Chronic Myeloid Leukemia, Version 2.2021, NCCN Clinical Practice Guidelines in Oncology

Deininger, Michael W.; Shah, Neil P.; Altman, Jessica K.; Berman, Ellin; Bhatia, Ravi; Bhatnagar, Bhavana; DeAngelo, Daniel J.; Gotlib, Jason; Hobbs, Gabriela; Maness, Lori J.; Mead, Monica; Metheny, Leland; Mohan, Sanjay; Moore, Joseph O.; Naqvi, Kiran; Oehler, Vivian G.; Pallera, Arnel; Patnaik, Mrinal M.; Pratz, Keith W.; Pusic, Iskra; Rose, Michal G.; Smith, B. Douglas; Snyder, David S.; Sweet, Kendra; Talpaz, Moshe; Thompson, James E.; Yang, David T.; Gregory, Kristina M.; Sundar, Hema

doi:10.6004/jnccn.2020.0047

Cited by 186 publications

(233 citation statements)

References 268 publications

(370 reference statements)

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“…Guidelines also suggest proper follow-up includes frequent molecular monitoring, with monthly visits for the first six months and then every three months thereafter. In general, though, the reference criteria in TKI discontinuation eligibility outside of a clinical trial are quite strict as shown by both the ESMO and the very recently updated NCCN guidelines (17). A shared recommendation is to exclude patients with high Sokal risk or with a previous history of accelerated phase or blast phase CML.…”

Section: Discussionmentioning

confidence: 99%

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Accelerated Phase Chronic Myeloid Leukemia and Treatment Free Remission Maintained After Five Years of Nilotinib: A Case Report

et al. 2021

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The present article reports the case of a patient presenting with chronic myeloid leukemia, diagnosed during the accelerated phase (>20% blasts in peripheral blood samples and megakaryocyte agglomerates in the bone marrow). The subject was treated with first-line therapy with the tyrosine kinase inhibitor nilotinib and reached complete clinical and molecular remission (according to the European Leukemia Net-ELN-criteria), which persisted over five years of treatment. Five years after discontinuation of nilotinib (ten years from diagnosis), the patient is in good clinical condition, with no traces of BCL-ABL1 at molecular evaluation (molecular response, MR5). The case is discussed in the setting of current literature, providing an overview on chronic myeloid leukemia and a discussion on treatment options available.

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Section: Discussionmentioning

confidence: 99%

“…However, because data available on treatment-free remission (TFR) are only for patients in the chronic phase and not for CML in advanced phases, current clinical guidelines and recommendations suggest TFR for chronic-phase patients only (17)(18)(19).…”

Section: Introductionmentioning

confidence: 99%

Accelerated Phase Chronic Myeloid Leukemia and Treatment Free Remission Maintained After Five Years of Nilotinib: A Case Report

et al. 2021

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“…Furthermore, BM-MNCs of 30 healthy donors were used as normal controls (NC). Chronic myeloid leukemia was diagnosed by molecular biology, bone marrow morphology, immunology, and cytogenetics examination (19,20). Patients with severe cardiopulmonary, renal or liver failure or coagulation abnormality or pregnant were excluded.…”

Section: Specimen Collectionmentioning

confidence: 99%

HNRNPH1 Is a Novel Regulator Of Cellular Proliferation and Disease Progression in Chronic Myeloid Leukemia

et al. 2021

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RNA binding proteins act as essential modulators in cancers by regulating biological cellular processes. Heterogeneous nuclear ribonucleoprotein H1 (HNRNPH1), as a key member of the heterogeneous nuclear ribonucleoproteins family, is frequently upregulated in multiple cancer cells and involved in tumorigenesis. However, the function of HNRNPH1 in chronic myeloid leukemia (CML) remains unclear. In the present study, we revealed that HNRNPH1 expression level was upregulated in CML patients and cell lines. Moreover, the higher level of HNRNPH1 was correlated with disease progression of CML. In vivo and in vitro experiments showed that knockdown of HNRNPH1 inhibited cell proliferation and promoted cell apoptosis in CML cells. Importantly, knockdown of HNRNPH1 in CML cells enhanced sensitivity to imatinib. Mechanically, HNRNPH1 could bind to the mRNA of PTPN6 and negatively regulated its expression. PTPN6 mediated the regulation between HNRNPH1 and PI3K/AKT activation. Furthermore, the HNRNPH1–PTPN6–PI3K/AKT axis played a critical role in CML tumorigenesis and development. The present study first investigated the deregulated HNRNPH1–PTPN6–PI3K/AKT axis moderated cell growth and apoptosis in CML cells, whereby targeting this pathway may be a therapeutic CML treatment.

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“…Indeed, several current CML guidelines advocate the use of a sustained DMR, for at least 2 years, to select patients for consideration of TKI cessation. 10 , 11 …”

Section: Clinically Validated Tests For Detecting and Monitoring Bcr-abl1 And Kit Mutationsmentioning

confidence: 99%

Interrogating the molecular genetics of chronic myeloproliferative malignancies for personalized management in 2021

et al. 2021

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Chronic Myeloid Leukemia, Version 2.2021, NCCN Clinical Practice Guidelines in Oncology

Cited by 186 publications

References 268 publications

Accelerated Phase Chronic Myeloid Leukemia and Treatment Free Remission Maintained After Five Years of Nilotinib: A Case Report

Accelerated Phase Chronic Myeloid Leukemia and Treatment Free Remission Maintained After Five Years of Nilotinib: A Case Report

HNRNPH1 Is a Novel Regulator Of Cellular Proliferation and Disease Progression in Chronic Myeloid Leukemia

Interrogating the molecular genetics of chronic myeloproliferative malignancies for personalized management in 2021

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