Temporal association of marrow eosinophilia with inversion of chromosome 16 in recurrent blast crises of chronic myelogenous leukemia

Evers, Joseph P.; Bagg, Adam; Himoe, Eleanor; Zwiebel, James A.; Jacobson, Robert J.

doi:10.1016/0165-4608(92)90251-3

Cited by 18 publications

(8 citation statements)

References 23 publications

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“…Coexistence of inv(16) and t(9;22) is rare, with few reports in the literature (Table 1) [7][8][9][10][11][12][13][14][15][16][17][18][19][20]. These cases have been described mainly in blast phase of chronic myeloid leukemia, but some cases represent de novo acute myeloid leukemia (AML).…”

Section: Discussionmentioning

confidence: 97%

Coexistence of inversion 16 and the Philadelphia chromosome comprising P190 BCR/ABL in chronic myeloid leukemia blast crisis

et al. 2011

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A 63-year-old woman presented with leukocytosis (278 × 10(9)/L) with 72% blasts. Bone marrow blast cells showed cytogenetic abnormality with 46,XX, t(9;22), inv(16). Despite achievement of hematological remission by induction chemotherapy, Philadelphia chromosome did not disappear; chronic myeloid leukemia (CML) in blast crisis (BC) was thus diagnosed. The P190 BCR/ABL fusion transcript was detected. Imatinib mesylate introduced a hematological remission of short duration; however, infiltration into the central nervous system occurred, and the patient died 7 months after presentation. Coexistence of inv(16) and t(9:22) has been described in CML-BC and de novo AML, and CML-BC patients always carry P210 BCR/ABL, while de novo AML patients usually have P190 BCR/ABL. To the best of our knowledge, this is the first report of CML-BC with inv(16) and P190 BCR/ABL. We discuss this case with reference to the literature.

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Section: Discussionmentioning

confidence: 97%

Coexistence of inversion 16 and the Philadelphia chromosome comprising P190 BCR/ABL in chronic myeloid leukemia blast crisis

et al. 2011

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“…We describe 10 patients with simultaneous occurrence of BCR‐ABL1 and CBFB rearrangement. The co‐occurrence of BCR‐ABL1 and CBFB rearrangement is an extremely rare event with less than a total of 20 cases reported in the literature . There is a male predominance, and the disease can present in any age, although patients tend to be older than those with AML with inv(16)…”

Section: Discussionmentioning

confidence: 99%

Myeloid neoplasms with concurrent BCR‐ABL1 and CBFB rearrangements: A series of 10 cases of a clinically aggressive neoplasm

et al. 2017

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Chronic myeloid leukemia (CML) is defined by the presence of t(9;22)(q34;q11.2)/BCR-ABL1. Additional chromosomal abnormalities confer an adverse prognosis and are particularly common in the blast phase of CML (CML-BP). CBFB rearrangement, particularly CBFB-MYH11 fusion resulting from inv(16)(p13.1q22) or t(16;16)(p13.1;q22), is an acute myeloid leukemia (AML)-defining alteration that is associated with a favorable outcome. The co-occurrence of BCR-ABL1 and CBFB rearrangement is extremely rare, and the significance of this finding remains unclear. We identified 10 patients with myeloid neoplasms harboring BCR-ABL1 and CBFB rearrangement. The study group included six men and four women with a median age of 51 years (range, 20–71 years). The sequence of molecular alterations could be determined in nine cases: BCR-ABL1 preceded CBFB rearrangement in seven, CBFB rearrangement preceded BCR-ABL1 in one, and both alterations were discovered simultaneously in one patient. BCR-ABL1 encoded for p210 kD in all cases in which BCR-ABL1 preceded CBFB rearrangement; a p190 kD was identified in the other three cases. Two patients were treated with the FLAG-IDA regimen (fludarabine, cytarabine, idarubicin, and G-CSF) and tyrosine kinase inhibitors (TKI); seven with other cytarabine-based regimens and TKIs, and one with ponatinib alone. At last follow up (median, 16 months; range 2–85), 7 of 10 patients had died. The co-existence of BCR-ABL1 and CBFB rearrangement is associated with poor outcome and a clinical course similar to that of CML-BP, and unlike de novo AML with CBFB rearrangement, suggesting that high-intensity chemotherapy with TKI should be considered in these patients.

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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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Temporal association of marrow eosinophilia with inversion of chromosome 16 in recurrent blast crises of chronic myelogenous leukemia

Cited by 18 publications

References 23 publications

Coexistence of inversion 16 and the Philadelphia chromosome comprising P190 BCR/ABL in chronic myeloid leukemia blast crisis

Coexistence of inversion 16 and the Philadelphia chromosome comprising P190 BCR/ABL in chronic myeloid leukemia blast crisis

Myeloid neoplasms with concurrent BCR‐ABL1 and CBFB rearrangements: A series of 10 cases of a clinically aggressive neoplasm

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

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