Chromosomes in acute leukemia

Prigogina, E. L.; Fleischman, E. W.; Puchkova, G. P.; Kulagina, O E; Majakova, S A; Balakirev, S. A.; Frenkel, M. A.; Khvatova, N V; Peterson, Isaac

doi:10.1007/bf00289443

Cited by 138 publications

(21 citation statements)

References 18 publications

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“…10,11,[28][29][30][31][32][33][34][35][36][37][38][39][40][41][42][43][44][45][46] The fact that six of the leukemias (3%) were morphologically classified as AML is also in line with what has been reported before. In fact, out of the 362 published cases with t(4;11), 11 (3%) have been AML, the majority AML-M4 and AML-M5.…”

Section: Discussionsupporting

confidence: 75%

“…Clinical hallmarks of t(4;11)-positive leukemia include young age at presentation, hyperleukocytosis, hepatosplenomegaly, relatively high frequency of CNS involvement, overrepresentation of females, and poor response to therapy. 10,11,[28][29][30][31][32][33][34][35][36][37][38][39][40][41][42][43][44][45][46] The blast cells have, by morphologic, cytochemical, ultrastructural, molecular genetic and immunologic means, been shown to display a mixture of lymphoid and myeloid features, suggesting that the cell of origin is an early progenitor with the potential for both lymphoid and myelomonocytic differentiation. Most leukemias are classified morphologically, using standard light microscopic criteria, as ALL of L1 or L2 type, although a few cases of acute myeloid leukemias (AML), mostly myelomonocytic, have been reported.…”

Section: Introductionmentioning

confidence: 99%

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Hematologic malignancies with t(4;11)(q21;q23) – a cytogenetic, morphologic, immunophenotypic and clinical study of 183 cases

et al. 1998

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A total of 183 hematologic malignancies with t(4;11)(q21;q23), including five variant translocations, were collected by the Workshop. Clinical, morphologic and immunophenotypic features were compiled, and karyotypes with variant t(4;11) or secondary chromosomal aberrations were reviewed. All cases were acute leukemias (AL): 173 acute lymphoblastic leukemias (ALL), six acute myeloid leukemias (AML), three unclassifiable AL, and one biphenotypic AL. Ten patients had treatment-associated AL. Females were overrepresented (104 vs 79) and the age distribution was clearly nonrandom; 34% of the cases occurred in infants below the age of 12 months. The remaining AL were evenly distributed among the other age groups, with the oldest patient being 79 years old. An increased white blood cell count (WBC) was reported in more than 90% of the cases, with hyperleukocytosis (у100 × 10 9 /l) in 64%. Additional chromosomal changes were detected in 55 (30%) cases, most often gain of the X chromosome, i(7)(q10), and trisomy 8, with frequent breakpoints in 1p36, 1q21, 7q10, 11p15, 12p13, 17p11, and 17p10. All recurrent secondary changes resulted in genomic imbalances, in particular gains of 1q, 7q, 8, and X and losses of 7p and 17p. Event-free and overall survival (EFS and OS) could be ascertained in 170 and 171 patients, respectively. Kaplan-Meier estimates of EFS and OS showed no differences with regard to gender, WBC, or presence of secondary chromosomal abnormalities, and there was no increase of EFS or OS among the 55 cases that had undergone bone marrow transplantation. However, age had an important prognostic impact, with significantly (P Ͻ 0.0001) longer EFS and OS in children 2-9 years old than among infants and younger children, patients aged between 10 and 39 years and older adults.

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Section: Discussionsupporting

confidence: 75%

Section: Introductionmentioning

confidence: 99%

Hematologic malignancies with t(4;11)(q21;q23) – a cytogenetic, morphologic, immunophenotypic and clinical study of 183 cases

et al. 1998

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“…Of these, the t(11;19)(q23;q13) translocation is a very rare but recurrent aberration observed in acute myeloid leukemia (AML), acute lymphoblastic leukemia (ALL) and myelodysplastic syndromes (MDS): only 6 cases have ever been reported [2,3,4,5,6,7,8]. Recently, Yang et al [8] demonstrated that MLL was fused to ACTN4 , encoding an ubiquitously expressed actin-bundling protein at 19q13 by t(11;19)(q23;q13.1) in therapy-related MDS.…”

Section: Figmentioning

confidence: 99%

Translocation t(11;19)(q23;q13.1) without <b><i>MLL </i></b>Rearrangement in Acute Myeloid Leukemia: Heterogeneity of the 11q23 Breakpoints

Yamamoto

Kawamoto²,

Kakiuchi³

et al. 2015

Acta Haematol

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“…[2][3][4] Even before this, cytogeneticists had noted that translocations affecting the locus 11q23, and in particular the translocation t(4;11), characterize a special subset of ALL that was associated with poor survival. [5][6][7] Soon thereafter it became clear that these translocations of the locus 11q23 are also typical for mixed lineage leukemia. Whereas treatment of non-mixed lineage leukemia in children has become the textbook success story of modern medicine with 5-year survival rates approaching 90%, 8 mixed lineage leukemia treatment seems to have hit a roadblock with hardly 40% of all infants surviving five years after diagnosis ( Figure 1).…”

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confidence: 99%

The molecular biology of mixed lineage leukemia

Slany¹

2009

Haematologica

285

280

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Mixed lineage leukemia is a very aggressive blood cancer that predominantly occurs in pediatric patients. In contrast to other types of childhood acute leukemias, mixed lineage leukemia presents with a dismal prognosis and despite the availability of advanced treatment methods cure rates have stagnated over the last years. Mixed lineage leukemia is characterized by the presence of MLL fusion proteins that are the result of chromosomal translocations affecting the MLL gene at 11q23. These events juxtapose the amino-terminus of the histone methyltransferase MLL with a variety of different fusion partners that destroy normal histone methyltransferase function of MLL and replace it by heterologous functions contributed by the fusion partner. The resulting chimeras are transcriptional regulators that take control of targets normally controlled by MLL with the clustered HOX homeobox genes as prominent examples. Recent studies suggested that MLL fusion partners activate transcription by two different mechanisms. Some of these proteins are themselves chromatin modifiers that introduce histone acetylation whereas other fusion partners can recruit histone methyltransferases.In particular, histone H3 specific methylation at lysine 79 catalyzed by DOT1L has been recognized as a hallmark of chromatin activated by MLL fusion proteins. Interestingly, several frequent MLL fusion partners seem to coordinate DOT1L activity with a protein complex that stimulates the elongation phase of transcription by phosphorylating the carboxy-terminal repeat domain of RNA polymerase II. The discovery of these novel enzymatic activities that are essentially involved in MLL fusion protein function presents potential new targets for a rational drug development.

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Chromosomes in acute leukemia

Cited by 138 publications

References 18 publications

Hematologic malignancies with t(4;11)(q21;q23) – a cytogenetic, morphologic, immunophenotypic and clinical study of 183 cases

Hematologic malignancies with t(4;11)(q21;q23) – a cytogenetic, morphologic, immunophenotypic and clinical study of 183 cases

Translocation t(11;19)(q23;q13.1) without <b><i>MLL </i></b>Rearrangement in Acute Myeloid Leukemia: Heterogeneity of the 11q23 Breakpoints

The molecular biology of mixed lineage leukemia

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