in Patients with Lymphoid Neoplasms: An Illustration of Evolutive Host-Fungus Interactions.

Recent outbreaks of (CG) infections in North America have sparked renewed interest in the pathogenic potential of CG, and have underscored notable differences with in terms of geographic distribution, pathogen virulence, and host susceptibility. While cases of CG are increasingly reported in patients with a wide variety of underlying conditions, only very few have been reported in patients with lymphoid neoplasms. Herein, we report a case of autochthonous CG meningitis in a patient receiving ibrutinib for chronic lymphocytic leukemia in France, and review available data on the clinical epidemiology of CG infections in patients with lymphoid neoplasms.

Evaluation of Residual Disease and TKI Duration Are Critical Predictive Factors for Molecular Recurrence after Stopping Imatinib First-line in Chronic Phase CML Patients.

Purpose: Tyrosine kinase inhibitor (TKI) discontinuation is an emerging goal in chronic myelogenous leukemia (CML) management and several studies have demonstrated the feasibility of safely stopping imatinib. A sustained deep molecular response on long-term TKI is critical prior to attempting treatment-free remission. Reproducible results from several studies reported recently, failed to identify robust and reproducible predictive factors for the selection of the best candidates for successful TKI cessation.

The R178Q mutation is a recurrent cause of hemochromatosis and is associated with a novel pathogenic mechanism.

Hemochromatosis type 4 is one of the most common causes of primary iron overload, after -related hemochromatosis. It is an autosomal dominant disorder, primarily due to missense mutations in This gene encodes ferroportin 1 (FPN1), which is the sole iron export protein reported in mammals. Not all heterozygous missense mutations in are disease-causing.