Complete molecular response of e6a2 BCR-ABL–positive acute myeloid leukemia to imatinib then dasatinib

Ritchie, David; McBean, Michelle; Westerman, David; Kovalenko, S.; Seymour, John F.; Dobrovic, Alexander

doi:10.1182/blood-2007-08-107508

Cited by 21 publications

(6 citation statements)

References 16 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…These patients underwent allo-SCT in first CR after TKIs and chemotherapy. In these cases, dasatinib and nilotinib were effective treatments in inducing molecular remission after imatinib failure [22, 23] and against relapse after transplant maybe thanks to synergy between TKI and the graft versus-leukemia effect, reaching sustained response [21, 22]. They were alive at 24, 30 and 52 months from diagnosis [21–23].…”

Section: Discussionmentioning

confidence: 99%

A rare BCR-ABL1 transcript in Philadelphia-positive acute myeloid leukemia: case report and literature review

et al. 2019

View full text Add to dashboard Cite

BackgroundPhiladelphia (Ph) chromosome results from the reciprocal translocation t(9;22)(q34.1;q11.2) and is diagnostic for chronic myeloid leukemia (CML). However, this translocation is also found in acute lymphoid leukemia (ALL), as well as in rare cases of acute myeloid leukemias (AML). Most patients with CML harbor either the e13a2 or the e14a2 BCR-ABL fusion product, while a small subset of the cases expresses e1a2 or e19a2 transcripts. Moreover, several atypical BCR-ABL1 transcripts, beside the most common e1a2, e13a2 and e14a2, have been described, mainly in patients with CML. However, ALL and de novo AML may also carry BCR-ABL1 atypical transcripts which will confer a poor prognosis.Case presentationA 78-years old male was admitted at our hospital with clinical and laboratory features allowing to make the diagnosis of AML. No evidence of a preceding CML (splenomegaly or basophilia) was found. The karyotype on G-banded metaphases was 46,XY, t(9;22)(q34;q11). While the molecular analysis was ongoing, the patient started treatment based on hydroxyurea followed by 5-aza-2′-deoxycytidine. The molecular biology analysis revealed the simultaneous presence of the common p190 e1a2 and the rare e6a2 isoforms. Because of persistent pancytopenia and presence of blasts, according to the molecular data, he was then switched to tyrosine kinase inhibitors (TKIs) treatment. Nevertheless, after 2 months, the patient was still refractory to second line treatment dying because of a pulmonary infection.ConclusionThe atypical p190 e6a2 transcript seems to be associated in AML with aggressive disease. TKI therapy alone does not seem to control the disease. Prompt observations on these patients carrying rare BCR-ABL1 transcripts may help to establish optimal treatment approaches on these aggressive BCR-ABL1 phenotypes in different setting of patients.

show abstract

Section: Discussionmentioning

confidence: 99%

A rare BCR-ABL1 transcript in Philadelphia-positive acute myeloid leukemia: case report and literature review

et al. 2019

View full text Add to dashboard Cite

show abstract

“…A good initial response was seen to a tyrosine kinase inhibitor, despite this and the presence of monosomy-7, another poor prognostic indicator. Although there are reported cases of good responses to tyrosine kinase inhibitors in Philadelphia-positive acute myeloid leukaemia (Kindler et al, 2003;Ritchie et al, 2008), none to our knowledge have presented with monosomy 7. It is perhaps not surprising, however, that relapse did eventually occur requiring myeloablative chemotherapy and allogeneic stem-cell transplant.…”

Section: Previously Undescribed Lytic Foci In the Axial Skeletonmentioning

confidence: 62%

Lytic bone disease as the presenting feature of Philadelphia-positive monosomy 7 myelodysplasia progressing to acute myeloid leukaemia

Tucker

Hamilton

Kerr

et al. 2012

Gene

View full text Add to dashboard Cite

“…Several case reports demonstrating the efficacy of tyrosine kinase inhibitors like imatinib and dasatinib towards BCR-ABL1 + AML [3,11,12,13,14,15] have been published, but there is only one report on nilotinib [16]. …”

Section: Discussionmentioning

confidence: 99%

BCR-ABL1+ Acute Myeloid Leukemia: Clonal Selection of a BCR-ABL1- Subclone as a Cause of Refractory Disease with Nilotinib Treatment

Neuendorff¹,

Schwarz²,

Hemmati³

et al. 2014

Acta Haematol

View full text Add to dashboard Cite

The presence of a Philadelphia chromosome with a corresponding BCR-ABL1 rearrangement is the hallmark of chronic myeloid leukemia, but is considered a very rare event in de novo acute myeloid leukemia (AML). Here, we report the first case in which a dominant Philadelphia chromosome-positive subclone was detected upon relapse in a formerly Philadelphia chromosome-negative MLL-AF6⁺ AML. Due to refractory disease under salvage chemotherapy, the patient was started on nilotinib treatment. As a result, the Philadelphia chromosome-positive subclone was eradicated within 1 month; however, disease progressed and was again dominated by the Philadelphia chromosome-negative founding clone, demonstrating rapid clonal expansion under nilotinib-induced selection pressure. © 2014 S. Karger AG, Basel

show abstract

Complete molecular response of e6a2 BCR-ABL–positive acute myeloid leukemia to imatinib then dasatinib

Cited by 21 publications

References 16 publications

A rare BCR-ABL1 transcript in Philadelphia-positive acute myeloid leukemia: case report and literature review

A rare BCR-ABL1 transcript in Philadelphia-positive acute myeloid leukemia: case report and literature review

Lytic bone disease as the presenting feature of Philadelphia-positive monosomy 7 myelodysplasia progressing to acute myeloid leukaemia

<b><i>BCR-ABL1</i></b><sup><i>+</i></sup> Acute Myeloid Leukemia: Clonal Selection of a <b><i>BCR-ABL1</i></b><sup><i>-</i></sup> Subclone as a Cause of Refractory Disease with Nilotinib Treatment

Contact Info

Product

Resources

About