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Ki-67, MCM-3, and MCM-7, but not MCM-5 are reliable proliferative and diagnostic markers in discerning benign and malignant adrenocortical tumors.
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Our results indicate that MCM7 may exert certain functions on spindle formation to prevent cytokinesis during early mitosis by regulating CDK1 activity.
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MCM7 is helpful for us to make differential diagnosis in pathological grade, MCM7 combination of Ki67 may serve as more sensitive proliferation markers for evaluation of gastric carcinoma and precancerous lesions
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CDT1, MCM7, and NUDT1 were shown to be up-regulated in hepatocellular carcinoma tissues and provide a more accurate diagnosis than alpha-fetal protein alone.
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High expression of MCM-7 was reduced in BVP-treated cancer cells.
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Data indicate that RACK1 increases interactions between Akt and MCM7 and promotes Akt-dependent MCM7 phosphorylation, which in turn increases MCM7 binding to chromatin and miniature chromosome maintenance (MCM) complex formation.
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our findings suggested that MCM7 promoted tumor cell proliferation, colony formation and migration of ESCC cells via activating AKT1/mTOR signaling pathway
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Results proved that MCM7 proliferative index is a better method for identifying patients with risk of recurrence in patients surgically resected for meningiomas compared with the traditional methods used in the current clinical practice.
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MCM7-cyclin D1 pathway may participate in cancer progression.
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The MCM7 directly binds to the centrosomal linker protein Cep68 in vitro and complexes with Cep68 and VHL in vivo.
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The results clearly demonstrate 7q21-22 amplification, MCM7, and its intronic miR-25 are the major molecular switches involved in the complex oncogenic circuits of gastric cancer.
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High MCM7 expression is associated with non-small cell lung cancer.
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MCM4 and MCM7 expression is significantly correlated with Ki-67, Bmi1, and cyclin E expression in esophageal adenocarcinoma, squamous cell carcinoma and precancerous lesions.
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Data suggest that interaction of Mcm10 with Mcm2-7 multimer requires Mcm10 domain that contains amino acids 530-655, which overlaps with domain required for stable retention of Mcm10 on chromatin; Mcm10 conserved domain (amino acids 200-482) is essential for DNA replication; both conserved domain and Mcm2-7-binding domain are required for full activity of Mcm10.
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Results show that the expression of MCM7 gene and its microRNA, miR-106b-25 cluster is reduced under hypoxia.
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This MCM4 mutation affected human MCM4/6/7 complex formation, since the complex containing the mutant MCM4 protein is unstable and the mutant MCM4 protein is tend to be degraded.
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Authors found that MCM7 highly expressed in K562 cells rather than that in normal neutrophils. Thus, lentivirus-mediated shRNA targeting MCM7 was used to suppress its endogenous expression in K562 cells and develop a novel therapeutic strategy for leukemia.
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MCM7 polymorphisms were associated with survival rate and prognosis in acute myeloid leukemia patients.
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The BCL2, MCM7, and CCNE1 genes might play distinctive roles in cisplatin resistance in bladder cancer.
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Purified MCM4/6/7 complex containing the G364R MCM4 exhibited similar levels of single-stranded DNA binding and ATPase activities to the complex containing wild-type MCM4
