1 alpha,25-dihydroxyvitamin D3 transrepresses retinoic acid transcriptional activity via vitamin D receptor in myeloid cells.

Granulocytes and monocytes originate from a common committed progenitor cell. Commitment to either granulocytic or monocytic lineage is triggered by specific extracellular signals involving cytokines or nuclear receptor ligands (all-trans-retinoic acid (RA) and 1 alpha,25-dihydroxyvitamin D(3)). Here we show that the stimulatory effect of 1 alpha,25-dihydroxyvitamin D(3) on the production of monocytic colonies (CFU-M) is accompanied by a repression of granulocytic colony (CFU-G) production.

Proton nuclear magnetic resonance spectroscopy reveals cellular lipids involved in resistance to adriamycin and taxol by the K562 leukemia cell line.

Proton nuclear magnetic resonance spectroscopy was performed on whole cells to study lipids and metabolites in Adriamycin- and Taxol-resistant K562 cells expressing multidrug resistance (MDR) and their sensitive counterparts. With one-dimensional spectra, both resistant cell lines showed lower fatty acid methylene:methyl ratios and higher choline:methyl ratios than sensitive cells. Using two-dimensional COSY spectra, a decrease in the glutamine content was evidenced in resistant cells.

In vitro treatment with retinoids or the topoisomerase inhibitor, VP-16, evidences different functional apoptotic pathways in acute promyelocytic leukemic cells.

Understanding the mechanisms inherent to malignant cell eradication is a major determinant for cancer therapy. Recent data have demonstrated that apoptosis may be one of the mechanisms through which both cytotoxic and differentiating drugs may eliminate malignant cells. Treatment of acute promyelocytic leukemia (APL) by all-trans retinoic acid (ATRA) is the first model of differentiation therapy allowing achievement of more than 90% complete remission (CR).

Selective induction of apoptosis in myeloid leukemic cell lines by monoacetone glucose-3 butyrate.

Butyric acid is a potent cell growth inhibitor and differentiation inducer. Our previous studies have shown that MAG=3but, a monosaccharide ester of butyric acid, used at 1 mM, induces apoptosis in the HL-60 cell line. We report here that this drug can also induce apoptosis in the U-937 leukemic cell lines whereas the myeloblastic KG1 and the NB4 promyelocytic leukemic cell lines were refractory to induction of apoptosis.

Butyric acid and its monosaccharide ester induce apoptosis in the HL-60 cell line.

Butyric acid is a potent cell growth inhibitor and differentiation inducer (1-4). However, the short plasma half-life of this fatty acid limits its potential therapeutic use (5,6). The recent synthesis of several monosaccharide esters of butyric sodium salt (BuONa) with a prolonged plasma half-life and similar biological properties as the sodium salt opens new perspectives (7-12).