The Hepatic Microenvironment Uniquely Protects Leukemia Cells through Induction of Growth and Survival Pathways Mediated by LIPG

Scientists demonstrated a unique role for liver in modulating the pathogenesis of leukemic disease and suggest that the hepatic microenvironment may protect leukemia cells from chemotherapeutic challenge.
[Cancer Discovery]
The hepatic microenvironment uniquely protects leukemia cells through induction of growth and survival pathways mediated by LIPG | Cancer Discovery. (n.d.). Retrieved October 13, 2020, from https://cancerdiscovery.aacrjournals.org/content/early/2020/10/07/2159-8290.CD-20-0318 Cite
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Biologically Synthesized of Au/Pt/ZnO Nanoparticles Using Arctium lappa Extract and Cytotoxic Activity against Leukemia

Investigators assessed the cytotoxicity of Au/Pt/ZnO nanoparticles by means of MTT assay, and analyzed apoptosis as well as the influence of the cultivation time and concentration of Au/Pt/ZnO nanoparticles on the percentage of dead cells.
[Biomedical Microdevices]
Dobrucka, R., Romaniuk-Drapała, A., & Kaczmarek, M. (2020). Biologically synthesized of Au/Pt/ZnO nanoparticles using Arctium lappa extract and cytotoxic activity against leukemia. Biomedical Microdevices, 22(4), 72. https://doi.org/10.1007/s10544-020-00526-z Cite
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TGFβR-SMAD3 Signaling Induces Resistance to PARP Inhibitors in the Bone Marrow Microenvironment

Scientists identified a constitutive mechanism of resistance to PARP inhibitor (PARPi). They report that the bone marrow microenvironment facilitates DNA double-strand break repair activity in leukemia cells to protect them against PARPi-mediated synthetic lethality.
[Cell Reports]
Le, B. V., Podszywalow-Bartnicka, P., Maifrede, S., Sullivan-Reed, K., Nieborowska-Skorska, M., Golovine, K., Yao, J.-C., Nejati, R., Cai, K. Q., Caruso, L. B., Swatler, J., Dabrowski, M., Lian, Z., Valent, P., Paietta, E. M., Levine, R. L., Fernandez, H. F., Tallman, M. S., Litzow, M. R., … Skorski, T. (2020). TGFβR-SMAD3 Signaling Induces Resistance to PARP Inhibitors in the Bone Marrow Microenvironment. Cell Reports, 33(1). https://doi.org/10.1016/j.celrep.2020.108221 Cite
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Activation of CpG-Rich Promoters Mediated by MLL Drives MOZ-Rearranged Leukemia

The authors describe the circuitry of a transactivation system responsible for oncogenic self-renewal. MLL recruited RNA polymerase II to unmethylated CpG-rich promoters by its CXXC domain and activated transcription by transcriptional regulators, including the AF4 family/ENL family/P-TEFb complex, DOT1L, and p300/CBP histone acetyl transferases.
[Cell Reports]
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Cellular and Molecular Aspects of Anti-Melanoma Effect of Minocycline—A Study of Cytotoxicity and Apoptosis on Human Melanotic Melanoma Cells

Scientists investigated the potential and mechanisms of anti-melanoma action of minocycline.
[International Journal of Molecular Sciences]
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Multi-Omics Analyses Identify HSD17B4

HSD17B4 was highly expressed in the vast majority of human cancers, and its methylation was present only in breast cancers and one lymphoblastic leukemia cell line.
[Scientific Reports]
Yamashita, S., Hattori, N., Fujii, S., Yamaguchi, T., Takahashi, M., Hozumi, Y., Kogawa, T., El-Omar, O., Liu, Y.-Y., Arai, N., Mori, A., Higashimoto, H., Ushijima, T., & Mukai, H. (2020). Multi-omics analyses identify HSD17B4 methylation-silencing as a predictive and response marker of HER2-positive breast cancer to HER2-directed therapy. Scientific Reports, 10(1), 15530. https://doi.org/10.1038/s41598-020-72661-9 Cite
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Covalent Inhibition of NSD1 Histone Methyltransferase

Compound BT5 demonstrated on-target activity in NUP98-NSD1 leukemia cells, including inhibition of histone H3 lysine 36 dimethylation and downregulation of target genes, and impaired colony formation in an NUP98-NSD1 patient sample.
[Nature Chemical Biology]
Huang, H., Howard, C. A., Zari, S., Cho, H. J., Shukla, S., Li, H., Ndoj, J., González-Alonso, P., Nikolaidis, C., Abbott, J., Rogawski, D. S., Potopnyk, M. A., Kempinska, K., Miao, H., Purohit, T., Henderson, A., Mapp, A., Sulis, M. L., Ferrando, A., … Cierpicki, T. (2020). Covalent inhibition of NSD1 histone methyltransferase. Nature Chemical Biology, 1–8. https://doi.org/10.1038/s41589-020-0626-6 Cite
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CARD8 Inflammasome Activation Triggers Pyroptosis in Human T Cells

Investigators showed that blocking dipeptidyl‐peptidases using Val‐boroPro triggers a lytic form of cell death in primary human CD4 and CD8 T cells, while other prototypical inflammasome stimuli were not active.
[EMBO Journal]
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T Cell Exhaustion and a Failure in Antigen Presentation Drive Resistance to the Graft-versus-Leukemia Effect

Investigators report that graft-versus-leukemia failed due to insufficient H60 presentation and T cell exhaustion. Leukemia-derived H60 was inefficiently cross-presented whereas direct T cell recognition of leukemia cells intensifies exhaustion.
[Nature Communications]
Zhou, M., Sacirbegovic, F., Zhao, K., Rosenberger, S., & Shlomchik, W. D. (2020). T cell exhaustion and a failure in antigen presentation drive resistance to the graft-versus-leukemia effect. Nature Communications, 11(1), 4227. https://doi.org/10.1038/s41467-020-17991-y Cite
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LW-213 Induces Cell Apoptosis in Human Cutaneous T-cell Lymphomas by Activating PERK–eIF2α–ATF4–CHOP Axis

Researchers showed that LW-213 dose-dependently inhibited human cutaneous T-cell lymphoma cell lines with IC50 values of around 10 μM, meanwhile it potently inhibited primary leukemia cells derived from peripheral blood of T-cell lymphoma patients.
[Acta Pharmacologica Sinica]
Yu, X., Zhu, M., Wang, J., Li, H., Hu, P., Qing, Y., Wang, X., Wang, H., Wang, Z., Xu, J., Guo, Q., & Hui, H. (2020). LW-213 induces cell apoptosis in human cutaneous T-cell lymphomas by activating PERK–eIF2α–ATF4–CHOP axis. Acta Pharmacologica Sinica, 1–11. https://doi.org/10.1038/s41401-020-0466-7 Cite
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Polymethine Dye-Functionalized Nanoparticles for Targeting CML Stem Cells

Researchers investigated the uptake behavior of various polymethine dyes on leukemia cell lines and searched for carrier proteins that guide dye transport using RNA interference.
[Molecular Therapy-Oncolytics]
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