Antecedent CHIP in CML?

Walter, Matthew J.

doi:10.1182/blood-2016-11-746842

Cited by 4 publications

(3 citation statements)

References 10 publications

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“…Here we reported a case of a post-transplant molecular relapsed ALL patient treated with the combo ponatinib-DLI, who achieved a sustained long-term response with MRD negativity (+22 months). TKI inhibitors are known to be unable to eradicate leukemic clones, mainly due to the fact that stem leukemic clones are often Ph-or BCR-ABL independent, thus being not targetable with current drugs (12). On the other hands, the infusion of DLI from an allogeneic donor could induce deep remissions but at the cost of significant toxicity (such as GVHD) (13,14).…”

Section: Discussionmentioning

confidence: 99%

Long-Term Remission Achieved by Ponatinib and Donor Lymphocytes Infusion in a Ph+ Acute Lymphoblastic Leukemia Patient in Molecular Relapse After Allogenic Stem Cell Transplant and Dasatinib: A Case Report

et al. 2020

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Currently, the prognosis of Ph+ acute lymphoblastic leukemia (Ph+ ALL) patients relapsing after an allogenic hematopoietic stem cell transplantation (allo-SCT) remains poor, with few therapeutic options available. Here we present the case of a 32 years old patient with dasatinib-resistant post-transplant molecular relapse of ALL, who received, as second-line therapy, the combination of ponatinib and donor lymphocyte infusion (DLI). The therapy was safe and the patient achieved a sustained minimal residual disease negative disease, still ongoing after 22 months, which was accompanied by several changes in the immune populations distribution within the bone marrow (i.e., the increase in the CD8/CD4 lymphocytes ratio). Our report provides evidence of the efficacy of the third generation TKI inhibitor ponatinib in combination with DLI as second line therapy for Ph+ ALL relapsing after an allo-SCT.

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Section: Discussionmentioning

confidence: 99%

Long-Term Remission Achieved by Ponatinib and Donor Lymphocytes Infusion in a Ph+ Acute Lymphoblastic Leukemia Patient in Molecular Relapse After Allogenic Stem Cell Transplant and Dasatinib: A Case Report

et al. 2020

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“…Secondary hematologic neoplasms reported in the previous studies occurred primarily in older patients, suggesting that a possible antecedent clonal hematopoiesis of indeterminate potential (CHIP) progressed while CML was well controlled on TKIs. 2,10,11 Recent genomic studies have demonstrated the clonal diversity in the evolution of CML and showed that the mutational persistence does not alter the response to TKIs. These mutations are predominantly in epigenetic machinery (TET2, ASXL1, and DNMT3A) that are commonly attributed to the development of CHIP.…”

Section: Discussionmentioning

confidence: 99%

Not So Typical: Development of Atypical Chronic Myeloid Leukemia in a Patient With Chronic Myeloid Leukemia

Saba

Bhamidipati

Cashen

2017

JCO Precision Oncology

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“…However, the finding of ASXL1 mutations in CML patients with a lower median age (<60 years) and at even higher frequency among children and young adults (29%), and, on the other hand, the identification of DNMT3A mutations at lower frequency in CML compared to CHIP and other myeloid neoplasms suggest that the acquisition of these mutations in CML is not an age- but a disease-related event [ 133 , 142 , 143 ]. At this stage, the role played by CHIP-related mutations in the initiation and mutational landscape of CML is still to be clarified [ 144 ].…”

Section: Baseline Prognostic Factorsmentioning

confidence: 99%

Prognosis in Chronic Myeloid Leukemia: Baseline Factors, Dynamic Risk Assessment and Novel Insights

Iezza

Cortesi

Ottaviani

et al. 2023

Cells

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The introduction of tyrosine kinase inhibitors (TKIs) has changed the treatment paradigm of chronic myeloid leukemia (CML), leading to a dramatic improvement of the outcome of CML patients, who now have a nearly normal life expectancy and, in some selected cases, the possibility of aiming for the more ambitious goal of treatment-free remission (TFR). However, the minority of patients who fail treatment and progress from chronic phase (CP) to accelerated phase (AP) and blast phase (BP) still have a relatively poor prognosis. The identification of predictive elements enabling a prompt recognition of patients at higher risk of progression still remains among the priorities in the field of CML management. Currently, the baseline risk is assessed using simple clinical and hematologic parameters, other than evaluating the presence of additional chromosomal abnormalities (ACAs), especially those at “high-risk”. Beyond the onset, a re-evaluation of the risk status is mandatory, monitoring the response to TKI treatment. Moreover, novel critical insights are emerging into the role of genomic factors, present at diagnosis or evolving on therapy. This review presents the current knowledge regarding prognostic factors in CML and their potential role for an improved risk classification and a subsequent enhancement of therapeutic decisions and disease management.

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Antecedent CHIP in CML?

Cited by 4 publications

References 10 publications

Long-Term Remission Achieved by Ponatinib and Donor Lymphocytes Infusion in a Ph+ Acute Lymphoblastic Leukemia Patient in Molecular Relapse After Allogenic Stem Cell Transplant and Dasatinib: A Case Report

Long-Term Remission Achieved by Ponatinib and Donor Lymphocytes Infusion in a Ph+ Acute Lymphoblastic Leukemia Patient in Molecular Relapse After Allogenic Stem Cell Transplant and Dasatinib: A Case Report

Not So Typical: Development of Atypical Chronic Myeloid Leukemia in a Patient With Chronic Myeloid Leukemia

Prognosis in Chronic Myeloid Leukemia: Baseline Factors, Dynamic Risk Assessment and Novel Insights

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