Monozygotic twins with congenital acute lymphoblastic leukemia (ALL) and t(4;11)(q21;q23)

Bayar, Emel; Kurczynski, Thaddeus W.; Robinson, Margaret G.; Tyrkus, Michael; Saadi, A. Al

doi:10.1016/0165-4608(94)00293-2

Cited by 15 publications

(9 citation statements)

References 7 publications

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“…Occasionally, monozygotic twins present in the first month of life with genetically identical leukaemia, indicating an intrauterine origin with transmission from one twin to the other via intrauterine placental sharing. This has been reported in pro-B ALL with t(11;19)(q23;p13) (Mahmoud et al, 1995), pro-B ALL with t(4;11)(q21;q23) (Bayar et al, 1996) and acute monocytic leukaemia with t(9;11)(p21;q23) (Park et al, 2001), KMT2A rearrangement being predicted with each of these translocations. In addition, monozygotic twins presenting at 7 weeks of age had pro-B ALL associated with t(1;11)(p13;q32) and KMT2A-EPS15, suggesting that the leukaemia was already present at birth, and had spread from one twin to the other (Kotecha et al, 2012).…”

Section: Differential Diagnosissupporting

confidence: 61%

“…Neonatal leukaemia with KMT2A/11q23.3 rearrangement (Tables I and II) In non-DS neonatal leukaemia, the underlying cytogenetic/ molecular genetic abnormality is often t(4;11)(q21.3;q23.3)/ KMT2A-AFF1. The leukaemia may be AML (particularly acute monoblastic/monocytic or myelomonocytic leukaemia) (Bresters et al, 2002;Ishii et al, 2006) but is usually ALL (early precursor or pro-B ALL, often with coexpression of CD15 or CD33) (Bayar et al, 1996;Ishii et al, 2006;Bas Su arez et al, 2011) or MPAL (most often monocytic/monoblastic/pro-B) (Pui et al, 1987;Ridge et al, 1995). Lineage switch can occur during treatment or at relapse, for example, cases presenting with B-lineage blasts that relapse as or 'switch' after treatment to a monoblastic immunophenotype .…”

Section: Differential Diagnosismentioning

confidence: 99%

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Neonatal leukaemia

et al. 2018

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Neonatal leukaemia is defined as occurring within the first 28 days of life and most, if not all, cases are congenital. With the exception of Down syndrome-associated transient abnormal myelopoiesis, which is not considered here, neonatal leukaemias are rare. In two-thirds of patients the disease manifests as an acute myeloid leukaemia, frequently with monocytic/monoblastic characteristics. Most other cases are acute lymphoblastic leukaemia, particularly B lineage, but some are mixed phenotype or blastic plasmacytoid dendritic cell neoplasms. The most frequently observed cytogenetic/molecular abnormality is t(4;11)(q21.3;q23.3)/KMT2A-AFF1 followed by t(1;22)(p13.3;q13.1)/RBM15-MKL1 and t(8;16)(p11.2;p13.3)/KAT6A-CREBBP. Common clinical features include prominent hepatosplenomegaly and a high incidence of skin involvement, sometimes in the absence of bone marrow disease. A distinctive feature is the occurrence of spontaneous remission in some cases, particularly in association with t(8;16). In this review, we summarise current knowledge of the clinical, cytogenetic and molecular features of neonatal leukaemia and discuss clinical management of these cases.

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Section: Differential Diagnosissupporting

confidence: 61%

Section: Differential Diagnosismentioning

confidence: 99%

Neonatal leukaemia

et al. 2018

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“…The identical, clonal, nonconstitutional rearrangements suggested that the translocations occurred in utero and that there had been intraplacental metastasis from one twin to the other (7)(8)(9). Monozygous twins with congenital ALL and t(4;11)(q21;q23) have also been described (10).…”

Section: Introductionmentioning

confidence: 99%

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

Megonigal

Rappaport

Jones

et al. 1998

Proc. Natl. Acad. Sci. U.S.A.

153

123

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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)

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“…Bayar et al [20] reported a pair of monozygotic twins with congenital acute lymphoblastic leukemia (cALL) and t(4;11)(q21;q23). A high concordance rate (20-25%) in ALL occurring in identical twins has been described.…”

Section: Discussionmentioning

confidence: 98%