All of these protein-based drugs combine part of an anti-B cell antibody with a bacterial toxin to kill the cells on internalization. BL22 and HA22 attack a common protein called CD22, which is present on hairy cells and healthy B cells. LMB-2 attacks a protein called CD25, which is not present in HCL-variant, so LMB-2 is only useful for patients with HCL-classic or the Japanese variant. HA-22, now renamed moxetumomab pasudotox, is being studied in patients with relapsed hairy cell leukemia at the National Cancer Institute in Bethesda, Maryland, MD Anderson Cancer Center in Houston, Texas, and Ohio State University in Columbus, Ohio. Other sites for the study are expected to start accepting patients in late 2014, including The Royal Marsden Hospital in London, England.Other clinical trials are studying the effectiveness of cladribine followed by rituximab in eliminating residual hairy cells that remain after treatment by cladribine or pentostatin. It is not currently known if the elimination of such residual cells will result in more durable remissions. BRAF mutation has been frequently detected in HCL (Tiacci et al. NEJM  2011) and some patients may respond to Vemurafenib. The major remaining research questions are identifying the cause of HCL and determining what prevents hairy cells from maturing normally. See also
Annexin A1
List of cutaneous conditions

References
External links

About HCL at the US National Cancer Institute
History of HCL and the Godmother of HCL
Hyperglycinemia may refer to one of two related inborn amino acid disorders that are characterized by elevated levels of glycine in the blood. Propionic acidemia, also known as "ketotic glycinemia"
Glycine encephalopathy, also known as "non-ketotic hyperglycinemia"