ABSTRACT
This Article has been retracted; see accompanying Retraction Note.
ABSTRACT
BACKGROUND: Evidence indicates RFC1 G80A polymorphism as a risk factor for a number of cancers. Increasing studies have been conducted on the association of RFC1 G80A polymorphism with acute lymphoblastic leukemia (ALL) risk. However, the results were controversial. The aim of the present study was to derive a more precise estimation of the relationship. MATERIALS AND METHOD: PubMed, Embase, Web of Science, Cochrane database, and Google Scholar were searched to get the genetic association studies between RFC1 G80A polymorphism and ALL. All eligible studies for the period up to February 2016 were identified. Subgroup analyses regarding ethnicity were also implemented. All statistical analyses were done with CMA 2.0. RESULTS: A total of ten studies comprising of 2,168 ALL cases and 2,693 healthy controls were included in this meta-analysis. Overall, no significant association was detected for allelic model (OR = 1.029, 95 % CI 0.754- 1.405, P=0.000), Dominant model (OR = 1.619, 95 % CI 0.847-3.094, P=0.145), recessive model (OR = 1.169, 95 % CI 10.764-1.790, P=0.429), and homozygote model (OR = 1.288, 95 % CI 0.928-1.788, P=0.130). However, there was an obvious association under the heterozygote model (OR = 1.368, 95 % CI 1.056- 1.772, P=0.018). Also, in the stratified analysis by ethnicity, no significant association of this polymorphism with risk of OC was found in the Asian and Caucasian populations. However, there was not significant heterogeneity between heterozygote genetic model (P = 0.15, I(2) = 33%) in Caucasian. Therefore, we utilized the fixed-effect model to merge OR value. CONCLUSION: Based on the available evidence, no association between RFC1 G80A Polymorphism and ALL risk was observed, even in the subanalysis by ethnicity. The direction of further research should focus not only on the simple relationship of RFC1 G80A Polymorphism and ALL risk, but also on gene-gene and gene-environment interaction.
ABSTRACT
High-grade serous ovarian cancers (HGSCs) are deadly malignancies that relapse despite carboplatin chemotherapy. Here we show that 16 independent primary HGSC samples contain a CA125-negative population enriched for carboplatin-resistant cancer initiating cells. Transcriptome analysis reveals upregulation of homologous recombination DNA repair and anti-apoptotic signals in this population. While treatment with carboplatin enriches for CA125-negative cells, co-treatment with carboplatin and birinapant eliminates these cells in HGSCs expressing high levels of the inhibitor of apoptosis protein cIAP in the CA125-negative population. Birinapant sensitizes CA125-negative cells to carboplatin by mediating degradation of cIAP causing cleavage of caspase 8 and restoration of apoptosis. This co-therapy significantly improves disease-free survival in vivo compared with either therapy alone in tumour-bearing mice. These findings suggest that therapeutic strategies that target CA125-negative cells may be useful in the treatment of HGSC.
Subject(s)
Antineoplastic Combined Chemotherapy Protocols/pharmacology , Apoptosis/drug effects , Carboplatin/pharmacology , Dipeptides/pharmacology , Drug Resistance, Neoplasm/genetics , Gene Expression Regulation, Neoplastic/genetics , Indoles/pharmacology , Inhibitor of Apoptosis Proteins/drug effects , Neoplasms, Cystic, Mucinous, and Serous/genetics , Ovarian Neoplasms/genetics , Animals , Apoptosis/genetics , CA-125 Antigen/metabolism , Caspase 8/drug effects , Caspase 8/metabolism , Female , Gene Expression Profiling , Humans , Inhibitor of Apoptosis Proteins/metabolism , Membrane Proteins/metabolism , Mice , Neoplasm Transplantation , Neoplasms, Cystic, Mucinous, and Serous/drug therapy , Ovarian Neoplasms/drug therapy , Recombinational DNA Repair/genetics , Up-RegulationABSTRACT
We examine the statistical properties of mode-locked laser light in which each frequency component is subsequently given a constant, independent, and random phase shift. We find that, under certain conditions, this random phase encoding produces a pseudorandom light intensity that is statistically equivalent to that of a free-running multimode laser, with a negative exponential intensity-probability distribution.
ABSTRACT
We demonstrate the spreading of femtosecond optical pulses into picosecond-duration pseudonoise bursts. Spreading is accomplished by encoding pseudorandom binary phase codes onto the optical frequency spectrum. Subsequent decoding of the spectral phases restores the original pulse. We propose that frequency-domain encoding and decoding of coherent ultrashort pulses could form the basis for a rapidly reconfigurable, code-division multiple-access optical telecommunications network.
ABSTRACT
Sands from various geographic locations reduce N(2) from the air to NH(3) and traces of N(2)H(4) on exposure to sunlight. This N(2) photofixation occurs under sterile conditions on the surface of finely dispersed titanium minerals such as rutile, utilizing reducing equivalents generated through the photolysis of chemisorbed H(2)O. Abiological N(2) photofixation is suggested to be part of the nitrogen cycle in arid and semiarid regions. It is estimated that about 10 x 10(5) tons of N(2) is photoreduced on the total surface of the earth's deserts per year.
