Editorial: Recovery from chemotherapy depends on STAT1 for replenishment of B lymphopoiesis

Strobl, Birgit; Moriggl, Richard

doi:10.1189/jlb.0114051

Cited by 2 publications

(2 citation statements)

References 12 publications

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“…Therefore, it may be hypothesized that decreased STAT-1 expression results in reduced tumor radiosensitivity via the ATM checkpoint. Similar studies have revealed that STAT-1-positive cancer may improve chemosensitivity of the tumor (10,13,14), whereas STAT-1 activation by IFN-α/β and antineoplastic drugs may exert a synergistic effect on the induction of apoptosis (5). In addition, the functions of the topoisomerase I inhibitor irinotecan on squamous cell carcinoma, and those of the antimetabolite raltitrexed, appear to depend on the expression of STAT-1 (15), thus suggesting that similar mechanisms may exist in glioma.…”

Section: Discussionmentioning

confidence: 68%

“…STAT-1 has been identified as a tumor-inhibiting factor, and reduced STAT-1 expression is associated with the occurrence and progression of malignant tumors (4). In addition, it has been demonstrated that the activation of STAT-1 expression in tumor cells by exogenous or endogenous stimuli can improve the sensitivity of these cells to chemotherapy (5). The p53 gene has been classified as a tumor suppressor gene that can effectively inhibit cellular growth and response to stress in various cell types by inducing temporary or permanent suppression of proliferation, or by activating cell death processes.…”

Section: Introductionmentioning

confidence: 99%

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A study on the correlation between STAT‑1 and mutant p53 expression in glioma

Yang

Wang

et al. 2018

Mol Med Report

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Glioma is the most common primary brain tumor in adults and the second most common malignant tumor in children. Aberrant expression of signal transducer and activator of transcription 1 (STAT‑1) and p53 are known to affect the occurrence and progression of malignant tumors. The aim of the present study was to investigate the expression of STAT‑1 and mutant p53 gene, as well as their correlation, in patients with glioma. The present study included 50 patients who underwent glioma resection at the First Affiliated Hospital of Inner Mongolia Medical University between December 2007 and December 2011, and 10 patients with acute cerebral contusion who underwent intracerebral hematoma removal at the same hospital between January 2013 and January 2014. The expression of STAT‑1 and mutant p53 protein in patients with different grades of glioma was assessed by immunohistochemistry. Spearman's correlation coefficient was employed to examine the correlation between STAT‑1 and the grade of glioma, and mutant p53 expression. The results demonstrated that the mean expression of STAT‑1 in glioma was significantly lower compared with normal brain tissue (P<0.05). However, there was no significant difference in the STAT‑1 positive expression rate between the two groups (χ2=1.38, P>0.05). The expression score (P<0.05) and positive expression rate (χ2=31.27, P<0.05) of mutant p53 in glioma was significantly higher compared with those in normal brain tissue. Statistical analysis revealed a negative correlation between STAT‑1 expression and the grade of glioma (r=‑0.767, P<0.05). In addition, mutant p53 expression was negatively correlated with STAT‑1 expression in glioma (r=‑0.876, P<0.05). The observed negative correlation between STAT‑1 and the pathological grade of glioma suggested an association between STAT‑1 and the occurrence and development of glioma, thus revealing the potential of STAT‑1 as a diagnostic biomarker and therapeutic target for glioma.

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Section: Discussionmentioning

confidence: 68%

Section: Introductionmentioning

confidence: 99%

A study on the correlation between STAT‑1 and mutant p53 expression in glioma

Yang

Wang

et al. 2018

Mol Med Report

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Differential signaling through p190 and p210 BCR-ABL fusion proteins revealed by interactome and phosphoproteome analysis

et al. 2017

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Two major types of leukemogenic BCR-ABL fusion proteins are p190and p210. Although the two fusion proteins are closely related, they can lead to different clinical outcomes. A thorough understanding of the signaling programs employed by these two fusion proteins is necessary to explain these clinical differences. We took an integrated approach by coupling protein-protein interaction analysis using biotinylation identification with global phosphorylation analysis to investigate the differences in signaling between these two fusion proteins. Our findings suggest that p190 and p210 differentially activate important signaling pathways, such as JAK-STAT, and engage with molecules that indicate interaction with different subcellular compartments. In the case of p210, we observed an increased engagement of molecules active proximal to the membrane and in the case of p190, an engagement of molecules of the cytoskeleton. These differences in signaling could underlie the distinct leukemogenic process induced by these two protein variants.

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Editorial: Recovery from chemotherapy depends on STAT1 for replenishment of B lymphopoiesis

Abstract: Discussion of how B cell immune function is affected after hematopoietic reconstitution in a situation of chemotherapy upon STAT1 deficiency, possibly impairing bone marrow transplants.

Cited by 2 publications

References 12 publications

A study on the correlation between STAT‑1 and mutant p53 expression in glioma

A study on the correlation between STAT‑1 and mutant p53 expression in glioma

Differential signaling through p190 and p210 BCR-ABL fusion proteins revealed by interactome and phosphoproteome analysis

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