t(11;22)(q23;q11.2) in acute myeloid leukemia of infant twins fuses MLL with hCDC rel , a cell division cycle gene in the genomic region of deletion in DiGeorge and velocardiofacial syndromes

Abstract

Medical Sciences. In the article "t(11;22)(q23;q11.2) in acute myeloid leukemia of infant twins fuses MLL with hCDCrel, a cell division cycle gene in the genomic region of deletion in DiGeorge and velocardiofacial syndromes" by Maureen D. Megonigal, Eric F. Rappaport, Douglas H. Jones, Terrence M. Williams, Brian D. Lovett, Kara M. Kelly, Paul H. Lerou, Thomas Moulton, Marcia L. Budarf, and Carolyn A. Felix, which appeared in number 11, May 26, 1998, of Proc. Natl. Acad. Sci. USA (95, pp. 6413-6418), the authors wish to note the following corrections. On page 6414, column 2, line 4, the text should read: "The 24-l ligation reaction mixture contained 0.5 g" not "0.05 g" as printed. Also, on page 6415, column 1, line 56, the text should read: "AmpliTaq DNA polymerase, all four dNTPs (each at 200 M)" not "(each at 250 M)" as printed.Medical Sciences. In the article "Potent inhibition of human immunodeficiency virus type 1 replication by an intracellular anti-Rev single-chain antibody" by Lingxun Duan, Omar Bagasra, Mark A. Laughlin, Joseph W. Oakes, and Roger J. Pomerantz, which appeared in number 11, May 24, 1994, of Proc. Natl. Acad. Sci. USA (91, 5075-5079), the undersigned authors wish to note the following: "The sequence of the heavy chain of the D8 anti-Rev single chain variable fragment (SFv) has been reanalyzed and found to be not what was reported in the article. It is likely that the coding DNA was derived from the fusion partner cell line used to make the original D8 hybridoma, and not from the heavy chain gene expressed by the B cell precursor to this hybridoma. There is a deletion in the framework region 3 (FR3) leading to a framehsift in CDR3 and downstream regions of the heavy chain gene. Individual nucleotide differences make this sequence very close to that described [Thammana, P. (1994)

MLL-SEPTIN6 fusion recurs in novel translocation of chromosomes 3, X, and 11 in infant acute myelomonocytic leukaemia and in t(X;11) in infant acute myeloid leukaemia, and MLL genomic breakpoint in complex MLL-SEPTIN6 rearrangement is a DNA topoisomerase II cleavage site

“…MLL translocations in infant leukaemias are in utero events (Ford et al, 1993;Gale et al, 1997;Gill-Super et al, 1994;Mahmoud et al, 1995;Megonigal et al, 1998). MLL has many partner genes that encode proteins of several different types (reviewed in Ayton and Cleary, 2001;Felix, 2000;Rowley, 1998).…”

Monitoring of minimal residual leukemia in patients with MLL-AF9 positive acute myeloid leukemia by RT-PCR

“…2 At least 14 partner genes (on chromosomes 1, 4, 6, 9, 10, 16, 17, 19, 22 and X) have been fully characterized. [3][4][5][6][7][8][9][10][11][12][13][14][15] The role of these partner genes in leukemogenesis and the possible prognostic impact of distinct 11q23 translocations is largely unexplored.…”

Dysplastic changes in the peripheral blood of children with microdeletion 22q11.2

“…This gene maps to the central portion of a 1.3-megabase sequence that is part of the region commonly deleted in patients with del22q11.2. On investigation of two infant twins with acute myeloid leukemia, the authors demonstrated fusion of the MLL gene this resulted in the chromosomal anomaly t(11;22)(q23;q11.2) and also caused acute myeloid leukemia [14]. The above-mentioned reports suggest that the 22q11 region includes gene(s) that may be involved in the pathogenesis of MD and certain malignancies.…”

“…Two other reports described a 7-month-old boy and a 10-month-old girl with DGS who developed B-cell lymphoma and B-cell non-Hodgkin's lymphoma, respectively [12,13]. In addition to these accounts, a recent study described a role for the human cell division cyclerelated (hCDCrel) gene in malignant conditions [14]. This gene maps to the central portion of a 1.3-megabase sequence that is part of the region commonly deleted in patients with del22q11.2.…”