Blinatumomab + ponatinib for relapsed/refractory Philadelphia chromosome-positive acute lymphoblastic leukemia in adults.

We retrospectively examined the results of a new chemo-free approach combining blinatumomab with ponatinib (blina/pona) in 26 relapsed/refractory Philadelphia positive (Ph+) acute lymphoblastic leukemia (ALL) patients. All but one achieved complete morphologic remission, and 23 achieved a complete molecular response. With a median follow-up of 34.

Late molecular recurrences in patients with chronic myeloid leukemia experiencing treatment-free remission.

Treatment-free remission (TFR) is an opportunity for patients with chronic myeloid leukemia (CML). Reported cumulative incidence curves of molecular recurrence (MRec) arbor a 2-phase shape with mainly early events, but also some late events (late MRec [LMRec]). Having discontinued our first patient in 2004, we have access to a prolonged follow-up, enabling us to characterize these late events.

Highlighting the Potency of Biosurfactants Produced by Strains as Anti- Agents.

, the causative agent of Legionnaires' disease, is a waterborne bacterium mainly found in man-made water systems in close association with free-living amoebae and multispecies biofilms. strains, originating from various environments including freshwater systems or isolated from hospitalized patients, were tested for their antagonistic activity towards . A high amount of tested strains was thus found to be active.

Specific Anti-Leukemic Activity of the Peptide Warnericin RK and Analogues and Visualization of Their Effect on Cancer Cells by Chemical Raman Imaging.

Antimicrobial peptides can be used as therapeutic agents against cancer cells. Warnericin RK and derivatives (WarnG20D and WarnF14V) were tested on various, solid tumor or leukemia, cancer cells. These peptides appeared to be cytotoxic on all the cell types tested, cancerous as well healthy, but very interestingly displayed no deleterious effect on healthy mononuclear cells.

Legionella pneumophila: The Paradox of a Highly Sensitive Opportunistic Waterborne Pathogen Able to Persist in the Environment.

Legionella pneumophila, the major causative agent of Legionnaires' disease, is found in freshwater environments in close association with free-living amoebae and multispecies biofilms, leading to persistence, spread, biocide resistance, and elevated virulence of the bacterium. Indeed, legionellosis outbreaks are mainly due to the ability of this bacterium to colonize and persist in water facilities, despite harsh physical and chemical treatments. However, these treatments are not totally efficient and, after a lag period, L.

New therapeutic approaches in myelodysplastic syndromes: Hypomethylating agents and lenalidomide.

Recent advances in the treatment of myelodysplastic syndromes have come from the use of the hypomethylating agents decitabine and azacitidine as well as the immunomodulatory drug lenalidomide. Their clinical benefit has been demonstrated by randomized phase III clinical trials, mostly in high-risk and del(5q) myelodysplastic syndromes, respectively. Neither drug, however, appears to eradicate myelodysplastic stem cells, and thus they currently do not represent curative options.

Effect of amino acid substitution in the staphylococcal peptides warnericin RK and PSMα on their anti-Legionella and hemolytic activities.

Warnericin RK from Staphylococcus warneri and PSMα from Staphylococcus epidermidis are anti-Legionella peptides which were differently classified in a previous study according to their mode of action. Indeed, warnericin RK is highly hemolytic with a bactericidal mode of action, whereas PSMα is poorly hemolytic with a bacteriostatic mode of action toward L. pneumophila.

Surfactin from Bacillus subtilis displays an unexpected anti-Legionella activity.

A contaminant bacterial strain was found to exhibit an antagonistic activity against Legionella pneumophila, the causative agent of Legionnaires' disease. The bacterial strain was identified as a Bacillus subtilis and named B. subtilis AM1.

Genetic variations creating microRNA target sites in the FXN 3'-UTR affect frataxin expression in Friedreich ataxia.

Friedreich's ataxia (FRDA) is a severe neurodegenerative disease caused by GAA repeat expansion within the first intron of the frataxin gene. It has been suggested that the repeat is responsible for the disease severity due to impaired transcription thereby reducing expression of the protein. However, genotype-phenotype correlation is imperfect, and the influence of other gene regions of the frataxin gene is unknown.