Beta-Catenin Mutations are not Observed in Chronic Myeloid Leukemia

Sercan, Zeynep; Pehlivan, Melek; Göktürk, Dilek; Sercan, Hakki Ogun

doi:10.1177/030089160909500633

Cited by 8 publications

(7 citation statements)

References 23 publications

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“…Studies have demonstrated that deregulation of Wnt signaling pathway plays a role in the pathogenesis of CML. However, β-catenin amino-terminal mutations are not observed or are very rare and therefore are not the underlying mechanism of activated Wnt signaling in CML[54]. There must be other mechanisms for deregulating canonical Wnt signaling in CML.…”

Section: Introductionmentioning

confidence: 99%

Role of Wnt canonical pathway in hematological malignancies

Wang

2010

J Hematol Oncol

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Wnt canonical signaling pathway plays a diverse role in embryonic development and maintenance of organs and tissues in adults. It has been observed that Wnt/β-catenin signaling pathway is involved in the pathogenesis of many carcinomas. Moreover, Wnt/β-catenin pathway has been revealed to be associated with angiogenesis. Wnt canonical pathway signaling has great potential as a therapeutic target. It has been disclosed that some hematological malignancies, such as chronic lymphocytic leukemia, mantle cell lymphoma, may occur partly due to the constitutive activation of Wnt canonical signaling pathway. This review will summarize the latest development in Wnt canonical signaling pathway and its roles in tumorigenesis and angiogenesis.

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Section: Introductionmentioning

confidence: 99%

Role of Wnt canonical pathway in hematological malignancies

Wang

2010

J Hematol Oncol

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“…29 Nuclear accumulation of β-catenin is limited to HSCs, where it is the driving force of self-renewal. [8][9][10][11] Granulocyte-macrophage progenitors from CML blast crisis or therapy resistant disease also displays self-renewal capacity, a feature they normally do not posses. 16 Aberrant Wnt signaling and β-catenin nuclear accumulation in granulocyte-macrophage progenitors were shown to be responsible for this observation.…”

Section: Discussionmentioning

confidence: 99%

“…19,20 Although mutations of β-catenin, APC, and Axin-2 are frequently observed in a variety of epithelial cancers, they are infrequent in CML and in leukemia in general. 9 Epigenetic silencing of Wnt inhibitors and the stabilization and accumulation of β-catenin in cancers with or without mutational activation of Wnt/β-catenin signaling are another mechanisms that are observed in many cancers. [21][22][23][24][25] These proteins are able to inhibit and/or change the activity of Wnt proteins, thereby act as moderators of the signaling cascade and demonstrate a high frequency of aberrant promoter methylation in tumors.…”

Section: Introductionmentioning

confidence: 99%

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Forced expression of Wnt antagonists sFRP1 and WIF1 sensitizes chronic myeloid leukemia cells to tyrosine kinase inhibitors

et al. 2017

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Chronic myeloid leukemia is a clonal myeloproliferative disorder that arises from the neoplastic transformation of the hematopoietic stem cell, in which the Wnt/β-catenin signaling pathway has been demonstrated to play an important role in disease progression. However, the role of Wnt signaling antagonists in therapy resistance and disease progression has not been fully investigated. We aimed to study the effects of Wnt/β-catenin pathway antagonists-secreted frizzledrelated protein 1 and Wnt inhibitory factor 1-on resistance toward tyrosine kinase inhibitors in chronic myeloid leukemia. Response to tyrosine kinase inhibitors was analyzed in secreted frizzled-related protein 1 and Wnt inhibitory factor 1 stably transfected K562 cells. Experiments were repeated using a tetracycline-inducible expression system, confirming previous results. In addition, response to tyrosine kinase inhibitor treatment was also analyzed using the secreted frizzled-related protein 1 expressing, BCR-ABL positive MEG01 cell line, in the presence and absence of a secreted frizzled-related protein 1 inhibitor. Our data suggests that total cellular β-catenin levels decrease in the presence of secreted frizzled-related protein 1 and Wnt inhibitory factor 1, and a significant increase in cell death after tyrosine kinase inhibitor treatment is observed. On the contrary, when secreted frizzled-related protein 1 is suppressed, total β-catenin levels increase in the cell and the cells become resistant to tyrosine kinase inhibitors. We suggest that Wnt antagonists carry the potential to be exploited in designing new agents and strategies for the advanced and resistant forms of chronic myeloid leukemia.

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“…74 They are not, however, seen in leukemia. 75 Analyses of conditional ␤-catenin knockout mice show that ␤-catenin is essential to maintain ISCs 76 and HFSCs. 77 The role of Wnt/␤-catenin signaling in regulating HSCs, however, remains controversial.…”

Section: Negative Feedbackmentioning

confidence: 99%

Two anatomically distinct niches regulate stem cell activity

Ema

Suda

2012

Blood

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The niche microenvironment controls stem cell number, fate, and behavior. The bone marrow, intestine, and skin are organs with highly regenerative potential, and all produce a large number of mature cells daily. Here, focusing on adult stem cells in these organs, we compare the structures and cellular components of their niches and the factors they produce. We then define the niche as a functional unit for stem cell regulation. For example, the niche possibly maintains quiescence and regulates fate in stem cells. Moreover, we discuss our hypothesis that many stem cell types are regulated by both specialized and nonspecialized niches, although hematopoietic stem cells, as an exception, are regulated by a nonspecialized niche only. The specialized niche is composed of 1 or a few types of cells lying on the basement membrane in the epithelium. The nonspecialized niche is composed of various types of cells widely distributed in mesenchymal tissues. We propose that the specialized niche plays a role in local regulation of stem cells, whereas the nonspecialized niche plays a role in relatively broad regional or systemic regulation. Further work will verify this dual-niche model to understand mechanisms underlying stem cell regulation. (Blood. 2012;120(11): 2174-2181)

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Beta-Catenin Mutations are not Observed in Chronic Myeloid Leukemia

Abstract: Beta-catenin amino-terminal mutations are not observed or very rare and therefore are not the underlying mechanism of activated Wnt signaling in CML.

Cited by 8 publications

References 23 publications

Role of Wnt canonical pathway in hematological malignancies

Role of Wnt canonical pathway in hematological malignancies

Forced expression of Wnt antagonists sFRP1 and WIF1 sensitizes chronic myeloid leukemia cells to tyrosine kinase inhibitors

Two anatomically distinct niches regulate stem cell activity

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