S. Kreil

Publications90
h-index21
Citations4,117
Highly Influential Citations138
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Widespread occurrence of the JAK2 V617F mutation in chronic myeloproliferative disorders.
TLDR
It is concluded that V617F is widespread in MPDs and detection of this acquired mutation is likely to have a major impact on the way patients with MPD are diagnosed, as well as serving as an obvious target for signal transduction therapy.
Molecular and chromosomal mechanisms of resistance to imatinib (STI571) therapy
TLDR
Although the heterogeneous development of imatinib resistance is challenging, the fact that BCR-ABL is active in many resistant patients suggests that the chimeric oncoprotein remains a good therapeutic target.
Frequent CBL mutations associated with 11q acquired uniparental disomy in myeloproliferative neoplasms.
TLDR
It is concluded that acquired, transforming CBL mutations are a novel and widespread pathogenetic abnormality in morphologically related, clinically aggressive MPNs.
Response and resistance in 300 patients with BCR‐ABL–positive leukemias treated with imatinib in a single center
TLDR
The advent of imatinib has considerably changed the treatment of chronic myeloid leukemia and the hematologic and cytogenetic responses in all phases of the disease after limited observation periods.
Roots of Clinical Resistance to STI-571 Cancer Therapy
Early reduction of BCR-ABL mRNA transcript levels predicts cytogenetic response in chronic phase CML patients treated with imatinib after failure of interferon α
The degree of tumor load reduction as measured by cytogenetic response is an important prognostic factor for chronic myelogenous leukemia (CML) patients on therapy. We sought to determine whether…
Dynamics of BCR-ABL mutated clones prior to hematologic or cytogenetic resistance to imatinib
TLDR
D-HPLC is a sensitive method for screening for BCR-ABL mutations before and during therapy with tyrosine kinase inhibitors and small numbers of mutated clones could provide clinical benefit by triggering early therapeutic interventions.
Analysis of genomic breakpoints in p190 and p210 BCR–ABL indicate distinct mechanisms of formation
TLDR
Although the t(9;22) does not arise from aberrant variable (V), joining (J) and diversity (D) (V(D)J) recombination, the data suggest that in a subset of ALL cases RAG might create one of the initiating double-strand breaks.
Dynamics of BCR-ABL mRNA expression in first-line therapy of chronic myelogenous leukemia patients with imatinib or interferon α/ara-C
TLDR
It is concluded that treatment with imatinib in newly diagnosed CML patients is associated with a rapid decrease of BCR-ABL transcript levels, and nested PCR may reveal residual BCR/ABL transcripts in samples that are negative by real-time PCR.
Molecular monitoring of response to imatinib (Glivec®) in CML patients pretreated with interferon alpha. Low levels of residual disease are associated with continuous remission
TLDR
It is concluded that in patients with CCR to imatinib, HM-FISH and RT-PCR usually reveal residual BCR-ABL+ cells; RT- PCR results derived from PB and BM are comparable in CP CML; and low levels of residual disease with ratios BCR -ABL/ABL <0.1% are associated with continuous remission.
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