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Current Opinion in Hematology: March 2002 - Volume 9 - Issue 2 - p 179
Errata
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In the abstract of the article Intravenous Rh immune globulin for treating immune thrombocytic purpura by S. Gerald Sandler, which appeared in the November 2001 issue of Current Opinion in Hematology (2001;8:417–420), the phrase “Rhesus factor” should be changed to “Rh.”

In the article Mouse models of acute promyelocytic leukemia by Jessica L. Pollock, PhD, Peter Westervelt, MD, PhD, Matthew J. Walter, MD, Andrew Lane, BE, and Timothy J. Ley, MD, that appeared in the July 2001 issue of Current Opinion in Hematology (2001;8:206–211), the following corrections should be made:

Correction on Page 207, right column, first full paragraph, line 10. “RAROC” should be RARα.

Revised Paragraph 1, page 208. The t(15/17) translocation also causes obligate haploinsufficiency for RARα (both isoforms 1 and 2) [30]. Knockout mice have been generated to assess the role of RARα during development and granulopoiesis. Homozygous RARα1−/− mice have no phenotype [31] (presumably because of retention of the RARα2 isoform), but RARα−/− mice (deficient for both isoforms) exhibit perinatal lethality [32]. Because RARγ may compensate for RARα in myeloid development [33], doubly deficient mice (RARα1−/− x RARγ−/−) were also generated; these mice (lacking only the α1 isoform of RARα) display a block in myeloid differentiation in methylcellulose assays [34]. In vivo, however, fetal liver cells from RARα−/− (i.e. lacking both RARα1 and RARα2) × RARγ−/− mice display an increase in myeloid differentiation [35•]. Similarly, mice fed a diet without retinoids can develop retinoic acid deficiency, causing expansion of the myeloid lineage in vivo [35•,36]. RARα deficient mice have not been intercrossed with the PML-RARα mouse models, so the importance of RARα haploinsufficiency for APL development is not known.

References

Papers of particular interest, published within the annual period of review, have been highlighted as:

• Of special interest

•• Of outstanding interest

Boylan JF, Lufkin T, Achkar CC, et al.: Targeted disruption of retinoic acid receptor α (RARα) and RARγ results in receptor-specific alterations in retinoic acid-mediated differentiation and retinoic acid metabolism. Mol Cell Biol 1995, 15:843–851.Kastner P, Lawrence HJ, Waltzinger C, et al.: Positive and negative regulation of granulopoiesis by endogenous RARα. Blood 2001, 97:1314–1320.

Studies were conducted with RARα−/− and RARα−/− × RARγ−/− cells to define the role of the RARγ isoforms in granulopoiesis. The RARα mutation caused loss of both isoforms of RARα, which made the findings more biologically representative of RARα loss in APL translocations. The results suggested both positive and negative influences of RARα on granulocyte differentiation.

© 2002 Lippincott Williams & Wilkins, Inc.