ABSTRACT
OBJECTIVE@#To analyze the expression level of miR-429 in patients with acute lymphoblastic leukemia(ALL) and its clinical prognostic value.@*METHODS@#One hundred and Twenty-six patients with ALL treated in our hospital from April 2016 to February 2018 were selected, and 100 healthy persons in the same period were selected as control group. Bone marrow mononuclear cells were collected. The expression level of miR-429 in bone marrow mononuclear cells was detected by RT-PCR, and the correlation of miR-429 expression with clinical characteristics and therapeutic efficacy was analyzed. Kaplan-Meier method and multi-factorial Cox regression model were used to analyze the correlation between the level of microRNA-429 and the prognosis of ALL patients.@*RESULTS@#The relative level of miR-429 in ALL patients was 2.47±0.07, which was signifi-cantly higher than that in control group (P0.05). The level of miR-429 was not significantly different between CR patients and control group (P>0.05); the level of miR-429 in PR patients was higher than that in control group and CR patients (P<0.05). The level of miR-429 in NR patients was higher than that in other groups (P<0.05). Kaplan-Meier survival analysis showed that the overall survival rate of ALL patients with low expression of miR-429 was better than that of ALL patients with high expression of miR-429 (P<0.05). Univariate Cox regression analysis showed that leukocyte level, ratio of bone marrow primordial cells, Hb and LDH level, risk grading and miR-429 were the factors influencing overall survival rate in ALL patients (P<0.05). Multivariate Cox regression analysis showed that leukocyte level, ratio of bone marrow primordial cells, risk grading, and miR-429 were the factors influencing overall survival rate (P<0.05).@*CONCLUSION@#The expression of miR-429 is high in ALL patients, which closely relates to the curative effect and pro-gnosis of ALL patients, and can be used as a reference index for evaluation of clinical prognosis of ALL patients.
ABSTRACT
<p><b>BACKGROUND</b>Previous cytogenetic studies revealed aberrations varied among the three subtypes of rhabdomyosarcoma. We profiled chromosomal imbalances in the different subtypes and investigated the relationships between clinical parameters and genomic aberrations.</p><p><b>METHODS</b>Comparative genomic hybridization was used to investigate genomic imbalances in 25 cases of primary rhabdomyosarcomas and two rhabdomyosarcoma cell lines. Specimens were reviewed to determine histological type, pathological grading and clinical staging.</p><p><b>RESULTS</b>Changes involving one or more regions of the genome were seen in all rhabdomyosarcomal patients. For rhabdomyosarcoma, DNA sequence gains were most frequently (> 30%) seen in chromosomes 2p, 12q, 6p, 9q, 10q, 1p, 2q, 6q, 8q, 15q and 18q; losses from 3p, 11p and 6p. In aggressive alveolar rhabdomyosarcoma, frequent gains were seen on chromosomes 12q, 2p, 6p, 2q, 4q, 10q and 15q; losses from 3p, 6p, 1q and 5q. For embryonic rhabdomyosarcoma, frequent gains were on 7p, 9q, 2p, 18q, 1p and 8q; losses only from 11p. Frequently gained chromosome arms of translocation associated with rhabdomyosarcoma were 12q, 2, 6, 10q, 4q and 15q; losses from 3p, 6p and 5q. The frequently gained chromosome arms of nontranslocation associated with rhabdomyosarcoma were 2p, 9q and 18q, while 11p and 14q were the frequently lost chromosome arms. Gains on chromosome 12q were significantly correlated with translocation type. Gains on chromosome 9q were significantly correlated with clinical staging.</p><p><b>CONCLUSIONS</b>Gains on chromosomes 2p, 12q, 6p, 9q, 10q, 1p, 2q, 6q, 8q, 15q and 18q and losses on chromosomes 3p, 11p and 6p may be related to rhabdomyosarcomal carcinogenesis. Furthermore, gains on chromosome 12q may be correlated with translocation and gains on chromosome 9q with the early stages of rhabdomyosarcoma.</p>
Subject(s)
Humans , Cell Line, Tumor , Chromosome Aberrations , Chromosomes, Human, Pair 12 , Genetics , Comparative Genomic Hybridization , Methods , Gene Fusion , Genetics , Oncogene Proteins, Fusion , Genetics , Rhabdomyosarcoma , Genetics , Tumor Cells, CulturedABSTRACT
<p><b>OBJECTIVE</b>To characterize the profile of chromosomal imbalances of rhabdomyosarcoma(RMS).</p><p><b>METHODS</b>Comparative genomic hybridization (CGH) was used to investigate genomic imbalances in 25 cases of primary RMS including 10 cases of alveolar rhabdomyosarcoma (ARM), 12 cases of embryonic rhabdomyosarcoma (ERMS), 3 cases of polymorphic rhabdomyosarcoma (PRMS) and 2 RMS cell lines (A240 originated from ARMS and RD from PRMS), with correlation to histological type, pathologic grading, clinical staging, gender and age, respectively.</p><p><b>RESULTS</b>All twenty-five rhabdomyosarcomas showed evidence of increased or decreased DNA sequence copy numbers involving one or more regions of the genome. (1) The frequently gained chromosome regions in RMS were 2p, 12q, 6p, 9q, 10q, 1p, 2q, 6q, 8q, 15q, 18q, and the frequently lost chromosome regions were 3p, 11p, 6p. (2) The frequently gained chromosome arms in ARMS were 12q, 2p, 6, 2q, 4q, 10q, 15q. The frequently lost chromosome arms were 3p, 6p, 1q, 5q. The frequently gained chromosome regions in ERMS were 7p, 9q, 2p, 18q, 1p, 8q. The frequently lost chromosome arms in ERMS were 11p. (3) The frequently gained chromosome arms in translocation associated RMS were 12q, 2, 6, 10q, 4q and 15q (> 30%), 3p, 6p, 5q (> 30%) were the frequently loss chromosome arms. The frequently gained chromosome regions in non-translocation associated RMS were 2p, 9q, 18q (> 30%), and 11p, 14q (> 30%) were the frequently loss chromosome regions. Gain of 12q was significantly correlated with the translocation-associated tumors (P < 0.05). (4) Gains of 9q was significantly correlated with clinical staging (P < 0.05).</p><p><b>CONCLUSIONS</b>Gain of 2p, 12q, 6p, 9q, 10q, 1p, 2q, 6q, 8q, 15q, 18q and loss of 3p, 11p, 6p may be involved in the tumorigenesis of RMS. Gains of 12q may be correlated with gene fusion/chromosomal translocation in ARMS. Gains of 9q may be correlated with an early tumor stage of RMS.</p>