Scientists hypothesized that targeted hyperactivation of the phosphatidylinositol-3-phosphate/AKT (PI3K/AKT)-signaling pathway may have been leveraged to trigger chronic lymphocytic leukemia cell death.
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The authors reported that cabozantinib could promote differentiation in erythroid leukemia cells and found that K562 erythroid leukemia cells treated with 1 μM cabozantinib for 72 hours underwent erythroid lineage differentiation.
[Cancer Gene Therapy]
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Investigators discovered that FLT3-ITD, one of the most frequent mutations in acute myeloid leukemia, was S-palmitoylated by the ZDHHC6 palmitoyl acyltransferase. Disruption of palmitoylation redirected FLT3-ITD to the plasma membrane and rewired its downstream signaling by activating AKT and ERK pathways in addition to STAT5.
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Rigosertib monotherapy or in combination therapy with immune checkpoint blockade were investigated using immunocompetent mouse models of BRAFwt and BRAFmut melanoma and analyzed in reference to patient data.
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Yan, C., Saleh, N., Yang, J., Nebhan, C. A., Vilgelm, A. E., Reddy, E. P., Roland, J. T., Johnson, D. B., Chen, S.-C., Shattuck-Brandt, R. L., Ayers, G. D., & Richmond, A. (2021). Novel induction of CD40 expression by tumor cells with RAS/RAF/PI3K pathway inhibition augments response to checkpoint blockade. Molecular Cancer, 20(1), 85. https://doi.org/10.1186/s12943-021-01366-y Cite
Investigators studied effects of recombinant D-dopachrome tautomerase (DDT) on cell proliferation and survival by clonogenic assay and annexin V-PI staining respectively. DDT-induced signaling was investigated by Western blot.
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Song, S., Liu, B., Habibie, H., Bor, J. van den, Smit, M. J., Gosens, R., Wu, X., Brandsma, C.-A., Cool, R. H., Haisma, H. J., Poelarends, G. J., & Melgert, B. N. (2021). D-dopachrome tautomerase contributes to lung epithelial repair via atypical chemokine receptor 3-dependent Akt signaling. EBioMedicine, 68. https://doi.org/10.1016/j.ebiom.2021.103412 Cite
The authors investigated the mechanisms of action of long non-coding RNA Bmp1 on damaged intestinal mucosa. They found that Bmp1 was increased in damaged intestinal mucosal tissue and Bmp1 overexpression was able to alleviate intestinal mucosal injury.
[Cell Death & Disease]
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DDR1 knockdown and DDR1 pharmacological inhibitor decreased cell growth and inhibited cell cycle progression in breast cancer cell lines, while enhanced the sensitivity of PIK3CA/AKT1 mutant cells to palbociclib.
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Investigators showed that gilteritinib and CUDC-907, a dual inhibitor of PI3K and histone deacetylases, synergistically induced apoptosis in FMS-like tyrosine kinase 3 (FLT3)-internal tandem duplication (ITD) acute myeloid leukemia (AML) cell lines and primary patient samples and had striking in vivo efficacy.
[Blood Cancer Journal]
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Researchers showed that conditional knockout of the demethylase Alkbh5 in bone marrow MSCs strengthened bone mass in mice.
[Cell Death & Disease]
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Scientists applied an oncogene-associated, multicolor reporter mouse model to the small intestine to show that oncogene-expressing mutant crypts altered the cellular organization of neighbouring wild-type crypts, thereby driving accelerated clonal drift.
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By probing a number of kinases downstream of integrin-β1, scientists determined that PI3K inhibition with either a tool compounds or a compound in clinical trials robustly sensitizes quiescent breast tumor cells seeded in organotypic bone marrow cultures to chemotherapy.
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