Philadelphia-positive patients who already harbor imatinib-resistant Bcr-Abl kinase domain mutations have a higher likelihood of developing additional mutations associated with resistance to second- or third-line tyrosine kinase inhibitors.

doi:10.1182/blood-2009-01-197186

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Community

Back to search

Article

Philadelphia-positive patients who already harbor imatinib-resistant Bcr-Abl kinase domain mutations have a higher likelihood of developing additional mutations associated with resistance to second- or third-line tyrosine kinase inhibitors.

Blood - 3 Sept 2009

Soverini Simona, Gnani Alessandra, Colarossi Sabrina, Castagnetti Fausto, Abruzzese Elisabetta, Paolini Stefania, Merante Serena, Orlandi Ester, de Matteis Silvia, Gozzini Antonella, Iacobucci Ilaria, Palandri Francesca, Gugliotta Gabriele, Papayannidis Cristina, Poerio Angela, Amabile Marilina, Cilloni Daniela, Rosti Gianantonio, Baccarani Michele, Martinelli Giovanni

Abstract excerpt

Dasatinib and nilotinib are tyrosine kinase inhibitors (TKIs) developed to overcome imatinib resistance in Philadelphia-positive leukemias. To assess how Bcr-Abl kinase domain mutation status evolves during sequential therapy with these TKIs and which mutations may further develop and impair their efficacy, we monitored the mutation status of 95 imatinib-resistant patients before and during treatment with...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Benzamides

Methodology Data sources Editorial policy Privacy Delete account & data About Contact Helena Bioinformatics

Share to Dasatinib

Share to Fusion Proteins, bcr-abl

Share to Imatinib Mesylate

Share to Leukemia, Myelogenous, Chronic, BCR-ABL Positive

Share to Piperazines

Share to Precursor Cell Lymphoblastic Leukemia-Lymphoma

Share to Thiazoles

Source

Open in PubMed

Identifiers

PMID: 19589924
DOI: 10.1182/blood-2009-01-197186

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-08.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence. Graph snapshot: 2026-09-29.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Philadelphia-positive patients who already harbor imatinib-resistant Bcr-Abl kinase domain mutations have a higher likelihood of developing additional mutations associated with resistance to second- or third-line tyrosine kinase inhibitors.PMID 19589924Read ↗

Patients with Philadelphia-positive leukemia with Y253H or F359V mutation have a high risk of developing new mutations in the setting of dasatinib resistance.Semantic proximity Read ↗

The landscape of BCR-ABL mutations in patients with Philadelphia chromosome-positive leukaemias in the era of second-generation tyrosine kinase inhibitors.Semantic proximity Read ↗

Dynamics of BCR-ABL kinase domain mutations in chronic myeloid leukemia after sequential treatment with multiple tyrosine kinase inhibitors.Semantic proximity Read ↗

In chronic myeloid leukemia patients on second-line tyrosine kinase inhibitor therapy, deep sequencing of BCR-ABL1 at the time of warning may allow sensitive detection of emerging drug-resistant mutants.Semantic proximity Read ↗

Emergence of BCR-ABL kinase domain mutations associated with newly diagnosed chronic myeloid leukemia: a meta-analysis of clinical trials of tyrosine kinase inhibitors.Semantic proximity Read ↗

Drug resistance and BCR-ABL kinase domain mutations in Philadelphia chromosome-positive acute lymphoblastic leukemia from the imatinib to the second-generation tyrosine kinase inhibitor era: The main changes are in the type of mutations, but not in the frequency of mutation involvement.Semantic proximity Read ↗

Patients with Philadelphia-positive leukemia with BCR-ABL kinase mutations before allogeneic transplantation predominantly relapse with the same mutation.Semantic proximity Read ↗

Presence or the emergence of a F317L BCR-ABL mutation may be associated with resistance to dasatinib in Philadelphia chromosome-positive leukemia.Semantic proximity Read ↗

Primary imatinib resistance in chronic myeloid leukemia patients in a developing country: BCR-ABL kinase domain mutations or BCR-ABL independent mechanisms?Semantic proximity Read ↗

Kinase domain point mutations in Philadelphia chromosome‐positive acute lymphoblastic leukemia emerge after therapy with BCR‐ABL kinase inhibitorsSemantic proximity Read ↗

BCR-ABL1 kinase domain mutations may persist at very low levels for many years and lead to subsequent TKI resistance.Semantic proximity Read ↗

Long-term outcome of patients with chronic myeloid leukemia treated with second-generation tyrosine kinase inhibitors after imatinib failure is predicted by the in vitro sensitivity of BCR-ABL kinase domain mutations.Semantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.