Early transformation to acute myeloblastic leukaemia with the acquisition of inv(16) in Ph positive chronic granulocytic leukaemia

Han, Mei; Ross, Fiona; Hall, J.L.; Hamblin, Terry J.

doi:10.1016/s0145-2126(97)00070-2

Cited by 16 publications

(15 citation statements)

References 10 publications

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“…Cytogenetics of the present case at the end stage revealed an additional abnormality of add (16)p13, at [20]. Although the additional chromosomal abnormality of our case was add(16)p13 and not inv(16)(p13;q22), the MYH11 gene may contribute to the emergence of the more malignant clone in these two cases.…”

Section: Discussionmentioning

confidence: 46%

A case of chronic myeloid leukemia with minor bcr-abl transcript following fluorouracil therapy for esophageal carcinoma

Nakamura

Inokuchi

Hanawa

et al. 2000

Annals of Hematology

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We report here a very rare case of chronic myeloid leukemia (CML) with a minor bcr-abl transcript, which developed following long-term chemotherapy with fluorouracil for esophageal carcinoma. A 64-year-old male patient was diagnosed with CML. Four years earlier, he had suffered from esophageal carcinoma, which was treated by surgical resection followed by oral administration of fluorouracil (200 mg/day) for 4 years. Molecular analysis of his Philadelphia chromosome (Ph) using reverse-transcriptase polymerase chain reaction (RT-PCR) and subsequent sequencing revealed a minor bcr-abl transcript. The clinical course of this patient was aggressive with a short chronic phase of CML. This is the first reported case of secondary CML with a minor bcr-abl transcript.

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Section: Discussionmentioning

confidence: 46%

A case of chronic myeloid leukemia with minor bcr-abl transcript following fluorouracil therapy for esophageal carcinoma

Nakamura

Inokuchi

Hanawa

et al. 2000

Annals of Hematology

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“…These results demonstrate that induction of AML by AME requires functions and/or functional cooperation of both AML1 and EVI1 oncogenic components. In addition, like AME, AML1/ETO, CBFb/MYH11 and overexpression of EVI1 have all been found in some cases of CML in the blast phase (Myint et al, 1997;Nucifora, 1997;Kojima et al, 1999). However, although AML1-and EVI1-related oncogenes studied here inhibit the maturation of myeloid cells in BCR/ABL-induced MPD to some extent, they are not sufficient to cooperate with BCR/ABL in the induction of AML in mice as AME does.…”

Section: Discussionmentioning

confidence: 63%

“…In addition to the AME fusion, the t(3;21)(q26;q22) translocation may result in an inframe fusion of AML1 to MDS1, producing an AML1/ MDS1 chimeric protein and an out-of-frame fusion of AML1 to the EAP gene, resulting in a protein similar to an alternative spliced form of AML1 without the transactivation domain (AML1a) (Nucifora et al, 1994). The CBFb gene has also been frequently found to be fused to the MYH11 gene, which encodes the smooth muscle myosin heavy chain (SMMHC), in inv(16)(p13;q22)-associated AML (M4Eo) as well as in some cases of CML in the blast phase (Liu et al, 1993;Myint et al, 1997). Aberrant expression of EVI1 has been found in some CML-BC, MDS and AML that are associated with the t(3;3)(q21q26) and inv(3)(q21q26) chromosome abnormalities (Nucifora, 1997).…”

Section: Introductionmentioning

confidence: 99%

Both AML1 and EVI1 oncogenic components are required for the cooperation of AML1/MDS1/EVI1 with BCR/ABL in the induction of acute myelogenous leukemia in mice

Cuenco

Ren

2004

Oncogene

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We have previously shown that BCR/ABL, a fusion protein generated by the t(9;22)(q34;q11) translocation found in the vast majority of chronic myelogenous leukemia (CML), cooperates with AML1/MDS1/EVI1 (AME), a fusion transcription factor generated by a t(3;21)(q26;q22) translocation identified as a secondary mutation in some cases of CML during the blast phase (CML-BC), in the rapid induction of an acute myelogenous leukemia (AML) in mice. In this study, we evaluated the leukemogenic potential of EVI1-, MDS1/EVI1-and AML1-related oncoproteins (AML1D, AML1/MDS1). We found that ectopic expression of either EVI1 or MDS1/EVI1 impaired hematopoiesis. However, neither EVI1 nor MDS1/EVI1 was sufficient for inducing AML in mice, although EVI1 did induce some hematologic neoplasia other than AML with a low efficiency. In addition, unlike AME, none of the EVI1-or AML1-related oncoproteins examined were capable of fully cooperating with BCR/ABL in the induction of AML. The results indicate that both the AML1 and EVI1 oncogenic components are required for the leukemogenic potential of AME and for the cooperation of AME and BCR/ABL in the induction of AML.

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“…Therefore, a clear distinction of de novo AML and CML blast crisis remains challenging even in these inv(16)+ cases. The distribution of BCR-ABL p190 and p210 in inv(16)-CBF-AML was notably different from CML blast crisis: 53 % (9 cases) carried the p190 transcript in AML, whereas p190 was only found in one of 19 published cases of CML-AP/BC with inv (16) [18,19,[39][40][41][42][43][44][45][46][47][48]. Therefore, the detection of the minor BCR-ABL transcript in AML with inv(16) might be helpful in identifying de novo BCR-ABL+ AML.…”

Section: Characteristic Features Of Bcr-abl+ Amlmentioning

confidence: 99%

BCR-ABL-positive acute myeloid leukemia: a new entity? Analysis of clinical and molecular features

et al. 2016

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BCR-ABL-positive acute myeloid leukemia (AML) is a rare subtype of AML that is now included as a provisional entity in the 2016 revised WHO classification of myeloid malignancies. Since a clear distinction between de novo BCR-ABL+ AML and chronic myeloid leukemia (CML) blast crisis is challenging in many cases, the existence of de novo BCR-ABL+ AML has been a matter of debate for a long time. However, there is increasing evidence suggesting that BCR-ABL+ AML is in fact a distinct subgroup of AML. In this study, we analyzed all published cases since 1975 as well as cases from our institution in order to present common clinical and molecular features of this rare disease. Our analysis shows that BCR-ABL predominantly occurs in AML-NOS, CBF leukemia, and AML with myelodysplasia-related changes. The most common BCR-ABL transcripts (p190 and p210) are nearly equally distributed. Based on the analysis of published data, we provide a clinical algorithm for the initial differential diagnosis of BCR-ABL+ AML. The prognosis of BCR-ABL+ AML seems to depend on the cytogenetic and/or molecular background rather than on BCR-ABL itself. A therapy with tyrosine kinase inhibitors (TKIs) such as imatinib, dasatinib, or nilotinib is reasonable, but-due to a lack of systematic clinical data-their use cannot be routinely recommended in first-line therapy. Beyond first-line treatment of AML, the use of TKI remains an individual decision, both in combination with intensive chemotherapy and/or as a bridge to allogeneic stem cell transplantation. In each single case, potential benefits have to be weighed against potential risks.

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Early transformation to acute myeloblastic leukaemia with the acquisition of inv(16) in Ph positive chronic granulocytic leukaemia

Cited by 16 publications

References 10 publications

A case of chronic myeloid leukemia with minor bcr-abl transcript following fluorouracil therapy for esophageal carcinoma

A case of chronic myeloid leukemia with minor bcr-abl transcript following fluorouracil therapy for esophageal carcinoma

Both AML1 and EVI1 oncogenic components are required for the cooperation of AML1/MDS1/EVI1 with BCR/ABL in the induction of acute myelogenous leukemia in mice

BCR-ABL-positive acute myeloid leukemia: a new entity? Analysis of clinical and molecular features

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