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Recurrent ETNK1 mutations in atypical chronic myeloid leukemia.
This study shows for the first time the evidence of recurrent somatic ETNK1 mutations in the context of myeloproliferative/myelodysplastic disorders.
Imatinib resistance in CML.
Increase sensitivity to chemotherapeutical agents and cytoplasmatic interaction between NPM leukemic mutant and NF-κB in AML carrying NPM1 mutations
The increased in vitro sensitivity of NPMc+ cells to chemotherapeutical agents and their reduced NF-κB activity is demonstrated and may provide a possible explanation for the increased rate of chemosensitivity observed among the N PMc+ patients.
BCR-ABL inactivates cytosolic PTEN through Casein Kinase II mediated tail phosphorylation
It is shown that nuclear exclusion of PTEN is associated with PTEN inactivation in the cytoplasm of CML cells, and a novel BCR-ABL/CKII/PTEN pathway is proposed as a potential target to achieve synthetic lethality with tyrosine kinase inhibitors.
The non-genomic loss of function of tumor suppressors: an essential role in the pathogenesis of chronic myeloid leukemia chronic phase
New insights on the role of FoxO, PP2A, p27, BLK, PTEN and other tumor suppressors in CML pathogenesis are described and strategies to promote tumor suppressor reactivation in C ML are described.
BCR-ABL disrupts PTEN nuclear-cytoplasmic shuttling through phosphorylation-dependent activation of HAUSP
This study identifies a new proto-oncogenic mechanism whereby BCR-ABL antagonizes the nuclear function of the PTEN tumor suppressor, with important therapeutic implications for the eradication of CML minimal residual disease.
The BCR-ABL/NF-κB signal transduction network: a long lasting relationship in Philadelphia positive Leukemias
The role of NF-κB in BCR-ABL-mediated leukemogenesis is summarized and new insights are provided on the long lasting BCR -ABL/NF-κBs connection.
The Role of PTEN in Myeloid Malignancies
The role of PTEN in the development of myeloid malignancies is described and Targeting those mechanisms that affect PTEN function could indeed promote PTEN reactivation with consequent cancer selective apoptosis induction.
Morgana acts as an oncosuppressor in chronic myeloid leukemia.
It is shown that morgana (+/-) mice spontaneously develop a lethal myeloproliferative disease resembling human atypical chronic myeloid leukemia (aCML), preceded by ROCK hyperactivation, centrosome amplification, and cytogenetic abnormalities in the bone marrow.
Landscape of Tumor Suppressor Mutations in Acute Myeloid Leukemia
This review summarizes the most relevant mutations affecting tumor suppressor genes that contribute to the onset and progression of AML pathology and suggests a new opportunity to exploit therapeutically.