Philadelphia Chromosome–Positive Acute Myeloid Leukemia

Soupir, Chad P.; Vergilio, Jo Anne; Cin, Paola Dal; Muzikansky, Alona; Kantarjian, Hagop M.; Jones, Dan; Hasserjian, Robert P.

doi:10.1309/b4nver1ajj84ctuu

Cited by 168 publications

(46 citation statements)

References 28 publications

(47 reference statements)

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“…The prognosis of BCR-ABL1 + AML is usually regarded as dismal [3], but given the paucity of cases and still-missing prospective data, a definitive prognostic impact of BCR-ABL1 in AML can hardly be established. This is also due to the fact that other adverse cytogenetic aberrations like monosomy 7 or complex-aberrant karyotypes [2] are present in several BCR-ABL1 + AML cases reported so far.…”

Section: Discussionmentioning

confidence: 99%

“…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%

“…The incidence of BCR-ABL1 transcripts in de novo AML ranges from 0.48 to 3% [1,2,3]. Here, we report on an AML patient who acquired a BCR-ABL1 + subclone upon relapse and was treated with nilotinib (Tasigna®, Novartis Pharma).…”

Section: Introductionmentioning

confidence: 99%

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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

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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

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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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

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“…Some reports have suggested that IM is effective in maintaining CHR and achieving molecular responses [6,7]. Although the possibility of resistance or relapse with IM therapy still exists [3,8], IM may be considered as part of first-line therapy for patients with de novo Ph+ AML. …”

Section: Discussionmentioning

confidence: 99%

“…De novo Ph+ acute myeloid leukemia (AML) is an infrequent disease found in only 1–2% of newly diagnosed AML patients [1,2] with a median survival of only 9 months [3]. Most patients do not achieve remission and many early relapses are observed following standard treatment with conventional chemotherapy [1].…”

Section: Introductionmentioning

confidence: 99%

Prolonged Survival with Imatinib Mesylate Combined with Chemotherapy and Allogeneic Stem Cell Transplantation in de novo Ph+ Acute Myeloid Leukemia

et al. 2012

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Background: De novo Philadelphia chromosome-positive (Ph+) acute myeloid leukemia (AML) is a rare disease with a poor prognosis. Imatinib mesylate (IM) is the standard treatment for Ph+ chronic myeloid leukemia and Ph+ acute lymphoblastic leukemia; however, its role in Ph+ AML has not been extensively investigated. Methods: Two patients aged of 46 and 19 years were diagnosed with de novo Ph+ AML according to the WHO Classification of Myeloid Neoplasms (2002) and the French-American-British (FAB) classification systems (1989). Cytogenetic analysis confirmed the presence of t(9;22). Standard RT-PCR was used to detect expression of the BCR-ABL1 fusion gene. Minimal residual disease was monitored by RQ-PCR for the BCR-ABL1/ABL ratio. Both patients received initial IM therapy combined with daunorubicin-based chemotherapy followed by allogeneic hematopoietic stem cell transplantation (allo-HSCT) and IM maintenance treatment after allo-HSCT. Results: Both patients achieved long-term disease-free survival with complete hematologic response, complete molecular response, and complete cytogenetic response for 44 and 48 months, respectively. Conclusions: Our cases indicate that IM combined with daunorubicin-based chemotherapy followed by allo-HSCT and IM maintenance treatment is associated with a favorable outcome for de novo Ph+ AML, especially when IM is used in an early phase of AML.

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Acute Myeloid Leukemia

Johansson¹,

Harrison²

2010

Cancer Cytogenetics

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Philadelphia Chromosome–Positive Acute Myeloid Leukemia

Cited by 168 publications

References 28 publications

<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

<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

Prolonged Survival with Imatinib Mesylate Combined with Chemotherapy and Allogeneic Stem Cell Transplantation in de novo Ph+ Acute Myeloid Leukemia

Acute Myeloid Leukemia

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