<div>Abstract<p><b>Purpose:</b> Rhabdoid tumors are highly aggressive pediatric tumors that are usually refractory to available treatments. The purpose of this study was to evaluate the therapeutic potential of two oncolytic viruses, myxoma virus (MV) and an attenuated vesicular stomatitis virus (VSV<sup>ΔM51</sup>), in experimental models of human rhabdoid tumor.</p><p><b>Experimental Design:</b> Four human rhabdoid tumor cell lines were cultured <i>in vitro</i> and treated with live or inactivated control virus. Cytopathic effect, viral gene expression, infectious viral titers, and cell viability were examined at various time points after infection. To study viral oncolysis <i>in vivo</i>, human rhabdoid tumor cells were implanted s.c. in the hind flank or intracranially in CD-1 nude mice and treated with intratumoral (i.t.) or i.v. injections of live or UV-inactivated virus. Viral distribution and effects on tumor size and survival were assessed.</p><p><b>Results:</b> All rhabdoid tumor cell lines tested <i>in vitro</i> were susceptible to productive lethal infections by MV and VSV<sup>ΔM51</sup>. I.t. injection of live MV or VSV<sup>ΔM51</sup> dramatically reduced the size of s.c. rhabdoid tumor xenografts compared with control animals. I.v. administration of VSV<sup>ΔM51</sup> or i.t. injection of MV prolonged the median survival of mice with brain xenografts compared with controls (VSV<sup>ΔM51</sup>: 25 days versus 21 days, log-rank test, <i>P</i> = 0.0036; MV: median survival not reached versus 21 days, log-rank test, <i>P</i> = 0.0007). Most of the MV-treated animals (4 of 6; 66.7%) were alive and apparently “cured” when the experiment was arbitrarily ended (>180 days).</p><p><b>Conclusions:</b> These results suggest that VSV<sup>ΔM51</sup> and MV could be novel effective therapies against human rhabdoid tumor.</p></div>
Abstract Purpose: Rhabdoid tumors are highly aggressive pediatric tumors that are usually refractory to available treatments. The purpose of this study was to evaluate the therapeutic potential of two oncolytic viruses, myxoma virus (MV) and an attenuated vesicular stomatitis virus (VSVΔM51), in experimental models of human rhabdoid tumor. Experimental Design: Four human rhabdoid tumor cell lines were cultured in vitro and treated with live or inactivated control virus. Cytopathic effect, viral gene expression, infectious viral titers, and cell viability were examined at various time points after infection. To study viral oncolysis in vivo, human rhabdoid tumor cells were implanted s.c. in the hind flank or intracranially in CD-1 nude mice and treated with intratumoral (i.t.) or i.v. injections of live or UV-inactivated virus. Viral distribution and effects on tumor size and survival were assessed. Results: All rhabdoid tumor cell lines tested in vitro were susceptible to productive lethal infections by MV and VSVΔM51. I.t. injection of live MV or VSVΔM51 dramatically reduced the size of s.c. rhabdoid tumor xenografts compared with control animals. I.v. administration of VSVΔM51 or i.t. injection of MV prolonged the median survival of mice with brain xenografts compared with controls (VSVΔM51: 25 days versus 21 days, log-rank test, P = 0.0036; MV: median survival not reached versus 21 days, log-rank test, P = 0.0007). Most of the MV-treated animals (4 of 6; 66.7%) were alive and apparently “cured” when the experiment was arbitrarily ended (>180 days). Conclusions: These results suggest that VSVΔM51 and MV could be novel effective therapies against human rhabdoid tumor.
To develop a chemiluminescence immunoassay (CLIA) kit for quantitative determination of tumor marker carbohydrate antigen 125 (CA125) and evaluate its value of clinical application, CLIA for quantitative determination of CA125 was established by using micro-plates coated with antibody to CA125, combined with HRP conjugated anti-CA125 antibody, as well as luminol chemiluminescence substrate system. The national reference control sera were used for evaluation of specificity, sensitivity, stability and accuracy of the established CLIA. CA125 levels in sera from 350 clinical samples were parallel determined by the established methods and reference kits produced by the Siemens. The results show that the efficiency of the CLIA reagents met the requirements of national reference standard. The intra coefficient variations (CV) were between 2.8%~3.6% and inter CV 3.7%. The kit showed good stability after being kept at 37˚C for 3d. The established CLIA showed good correlation with the reference kits (negative concordance rate, positive concordance rate and overall concordance rate were 99.5%, 99.3% and 99.4% respectively, and a correlation coefficient r = 0.9897. High degree of agreement was observed with a Kappa value of 0.99). A rapid, specific, sensitive and stable CLIA kit for quantitative determination of CA125 was successfully established and that will be fit for widely application in clinical laboratory.
Human erythrocyte NADH-cytochrome b_(5) reductase, or b_(5) reductase, plays a major role in the reduction of methemoglobin, deficiency of which will lead to hereditary methemoglobinemia. Determination of b_(5) reductase activity is usually done by spectrophotometry. A new method was developed for the qualitative and semi-quantitative detection of b_(5) reductase activity, in which antibodies against b_(5) reductase was dot-blotted onto nitrocellulose membrane, and this in turn was used to capture and enrich b_(5) reductase activity were visualized with the precipitable substrate MTT, or 3-(4, 5-dimethyl thiazolyl-2) -2, 5-diphenyl tetrozolium bromide. Being straightforward and easy to follow, this method provides a new approach for the diagnosis of hereditary methemoglobinemia.
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