STAT transcript levels in childhood acute lymphoblastic leukemia: STAT1 and STAT3 transcript correlations

Adamaki, Maria; Tsotra, Maria; Vlahopoulos, Spiros; Zampogiannis, A.; Papavassiliou, Athanasios G.; Moschovi, Maria

doi:10.1016/j.leukres.2015.09.004

Cited by 11 publications

(8 citation statements)

References 23 publications

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“…STAT3, STAT5A, and STAT5B are downstream targets of JAK proteins and promote cell proliferation through the CRLF2/IL7RA pathway . Low STAT1 and STAT3 levels have been related to improved outcome in childhood ALL . On the other hand, the ABCC3 (MRP3) drug transporter has been implicated in resistance to daunorubicin, doxorubicin, vincristine, and methotrexate and is a marker of poor prognosis in childhood ALL .…”

Section: Discussionmentioning

confidence: 99%

Copy number profiling of adult relapsed B‐cell precursor acute lymphoblastic leukemia reveals potential leukemia progression mechanisms

Ribera

Zamora

Morgades

et al. 2017

Genes Chromosomes & Cancer

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The outcome of relapsed adult acute lymphoblastic leukemia (ALL) remains dismal despite new therapeutic approaches. Previous studies analyzing relapse samples have shown a high degree of heterogeneity regarding gene alterations without an evident relapse signature. Bone marrow or peripheral blood samples from 31 adult B-cell precursor ALL patients at first relapse, and 21 paired diagnostic samples were analyzed by multiplex ligation probe-dependent amplification (MLPA). Nineteen paired diagnostic and relapse samples of these 21 patients were also analyzed by SNP arrays. A trend to acquire homozygous CDKN2A/B deletions and a significant increase in the number of copy number alterations (CNA) was observed from diagnosis to first relapse. Evolution from an ancestral clone was the main pattern of clonal evolution. Relapse samples were extremely heterogeneous regarding CNA frequencies. However, CDKN2A/B, PAX5, ETV6, ATM, IKZF1, VPREB1, and TP53 deletions and duplications of 1q, 8q, 17q, 21, X/Y PAR1, and Xp were frequently detected at relapse. Duplications of genes involved in cell proliferation, drug resistance and stem cell homeostasis regulation, as well as deletions of KDM6A and STAG2 genes emerged as specific alterations at relapse. Genomics of relapsed adult B-cell precursor ALL is highly heterogeneous, although some recurrent lesions involved in essential pathways deregulation were frequently observed. Selective and simultaneous targeting of these deregulated pathways may improve the results of current salvage therapies.

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Section: Discussionmentioning

confidence: 99%

Copy number profiling of adult relapsed B‐cell precursor acute lymphoblastic leukemia reveals potential leukemia progression mechanisms

Ribera

Zamora

Morgades

et al. 2017

Genes Chromosomes & Cancer

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“…197,281 In normal tissues, STAT3 would protect from excessive Th1 activity and inflammation. 147,287,288 Therefore, the activation of STAT3 by constitutive DNA damage in cancer cells could facilitate selective drug effects on the tumor nest through the circulation, while having discrete indirect effects on the local tissue microenvironment owing to the secretome of the tumor. [283][284][285][286] However, unlike malignant tissue niches, normal tissue uses the intact regulatory network of STAT3 and NF-jB as a common mechanism to recover from inflammation.…”

Section: Feasibility Of Treating Malignant Tumors With Cq: Strengths mentioning

confidence: 99%

“…[283][284][285][286] However, unlike malignant tissue niches, normal tissue uses the intact regulatory network of STAT3 and NF-jB as a common mechanism to recover from inflammation. 147,287,288 Therefore, the activation of STAT3 by constitutive DNA damage in cancer cells could facilitate selective drug effects on the tumor nest through the circulation, while having discrete indirect effects on the local tissue microenvironment owing to the secretome of the tumor. It is therefore beneficial to dissect effects experimentally by cell-selective agents.…”

Section: Feasibility Of Treating Malignant Tumors With Cq: Strengths mentioning

confidence: 99%

Dissecting pharmacological effects of chloroquine in cancer treatment: interference with inflammatory signaling pathways

2019

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Chloroquines are 4-aminoquinoline-based drugs mainly used to treat malaria. At pharmacological concentrations, they have significant effects on tissue homeostasis, targeting diverse signaling pathways in mammalian cells. A key target pathway is autophagy, which regulates macromolecule turnover in the cell. In addition to affecting cellular metabolism and bioenergetic flow equilibrium, autophagy plays a pivotal role at the interface between inflammation and cancer progression. Chloroquines consequently have critical effects in tissue metabolic activity and importantly, in key functions of the immune system. In this article, we will review the work addressing the role of chloroquines in the homeostasis of mammalian tissue, and the potential strengths and weaknesses concerning their use in cancer therapy.

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“…The study by Zhang et al (4) showed that miR-146a was the only miRNA species which was elevated in both childhood acute lymphoblastic leukemia (ALL) and acute myeloid leukemia (AML). The transcription factor, STAT1 exerts its pro-apoptotic function by inducing the expression of caspases or by inhibiting growth-promoting NF-κB signals (5). Bcl-xL is a member of the anti-apoptotic Bcl-2 family protein, key regulators of the mitochondrial apoptosis pathway (6).…”

Section: Introductionmentioning

confidence: 99%

The effect of miR-146a on STAT1 expression and apoptosis in acute lymphoblastic leukemia Jurkat cells

Wang¹,

Guo²,

Suo³

et al. 2016

Oncology Letters

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The effect of miR-146a-dependent regulation of STAT1 on apoptosis in acute lymphoblastic leukemia (ALL) Jurkat cells was investigated. The miR-146a mimic and miR-146a inhibitor vectors were constructed in vitro, and experimental grouping was as follows: Control group (untreated Jurkat cells), empty vector group (Jurkat cells transfected with empty vector), agonist group (Jurkat cells transfected with miR-146a mimic) and the inhibitor group (Jurkat cells transfected with miR-146a inhibitor). Western blot analysis was used to observe the expression, respectively, of STAT1, p-STAT1 and Bcl-xL, and flow cytometry was used to test apoptosis in Jurkat cells. STAT1 and p-STAT1 expression in the agonist group was higher than that in the control and empty vector groups, but lower in the inhibitor group, and differences were statistically significant (P<0.05). The rate of apoptosis in the agonist group was significantly higher than that of the control group and blank vector group, and it was significantly lower in the inhibitor group (P<0.05). As a tumor suppressor, miR-146a can regulate expression of apoptosis-promoting factor STAT1, and anti-apoptosis factor Bcl-xL, and is able to promote apoptosis of ALL Jurkat cells.

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STAT transcript levels in childhood acute lymphoblastic leukemia: STAT1 and STAT3 transcript correlations

Cited by 11 publications

References 23 publications

Copy number profiling of adult relapsed B‐cell precursor acute lymphoblastic leukemia reveals potential leukemia progression mechanisms

Copy number profiling of adult relapsed B‐cell precursor acute lymphoblastic leukemia reveals potential leukemia progression mechanisms

Dissecting pharmacological effects of chloroquine in cancer treatment: interference with inflammatory signaling pathways

The effect of miR-146a on STAT1 expression and apoptosis in acute lymphoblastic leukemia Jurkat cells

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