemia

Agios Pharmaceuticals, Inc. announced the withdrawal of its European Marketing Authorization Application for TIBSOVO® for the treatment of adult patients with relapsed or refractory acute myeloid leukemia with an isocitrate dehydrogenase-1 mutation.
[Agios Pharmaceuticals, Inc]
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Repolarization of HSC Attenuates HSCs Failure in Shwachman–Diamond Syndrome

The authors report that primitive hematopoietic cells from Shwachman–Diamond syndrome patients present with a reduced activity of the small RhoGTPase Cdc42 and concomitantly a reduced frequency of HSCs polar for polarity proteins.
[Leukemia]
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Consequences of Zmat3 Loss in c-MYC– and Mutant KRAS-Driven Tumorigenesis

To investigate which oncogenic drivers co-operate with Zmat3 loss to promote neoplastic transformation, researchers utilized Zmat3 knockout mice in models of c-MYC-driven lymphomagenesis and KrasG12D-driven lung adenocarcinoma development.
[Cell Death & Disease]
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