<i>BIRC6</i>/Apollon gene expression in childhood acute leukemia: impact on therapeutic response and prognosis

Ismail, Eman Abdel Rahman; Mahmoud, Hanan M.; Tawfik, Lamis M; Habashy, Deena Mohamed; Adly, Amira Abdel Moneam; Elsherif, Nayera H K; Abdelwahab, Mahmoud Ahmed

doi:10.1111/j.1600-0609.2011.01734.x

Cited by 28 publications

(39 citation statements)

References 49 publications

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“…Carter et al [10] did not find any prognostic significance for Survivin or XIAP expression in adult AML samples, whereas BIRC6 overexpression is associated with unfavorable clinical features and negatively impacts on the 3-year relapse-free survival in childhood acute myeloid leukemia (AML) [11]. Similar results were obtained by Ismail et al in childhood AML and acute lymphoblastic leukemia (ALL) [12]. Abe et al [13] found lower expression of BIRC6 in bone marrow-derived cells of healthy donors compared to de novo AML samples.…”

Section: Introductionmentioning

confidence: 70%

BIRC6 (APOLLON) is down-regulated in acute myeloid leukemia and its knockdown attenuates neutrophil differentiation

et al. 2012

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BackgroundInhibitors of apoptosis (IAPs) were intensively investigated in the context of cancer where they promote tumor growth and chemoresistence. Overexpression of the IAP BIRC6 is associated with unfavorable clinical features and negatively impacts relapse-free survival in childhood acute myeloid leukemia (AML). Currently, BIRC6 levels in adult primary AML have not been compared to the expression in normal myeloid cells. Thus, we compared for the first time BIRC6 levels in adult primary AML patient samples to normal myeloid cells and studied its regulation and function during neutrophil differentiation.FindingsWe found significantly lower BIRC6 levels in particular AML subtypes as compared to granulocytes from healthy donors. The lowest BIRC6 expression was found in CD34+ progenitor cells. Moreover, BIRC6 expression significantly increased during neutrophil differentiation of AML cell lines and knocking down BIRC6 in NB4 acute promyelocytic leukemia (APL) cells significantly impaired neutrophil differentiation, but not cell viability.ConclusionTogether, we found an association of low BIRC6 levels with an immature myeloid phenotype and describe a function for BIRC6 in neutrophil differentiation of APL cells.

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Section: Introductionmentioning

confidence: 70%

BIRC6 (APOLLON) is down-regulated in acute myeloid leukemia and its knockdown attenuates neutrophil differentiation

et al. 2012

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“…In their work, they pointed out the possible predictive meaning of the BIRC6 gene [27]. Furthermore, they suggest that BIRC6 gene expression may be recognized as a risk factor in children with acute leukemia [12]. Abe et al also revealed a much higher mRNA BIRC6 expression in marrow cells with MDS, in comparison to normal cells.…”

Section: Resultsmentioning

confidence: 98%

The expression BIRC6 gene in patients with chronic lymphocytic leukemia – a preliminary study

Chomik

Gil-Kulik

Filas

et al. 2014

Current Issues in Pharmacy and Medical Sciences

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The BIRC6 gene encodes the Bruce (Apollon) protein. This belongs to the III class of Inhibitors of the Apoptosis Protein (IAP) and demonstrates anti-apoptotic activity (binding, inhibiting and degrading the caspases). Moreover, the Bruce protein shows multilevel activities and additional functions. The Bruce protein is involved in the maintenance of cell viability, and it is also suggested that it plays an important role in cell proliferation and diversification. Many researchers have noticed elevated BIRC6 gene expression in cell lines of brain cancer and ovarian carcinoma, leukemia, breast cancer and even in colorectal cancer tissues. Resistance to chemotherapy-inducted apoptosis in cancers characterized by BIRC6 gene over-expression was also reported. The aim of the study was to assess the BIRC6 gene expression in peripheral blood lymphocytes of patients diagnosed with chronic lymphocytic leukemia.

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“…The risk factor and prognosis of patients with normal karyotype are analyzed by the abnormality of gene expression and molecular genetics change to direct the clinical individualized treatment, which has been a novel research direction for the leukemia treatment [12][13][14]. Meanwhile, the mutations of IDH2, ASXL1, and DNMT3A, which are closely related to the occurrence and development of acute leukemia, have attracted wide attention.…”

Section: Discussionmentioning

confidence: 99%

The Transcriptome Study of Subtype M2 Acute Myeloblastic Leukemia

Yang

Lin

et al. 2015

Cell Biochem Biophys

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Our objective is to explore the tumor-specific mutated genes by transcriptome sequencing of patients with acute myeloblastic leukemia. 96 patients with subtype M2 acute myeloid leukemia (AML), admitted during January 2007 to January 2012, were selected. Bone marrow and peripheral blood samples from the patients after the first visit and the patients who were improved or alleviated, were subjected to high-throughput sequencing to compare the gene expression. The single nucleotide mutation related to subtype M2 AML was detected. Meanwhile, real-time fluorescent quantitation RT-PCR was used to detect the AML1/ETO fusion gene and its correlation with prognosis after treatment. Among 96 patients, AML1-ETO fusion gene was positive in 52 cases, the positive rate was 54.17 %. The complete relief (CR) rate of AML1-ETO fusion gene positive patients was 84.62 %, and the CR rate of AML1/ETO fusion gene negative patients was 77.27 %; the CR rate of AML1-ETO positive patients was higher than that of patients without the fusion gene, however there was no statistical difference. In the analysis of recurrent gene mutation in AML-M2 patients, IDH2, ASXL1, TET2, JAK1 and JAK2 gene expressions were not significantly different before treatment and after CR, however, IDHI, JAK3, ABL1 and BCR gene expressions were significantly different. In the study of transcriptome in AML-M2 patients, high-throughput sequencing could effectively detect the difference of the gene expression before treatment and after CR. Furthermore, positive expression of AML1-ETO fusion gene had effect on the prognosis of patients.

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BIRC6/Apollon gene expression in childhood acute leukemia: impact on therapeutic response and prognosis

Abstract: This is the first report to study BIRC6 gene in pediatric ALL. Our results suggested that BIRC6 gene expression could be considered as an adverse risk factor in childhood acute leukemia and, hence, could be used to guide therapeutic regimens.

Cited by 28 publications

References 49 publications

BIRC6 (APOLLON) is down-regulated in acute myeloid leukemia and its knockdown attenuates neutrophil differentiation

BIRC6 (APOLLON) is down-regulated in acute myeloid leukemia and its knockdown attenuates neutrophil differentiation

The expression BIRC6 gene in patients with chronic lymphocytic leukemia – a preliminary study

The Transcriptome Study of Subtype M2 Acute Myeloblastic Leukemia

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