G<scp>ENETIC</scp> P<scp>ROFILE</scp><scp>OF</scp> A<scp>CUTE</scp> M<scp>YELOID</scp> L<scp>EUKEMIA</scp>

Mecucci, Cristina; Rosati, Roberto; Starza, Roberta La

doi:10.1046/j.1468-0734.2002.00060.x

Cited by 11 publications

(4 citation statements)

References 144 publications

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“…Accordingly, all the median sensitivities and specificities were 100%. This is in line with previous reports describing a unique biologic background for these subentities, [46][47][48] which is reflected in distinct gene expression profiles. [49][50][51][52] However, because the latter have not yet been assessed by microarray analysis in the context of the full spectrum of AML and the other leukemias, the present study adds important information by clearly demonstrating that, based on their distinct features, these subentities can be accurately predicted even in the context of the heterogeneous background of other leukemias.…”

Section: Discussionsupporting

confidence: 93%

Global approach to the diagnosis of leukemia using gene expression profiling

Haferlach

Kohlmann

Schnittger

et al. 2005

Blood

183

109

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Section: Discussionsupporting

confidence: 93%

Global approach to the diagnosis of leukemia using gene expression profiling

Haferlach

Kohlmann

Schnittger

et al. 2005

Blood

183

109

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“…The involvement of HMGA2 in different mesenchymal tumors and the promiscuous nature of the translocations involving this gene are reminiscent of that of another gene encoding a nuclear scaffold protein associated with neoplasia. The mixed lineage leukemia (MLL) gene is rearranged in numerous acute lymphoid and myeloid leukemias in humans and more than 40 different partner genes have been identified [21]. MLL contains three motifs located near its amino terminus that are highly homologous to the core AT hook DNA-binding domains of the HMGA2 protein; however, whether the HMGA proteins and MLL share any common mechanism of transformation remains to be shown.…”

Section: Discussionmentioning

confidence: 99%

Deregulation of HMGA2 in an aggressive angiomyxoma with t(11;12)(q23;q15)

et al. 2006

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Aggressive angiomyxoma is a soft-tissue neoplasm with a predilection for the pelvic and perineal regions and a tendency to recur locally. Cytogenetic data on this tumor type are limited to five cases, three of which showed rearrangement of chromosomal bands 12q13-15. Molecular investigation of two of the tumors identified the HMGA2 gene as the target of the 12q rearrangements. However, the two previously analyzed tumors were different at the molecular level: in one, the rearrangement of 12q13-15 resulted in a fusion product, whereas, in the second case, the breakpoint was telomeric (3') to the HMGA2, leaving the gene intact although expressed in its entire length. To shed more light on the pathobiology of aggressive angiomyxoma and to investigate the molecular mechanisms behind the involvement of the HMGA2 gene in this tumor type (fusion transcript vs deregulated expression), we investigated, cytogenetically and with molecular techniques, one such tumor which presented a t(11;12)(q23;q15) as the sole karyotypic aberration. FISH analyses demonstrated no structural alteration of HMGA2 at the cytogenetic level; however, expression of the full-length gene was detected molecularly.

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“…A large variety of genetic alterations, including point mutations, amplification, insertion, deletions, trisomy and chromosomal translocations, are important in leukemia initiation. Elucidation of genomic events and the cascade of their effects in cell function is crucial for identifying distinct subsets of leukemia and for developing new therapeutic strategies [136] . Two paradigms come from the identification of the key roles that PML-RARα and BCR-ABL fusion proteins play in APL and CML leukemogenesis, and from the development of ATRA/ATO and Imatinib, which greatly improve the prognosis of patients with APL or CML, respectively [137] .…”

Section: Discussionmentioning

confidence: 99%

From dissection of disease pathogenesis to elucidation of mechanisms of targeted therapies: leukemia research in the genomic era

Guo

Chen

2007

Acta Pharmacologica Sinica

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Leukemia is a group of heterozygous diseases of hematopoietic stem/progenitor cells that involves dynamic change in the genome. Dissection of genetic abnormalities critical to leukemia initiation provides insights into the elusive leukemogenesis, identifies distinct subsets of leukemia and predicts prognosis individually, and can also provide rational therapeutic targets for curative approaches. The past three decades have seen tremendous advances in the analysis of genotype-phenotype connection of leukemia, and in the identification of molecular biomarkers for leukemia subtypes. Intriguingly, differentiation therapy, targeted therapy and chemotherapy have turned several subtypes of leukemia from highly fatal to highly curable. The use of all-trans retinoic acid and arsenic trioxide, which trigger degradation of PML-RARalpha, the causative fusion protein generated by t (15;17) translocation in acute promyelocytic leukemia (APL), has led to a dramatic improvement of APL clinical outcome. Imatinib mesylate/ Gleevec/STI571, which inhibits the tyrosine kinase activity of BCR-ABL oncoprotein, has now become the new gold standard for the treatment of chronic myeloid leukemia. Optimal use of chemotherapeutic agents together with a stringent application of prognostic factors for risk-directed therapy in clinical trials has resulted in a steady improvement in the treatment outcome of acute lymphoblastic leukemia. Hence, the pace of progress extrapolates to a prediction of leukemia control in the twenty-first century.

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GENETIC PROFILEOF ACUTE MYELOID LEUKEMIA

Cited by 11 publications

References 144 publications

Global approach to the diagnosis of leukemia using gene expression profiling

Global approach to the diagnosis of leukemia using gene expression profiling

Deregulation of HMGA2 in an aggressive angiomyxoma with t(11;12)(q23;q15)

From dissection of disease pathogenesis to elucidation of mechanisms of targeted therapies: leukemia research in the genomic era

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