China
Africa
Explore chapters and articles related to this topic
Oncogenes and Cancer
Published in Pimentel Enrique, Oncogenes, 2020
In another study fresh human leukemia cells from different types of leukemia were obtained from leukapheresis in a total of 26 patients and human c-onc probes, not v-onc probes, were used for determining the expression of different proto-oncogenes by molecular hybridization.70 It was found that “different oncogenes are expressed in the different leukemic types and that the transcript copy number varies from one type of leukemia to another and within a given individual leukemic type”.70 The c-myc gene was expressed at detectable levels in all leukemia samples analyzed and the c-myb gene was expressed in all samples except in B-cell malignancies. A single 1.5 kb transcript of c-H-ras was present at low levels in all acute and chronic leukemias examined whereas c-sis was expressed only in the sample from one patient with chronic myeloid leukemia in blast transformation. This is the first reported case of c-sis transcriptional activity in human malignant diseases. The proto-oncogene c-abl was expressed at very low levels in a fraction of all leukemia types analyzed and the transcript sizes and levels were the same in chronic myeloid leukemia (where the c-abl gene is translocated) as in other forms of leukemia. However, in some samples of CML an aberrant 8.0 kb transcript was detected in addition to the normal 6.4 and 7.2 kb transcripts contained in control samples. The scr and erb proto-oncogenes were not expressed in the fresh human leukemia cell samples.
Immunopathology
Published in Constantin A. Bona, Francisco A. Bonilla, Textbook of Immunology, 2019
Constantin A. Bona, Francisco A. Bonilla
Chronic myelogenous leukemia (CML), like Burkitt’s lymphoma, is associated with a characteristic chromosomal aberration. Ninety percent of CMLs have a translocation involving chromosomes 9 and 22, t(9;22). This is called the Philadelphia chromosome. This translocation involves the c-abl proto-oncogene on chromosome 9, and a gene called BCR (breakpoint cluster region) on chromosome 22. The product of the c-abl gene is a tyrosine kinase, although its physiologic function is not known. The function of BCR is not known. The translocation joins these two genes so that a fusion protein is encoded. The fusion protein appears to have an increased tyrosine kinase activity. The mechanism of oncogenesis has not been determined.
Interferons and their Mechanisms of Action
Published in Velibor Krsmanović, James F. Whitfield, Malignant Cell Secretion, 2019
CML is characterized in more than 90 to 95% of cases by the presence of the Philadelphia chromosome, which results from a reciprocal translocation between chromosome 9 and 22. The result of the translocation is the fusion of the cellular oncogene c-abl proto-oncogene with another gene located on chromosome 22 known as the “bcr” gene. The site of the breakpoint within the bcr region appears to be variable. The fusion of c-abl and bcr leads to the production of a large messenger which codes for a 210-kDa protein. This protein retains the tyrosine kinase activity of the normal c-abl gene product.258 Monoclonal antibodies directed against the 210-kDa fusion protein also precipitates a 53-kDa polypeptide which appears to form a complex with the fusion protein. This 53-kDa protein, which is distinct from the abl-bcr protein, can be phosphorylated and may perhaps be one of the targets of the kinase activity of the 210-kDa protein.259
Correlation of the transcription factors IRF4 and BACH2 with the abnormal NFATC1 expression in T cells from chronic myeloid leukemia patients
Published in Hematology, 2022
Yikai Zhang, Xiangbo Zeng, Xianfeng Zha, Jing Lai, Guangxiao Tan, Shaohua Chen, Xibao Yu, Yangqiu Li, Ling Xu
Chronic myelogenous leukemia (CML) is a common leukemia that is characterized by the BCR-ABL fusion protein in adults [1]. Although tyrosine kinase inhibitor (TKI) targeted therapy is beneficial for most CML patients in the chronic phase, there is a portion of patients who have primary TKI resistance or TKI-induced ABL gene mutations as well as disease progression in the blast phase. Thus, new avenues for improving this therapeutic strategy are needed [2–5]. Effective therapy for such CML patients includes hematopoietic stem cell transplantation (HSCT), including allogenic-HSCT and haploidentical-HSCT; however, its application is limited for older patients [6,7]. Thus, exploration of novel therapeutic approaches such as immunotherapy in combination with TKIs is necessary for CML patients.
Antiproliferative Effect of Gaillardin from Inula oculus-christi in Human Leukemic Cells
Published in Nutrition and Cancer, 2020
Afshin Karami, Maryam Hamzeloo-Moghadam, Amir Yami, Mohieddin Barzegar, Pargol Mashati, Ahmad Gharehbaghian
Initially, cells (3 × 105/mL) were treated with various concentrations of VCR and GLN, and were incubated for 48 h. Total RNA was extracted from each well by the Hybrid-R RNA purification kit (Gene All, Korea) according to the manufacturer’s instructions. The quantity of the RNA samples was analyzed by UV-spectroscopy (Nano Drop TM 2000 Spectrophotometer, Thermo Scientific, USA) at 260 and 280 nm and the quality of extracted RNA was tested by the 1% agarose gel electrophoresis. RNA was reverse transcribed to first-strand cDNA using the Revert Aid First Strand cDNA Synthesis Kit (Thermo Scientific, USA) following the manufacturer’s instructions. The sequences of the primers are shown in Table 1. Real-time PCR analysis was performed using SYBR Premix Ex Taq (Tli RNase H Plus) kit (Takara Biomedical Technology, Japan) in Applied Rotor-Gene Q Real-Time PCR System (Qiagen, Valencia, CA). The expression of ABL gene was used as an endogenous control to normalize the expression of the target genes. Melting curve analysis of CASPASE-3, BCL-2, BAX, P21, C-MYC, and ABL showed a single peak. The mean Ct of the target genes was calculated from triplicate measurements and then normalized with the mean Ct of the ABL gene. Data extraction was executed using the Rotor-Gene Q series software v. 2.0.2, and the Livak method was used to calculate the relative expression of each gene (20).
Wilms’ tumor 1 mRNA expression: a good tool for differentiating between myelodysplastic syndrome and aplastic anemia in children?
Published in Hematology, 2019
Yingxi Zuo, Yifei Cheng, Leping Zhang, Yazhen Qin, Hong Luo
The PCR reactions and fluorescence measurements were performed using an ABI PRISM 7500 real-time PCR system (PE Applied Biosystems, USA). Levels of WT1 transcripts were measured using a TaqMan-based real-time quantitative PCR assay, as previously described [20]. The ABL gene was used as the control gene, and samples with <3 × 104 copies of ABL were considered poor quality. All experiments were performed in duplicate, and the quantitative WT1 expression levels were calculated as: WT1 copies/ABL copies (%).