Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.1.30.2 (endonuclease)
 18,621 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Laryngeal squamous cell carcinoma (LSCC) is one of the most common malignant tumors in the head and neck area. Melanoma-associated antigens A (MAGE-A) are strictly tumor-specific and are expressed in several types of tumors. To date, no studies have reported the potential of MAGE-A genes as markers for circulating tumor cells (CTCs) in patients with LSCC. The present study aimed to evaluate the expression and the possible prognostic significance of MAGE-A in the peripheral blood of patients with LSCC. In the present study, the expression of MAGE-A genes was determined by multiplex semi-nested PCR and restriction endonuclease treatment of the peripheral blood of patients with LSCC. The association between MAGE-A gene expression and clinicopathological parameters and prognosis was evaluated. The results demonstrated that the expression of MAGE-A was associated with the predictors that indicate poor prognosis. The expression levels of MAGE-A and each individual MAGE-A gene were also associated with a shorter overall survival time of patients with LSCC. In conclusion, the results of the present study suggested that the expression of MAGE-A genes may be a potential prognostic marker for patients with LSCC.
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PMID:MAGE-A genes as predictors of the outcome of laryngeal squamous cell carcinoma. 3279 12

Reduced NME1 expression in melanoma cell lines, mouse models of melanoma, and melanoma specimens in human patients is associated with increased metastatic activity. Herein, we investigate the role of NME1 in repair of double-stranded breaks (DSBs) and choice of double-strand break repair (DSBR) pathways in melanoma cells. Using chromatin immunoprecipitation, NME1 was shown to be recruited rapidly and directly to DSBs generated by the homing endonuclease I-PpoI. NME1 was recruited to DSBs within 30 min, in concert with recruitment of ataxia-telangiectasia mutated (ATM) protein, an early step in DSBR complex formation, as well as loss of histone 2B. NME1 was detected up to 5 kb from the break site after DSB induction, suggesting a role in extending chromatin reorganization away from the repair site. shRNA-mediated silencing of NME1 expression led to increases in the homologous recombination (HR) and non-homologous end-joining (NHEJ) pathways of double-strand break repair (DSBR), and reduction in the low fidelity, alternative-NHEJ (A-NHEJ) pathway. These findings suggest low expression of NME1 drives DSBR towards higher fidelity pathways, conferring enhanced genomic stability necessary for rapid and error-free proliferation in invasive and metastatic cells. The novel mechanism highlighted in the current study appears likely to impact metastatic potential and therapy-resistance in advanced melanoma and other cancers.
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PMID:Metastasis Suppressor NME1 Modulates Choice of Double-Strand Break Repair Pathways in Melanoma Cells by Enhancing Alternative NHEJ while Inhibiting NHEJ and HR. 3282 12


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