Osteogenic osteosarcoma: a model of curable disease by multidiscipIinary approach of treatment

Delepine, N.; Delépine, G.; Jc, Desbois; Cornille, H.; Jasmin, C

doi:10.1016/0753-3322(90)90148-3

Cited by 4 publications

(2 citation statements)

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“…The effective antiproliferative concentration of QB is within the concentration range of established anticancer drugs routinely used for treatment of patients. Namely, methotrexate, when used as part of a combination therapy (for acute lymphoblastic leukemia, non-Hodgkin lymphoma, or osteosarcoma), is administered at a high dose (e.g., to overcome the mechanisms of cellular resistance), peak methotrexate plasma concentration can reach C max values >1000 μM in 96% of patients. , …”

Section: Resultsmentioning

confidence: 99%

“…Namely, methotrexate, when used as part of a combination therapy (for acute lymphoblastic leukemia, non-Hodgkin lymphoma, or osteosarcoma), is administered at a high dose (e.g., to overcome the mechanisms of cellular resistance), peak methotrexate plasma concentration can reach C max values >1000 μM in 96% of patients. 38,39 As a side effect of chemotherapy, the destruction of bone marrow structure is observed, affecting the production of new blood cells and therefore reducing white blood cell counts. 40−42 Obviously, there is a need for new drugs with limited toxicity toward hematopoiesis.…”

Section: ■ Results and Discussionmentioning

confidence: 99%

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Quambalarine B, a Secondary Metabolite from Quambalaria cyanescens with Potential Anticancer Properties

et al. 2016

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Quambalarine B (QB) is a secondary metabolite produced by the basidiomycete Quambalaria cyanescens with potential anticancer activity. Here we report that QB at low micromolar concentration inhibits proliferation of several model leukemic cell lines (Jurkat, NALM6, and REH), whereas higher concentrations induce cell death. By contrast, the effect of QB on primary leukocytes (peripheral blood mononuclear cells) is significantly milder with lower toxicity and cytostatic activity. Moreover, QB inhibited expression of the C-MYC oncoprotein and mRNA expression of its target genes, LDHA, PKM2, and GLS. Finally, QB blocked the phosphorylation of P70S6K, a downstream effector kinase in mTOR signaling that regulates translation of C-MYC. This observation could explain the molecular mechanism behind the antiproliferative and cytotoxic effects of QB on leukemic cells. Altogether, our results establish QB as a promising molecule in anticancer treatment.

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Section: Resultsmentioning

confidence: 99%

Section: ■ Results and Discussionmentioning

confidence: 99%