Chronic Myelogenous Leukemia: Role of Stem Cell Transplant in the Imatinib Era

Jain, Nitin; Besien, Koen van

doi:10.1016/j.hoc.2011.09.003

Cited by 12 publications

(18 citation statements)

References 119 publications

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“…Moreover patients who have undergone HSCT are also at higher risk of developing SCs ( Tanaka et al, 2015 ). Total body irradiation (TBI) in combination with cyclophosphamide was the preferred regimen for conditioning prior to transplant in the past ( Jain & van Besien, 2011 ). In the more recent times non-myeloablative regimens or reduced intensity conditioning (RIC) are preferred and TBI (at 200 cGY) with fludarabine is one of them.…”

Section: Discussionmentioning

confidence: 99%

“…Although it can be safely assumed that most of the patients with CML who were diagnosed in the post TKI era, received TKIs as they are the treatment of choice for CML since FDA approval in May 2001. Currently, other therapies are restricted to a small number of patients who are resistant to second generation TKIs or harbor TKIs resistant mutations like T3151 ( Jain & van Besien, 2011 ).…”

Section: Introductionmentioning

confidence: 99%

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An observational study on risk of secondary cancers in chronic myeloid leukemia patients in the TKI era in the United States

Kumar

Garg

Chaudhary

et al. 2018

PeerJ

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IntroductionThe treatment with tyrosine kinase inhibitors (TKIs) has drastically improved the outcome of chronic myeloid leukemia (CML) patients. This study was conducted to examine the risk of secondary cancers (SCs) in the CML patients who were diagnosed and treated in the TKI era in the United States.MethodsThe surveillance epidemiology and end results (SEER) database was used to identify CML patients who were diagnosed and received treatment during January 2002–December 2014. Standardized incidence ratios (SIRs) and absolute excess risks (AER) were calculated.ResultsOverall, 511 SCs (excluding acute leukemia) developed in 9,200 CML patients followed for 38,433 person-years. The risk of developing SCs in the CML patients was 30% higher than the age, sex and race matched standard population (SIR 1.30, 95% CI: 1.2–1.40; p < 0.001). The SIRs for CLL (SIR 3.4, 95% CI: 2–5.5; p < 0.001), thyroid (SIR 2.2, 95% CI: 1.2–3.5; p < 0.001), small intestine (SIR 3.1, 95% CI: 1.1–7; p = 0.004), gingiva (SIR 3.7, 95% CI: 1.2–8.7; p = 0.002), stomach (SIR 2.1, 95% CI: 1.1–3.5; p = 0.005), lung (SIR 1.4, 95% CI: 1.1–1.7; p = 0.006) and prostate (SIR 1.3, 95% CI: 1.02–1.6; p = 0.026) cancer among CML patients were significantly higher than the general population. The risk of SCs was higher irrespective of age and it was highest in the period 2–12 months after the diagnosis of CML. The risk of SCs in women was similar to that of the general population.ConclusionCML patients diagnosed and treated in the TKI era in the United States are at an increased risk of developing a second malignancy. The increased risk of SCs in the early period after CML diagnosis suggests that the risk of SCs may be increased due to the factors other than TKIs treatment.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

An observational study on risk of secondary cancers in chronic myeloid leukemia patients in the TKI era in the United States

Kumar

Garg

Chaudhary

et al. 2018

PeerJ

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“…High morbidity and relapse rates may be anticipated. After transplantation, continuation of the TKI is preferred in lymphoid BC and in general, TKI treatment is recommended for myeloid BC [63]. Figure 2 provides a flow diagram for treatment decisions in BC.…”

Section: Treatment Of Bcmentioning

confidence: 99%

Management of chronic myeloid leukemia in blast crisis

Saußele

Silver

2015

Ann Hematol

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Due to the high efficacy of BCR-ABL tyrosine kinase inhibition (TKI) in chronic phase (CP) chronic myeloid leukemia (CML), the frequency of blast crisis (BC) is greatly reduced compared to the pre-TKI era. However, TKI treatment of BC has only marginally improved the number of favorable responses, including remissions, which for the most part have only been transitory. Occasionally, they provide a therapeutic window to perform an allogeneic stem cell transplantation (allo-SCT). The challenge remains to improve management of BC with the limited options available. We review and summarize articles pertaining to the treatment of BC CML published after 2002. Additionally, we will discuss whether there is a need for a new definition of BC and/or treatment failure.

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“…Molecular-targeted therapy drug of STI571 and specific RNA interference technology had a milestone in the treatment of CML (Zaree-Mahmodabady et al, 2010;Jain and van Besien, 2011), even expressing a trend to replace bone marrow transplant. With the further research, it was found that CML cells would gradually develop drug-resistant mechanisms against the above treatments.…”

Section: Discussionmentioning

confidence: 99%

Study on the treatment of the p15 gene combined with Bcr-abl-specific siRNA and STI571 for chronic myeloid leukemia

Wang

et al. 2014

Genet. Mol. Res.

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ABSTRACT. The aim of this study was to investigate the effect of the p15 gene combined with Bcr-abl-specific siRNA and STI571 on the proliferation, cell cycle and apoptosis of K562 chronic myeloid leukemia cells. Using the gene sequence results, we amplified the p15 gene from normal peripheral blood by RT-PCR, and constructed a p15-pcDNA3.1 vector. The K562 cell line with G418 resistance was screened, synthesized and transfected for bcr-abl gene fusion point for 21-nt siRNA. In p15-pcDNA3.1-K562 cells, the growth rate was slower than that of the control K562 cells, G0/G1-phase was increased and S-phase was decreased significantly. In the siRNA group, bcr-abl fusion gene expression was significantly decreased in K562 cells accompanied by the downregulation of BCL-xL protein expression and G1-phase arrest. Cell survival rate was significantly decreased compared with the sole p15-K562 cell group and the sole RNA interference-K562 cell group. In the combination of p15-pcDNA3.1-K562 cells with STI571, the proportion of apoptosis was significantly increased and the cell survival rate was significantly decreased compared with the p15-K562 cell group and STI571-K562 cell group. siRNA at 30 pM combined with 0.5 μM STI571 promoted apoptosis compared with sole application. The p15 gene combined with siRNA had a synergistic effect on the inhibition of proliferation and the induction of apoptosis in K562 cells. Exogenous p15 protein expression combined with STI571 appeared to have a synergistic effect on proliferation inhibition and apoptosis induction in K562 cells. The combination of low-dose RNA interference with STI571 showed a synergistic effect in inducing apoptosis.

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Chronic Myelogenous Leukemia: Role of Stem Cell Transplant in the Imatinib Era

Cited by 12 publications

References 119 publications

An observational study on risk of secondary cancers in chronic myeloid leukemia patients in the TKI era in the United States

An observational study on risk of secondary cancers in chronic myeloid leukemia patients in the TKI era in the United States

Management of chronic myeloid leukemia in blast crisis

Study on the treatment of the p15 gene combined with Bcr-abl-specific siRNA and STI571 for chronic myeloid leukemia

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