Recurrent chromosomal rearrangements involving breakpoints 3p21 and 19q13 in Chinese IgD multiple myeloma detected by G-banding and multicolor spectral karyotyping: A review of IgD karyotype literature

Ng, Margaret H.L.; Wong, Nathalie; Tsang, K. S.; Cheng, Suk‐Hang; Chung, Yuk-Fei; Lo, KW

doi:10.1053/hupa.2001.27122

Cited by 9 publications

(10 citation statements)

References 15 publications

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“…Der(11;15) and t(5;21) are unique among all leukemia-lymphoma cell lines at least according to Drexler [1]. In addition to UHKT-893 cells, t(1;6) translocation was documented only in patient's myeloma cells in one study [20] and in two of 52 myeloma cell lines, but also with distinct breakpoints [1]. Another translocation t(1;11) was described only in two other myeloma cell lines.…”

Section: Discussionmentioning

confidence: 96%

Novel human multiple myeloma cell line UHKT-893

Uherková¹,

Vančurová²,

Vyhlídalová³

et al. 2013

Leukemia Research

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Section: Discussionmentioning

confidence: 96%

Novel human multiple myeloma cell line UHKT-893

Uherková¹,

Vančurová²,

Vyhlídalová³

et al. 2013

Leukemia Research

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“…The patients were treated with chemotherapy regimen of the U.K. MRC AML 12 study, modified according to risk stratification (low-, standard-, and high-risk groups). Cytogenetic studies by G-banding and detection of the CBF -MYH11 rearrangement by RT-PCR technique were performed [3,4]. Correlations with the morphological findings and clinical course of the patients were made.…”

Section: Methodsmentioning

confidence: 99%

Childhood acute myeloid leukemia with CBFβ‐MYH11 rearrangement: Study of incidence, morphology, cytogenetics, and clinical outcomes of Chinese in Hong Kong

Chan¹,

Wong²,

Ng³

et al. 2004

American J Hematol

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We analyzed 43 consecutive cases of pediatric acute myeloid leukemia (AML) for the presence of the CBFb-MYH11 rearrangement using molecular techniques in a regional hospital in Hong Kong. Five cases (11.6%), 3 girls and 2 boys, ranging in age from 8 months to 14 years old, were found positive for the CBFb-MYH11 rearrangement. Morphologically, they were FAB M2 or M4 with or without eosinophilia (Eo). Typical M4Eo was observed in only one case. The molecular findings were in complete concordance with cytogenetic data, which revealed inv(16)(p13q22) in all and also gains of chromosome 4, 8, 22, and Y in one patient. Clinically, all 5 patients achieved complete remission after chemotherapy with favorable outcomes except for the patient with infantile AML, who relapsed 11 months after diagnosis, underwent cord blood transplantation, and was in second remission. This is the first clinicopathological study and documentation of the incidence of

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“…G-banded cytogenetic studies were performed as described previously. 31 The presence of t(8;21) and inv (16) translocations was confirmed by reverse-transcriptionpolymerase chain reaction (RT-PCR) detection of RUNX1-ETO and CBF␤-MYH11 fusion transcripts. 32 Patients were treated with the modified U.K. MRC AML 12 protocol, according to cytogenetics and their response to induction chemotherapy.…”

Section: Patient Samples and Cell Culturementioning

confidence: 99%

Transcriptional repression of the RUNX3/AML2 gene by the t(8;21) and inv(16) fusion proteins in acute myeloid leukemia

Cheng

et al. 2008

Blood

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RUNX3/AML2 is a Runt domain transcription factor like RUNX1/AML1 and RUNX2/ AML3. Regulated by 2 promoters P1 and P2, RUNX3 is frequently inactivated by P2 methylation in solid tumors. Growing evidence has suggested a role of this transcription factor in hematopoiesis. However, genetic alterations have not been reported in blood cancers. In this study on 73 acute myeloid leukemia (AML) patients (44 children and 29 adults), we first showed that high RUNX3 expression among childhood AML was associated with a shortened event-free survival, and RUNX3 was significantly underexpressed in the prognostically favorable subgroup of AML with the t(8;21) and inv(16) translocations. We further demonstrated that this RUNX3 repression was mediated not by P2 methylation, but RUNX1-ETO and CBF␤-MYH11, the fusion products of t(8; 21) and inv(16), via a novel transcriptional mechanism that acts directly or indirectly in collaboration with RUNX1, on 2 conserved RUNX binding sites in the P1 promoter. In in vitro studies, ectopically expressed RUNX1-ETO and CBF␤-MYH11 also inhibited endogenous RUNX3 expression. Taken together, RUNX3 was the first transcriptional target found to be commonly repressed by the t(8;21) and inv (16) IntroductionThe Runt domain transcription factor family includes RUNX1/ AML1, RUNX2/AML3, and RUNX3/AML2. These transcription factors share a conserved Runt domain for binding to a 6-base pair (bp) DNA sequence (TGT/cGGT) and heterodimerization with core-binding factor ␤ (CBF␤). CBF␤ does not bind DNA directly but increases the ability of RUNX proteins to bind DNA and regulate transcription. 1 RUNX1 and RUNX2 are essential for hematopoiesis and osteogenesis, respectively. 2,3 Moreover, RUNX1 regulates neuron and muscle function. 4,5 On the other hand, RUNX3 is involved in neurogenesis and thymopoiesis and acts as a tumor suppressor in gastric cancer. [6][7][8] In addition, RUNX3 is inactivated frequently by promoter methylation and less frequently by gene deletion, point mutations, and protein mislocalization in various solid tumors. 9 RUNX3 and RUNX1 show prominent expression in hematopoietic cells and different subsets of neurons, 4,10 while RUNX2 is expressed mainly in bone and also other tissues including hematopoietic stem cells. 11 The expression of RUNX3 and RUNX1 can be induced by retinoic acid, suggesting that these transcription factors may jointly regulate retinoic acid-mediated hematopoietic differentiation. 10 The functional overlap was supported by the observations that hematopoietic defects due to RUNX1 deficiency could be rescued by RUNX3. 12,13 Further evidence suggesting a role of RUNX3 in hematopoiesis was reduction of mature blood cell formation in zebrafish by RUNX3 depletion. 14 The role of RUNX3 in tumorigenesis and its potential involvement in hematopoiesis suggest a role of this transcription factor in hematological malignancies. However, genetic alterations of RUNX3 have not been reported in acute myeloid leukemia (AML). 15 t(8;21)(q22;q22) and inv(16)(p13;q22) are the 2 most common t...

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Recurrent chromosomal rearrangements involving breakpoints 3p21 and 19q13 in Chinese IgD multiple myeloma detected by G-banding and multicolor spectral karyotyping: A review of IgD karyotype literature

Cited by 9 publications

References 15 publications

Novel human multiple myeloma cell line UHKT-893

Novel human multiple myeloma cell line UHKT-893

Childhood acute myeloid leukemia with CBFβ‐MYH11 rearrangement: Study of incidence, morphology, cytogenetics, and clinical outcomes of Chinese in Hong Kong

Transcriptional repression of the RUNX3/AML2 gene by the t(8;21) and inv(16) fusion proteins in acute myeloid leukemia

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