0000000000053786

AUTHOR

T Kindler

Fatal sepsis due to mycobacterium tuberculosis after allogeneic bone marrow transplantation.

Mycobacterium tuberculosis is a serious, but rare infectious complication after allogeneic bone marrow transplantation. We describe a case of fatal sepsis due to Mycobacterium tuberculosis after allogeneic bone marrow transplantation for Philadelphia chromosome-positive ALL. The diagnosis was made after BAL. Although broad-spectrum antituberculous therapy was started immediately after diagnosis, blood cultures became positive for Mycobacterium tuberculosis. The patient developed severe pyrexias and finally died of multi-organ failure. Rapid progression of mycobacterial infection should be considered in patients post BMT with unexplained fever, particularly in patients from endemic areas.

research product

BCR-ABL as a target for novel therapeutic interventions.

The BCR-ABL oncogene is the result of a reciprocal translocation between the long arms of chromosome 9 and 22 t(9; 22). There is good experimental evidence demonstrating that BCR-ABL is the single causative abnormality in chronic myeloid leukaemia (CML), making it a unique model for the development of molecular targets. In addition to CML, BCR-ABL transcripts can be found in a minority of acute lymphoblastic leukaemias and very rarely in acute myeloid leukaemia (AML). Elucidating the molecular mechanisms and downstream pathways of BCR-ABL has led to the design of several novel therapeutic approaches. In this review, molecular targeting of BCR-ABL will be discussed based on the inhibition of…

research product

BAX inhibitor-1 is a Ca(2+) channel critically important for immune cell function and survival.

The endoplasmic reticulum (ER) serves as the major intracellular Ca(2+) store and has a role in the synthesis and folding of proteins. BAX (BCL2-associated X protein) inhibitor-1 (BI-1) is a Ca(2+) leak channel also implicated in the response against protein misfolding, thereby connecting the Ca(2+) store and protein-folding functions of the ER. We found that BI-1-deficient mice suffer from leukopenia and erythrocytosis, have an increased number of splenic marginal zone B cells and higher abundance and nuclear translocation of NF-κB (nuclear factor-κ light-chain enhancer of activated B cells) proteins, correlating with increased cytosolic and ER Ca(2+) levels. When put into culture, purifie…

research product