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Hamid Morjani

Researcher at University of Reims Champagne-Ardenne

Publications -  138
Citations -  3515

Hamid Morjani is an academic researcher from University of Reims Champagne-Ardenne. The author has contributed to research in topics: Apoptosis & Chemistry. The author has an hindex of 29, co-authored 115 publications receiving 2929 citations. Previous affiliations of Hamid Morjani include Centre national de la recherche scientifique.

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Telomestatin-induced Telomere Uncapping Is Modulated by POT1 through G-overhang Extension in HT1080 Human Tumor Cells

TL;DR: Results suggest that telomestatin induced a telomere dysfunction in which G-overhang length and POT1 level are important factors but also suggest the presence of additional DNA sites of action for the ligand.
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Overcoming MDR-associated chemoresistance in HL-60 acute myeloid leukemia cells by targeting sphingosine kinase-1.

TL;DR: F-12509a, a new sphingosine kinase inhibitor, induced classical apoptosis hallmarks namely nuclear fragmentation, caspase-3 cleavage as well as downregulation of antiapoptotic XIAP, and release of cytochrome c and SMAC/Diablo.
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Selective analysis of antitumor drug interaction with living cancer cells as probed by surface-enhanced Raman spectroscopy.

TL;DR: The ability to detect SERS signals from very dilute solutions of doxorubicin or adriamycin (DOX), and 4′O-tetrahydropyranyl-adriamicin (THP-ADM), as well as from their complexes with targets in vitro and in vivo, has been demonstrated.
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MRP3, BCRP, and P-Glycoprotein Activities are Prognostic Factors in Adult Acute Myeloid Leukemia

TL;DR: BCRP and MRP3 may also be involved in chemoresistance in AML, especially MRp3 in patients with M5 FAB, and additional modulation of BCRP or MRP2 to Pgp modulation may be necessary in some patients in order to improve the treatment outcome.
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Mechanism of acridine-based telomerase inhibition and telomere shortening.

TL;DR: It is shown that BRACO-19 produces short- and long-term growth arrest in cancer cell lines, and is significantly less potent in a normal cell line, and the cellular activity can be ascribed both to the uncapping of 3' telomere ends and toTelomere shortening that may preferentially affect cells with short telomeres.