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Fas ligand expression in metastatic renal cell carcinoma during interleukin-2 based immunotherapy: no in vivo effect of Fas ligand tumor counterattack. | ding patients (P = 0.034; P < 0.001; and P < 0.001; respectively). However; no correlation was observed between the number of intratumoral lymphocytes and tumor FasL expression level.These observations do not support the hypothesis that FasL tumor "counterattack" has an effect on the clinical outcome in metastatic renal cell carcinoma during IL-2-based immunotherapy. | 15585624 | [
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Hypermethylation of the GATA genes in lung cancer. | In lung cancer; DNA hypermethylation is known to be a common event.Gene expression and methylation status of GATA-4; GATA-5; and GATA-6 were analyzed with cell lines and primary human lung cancers. Methylation profiles of primary lung cancers were analyzed and correlated with clinical as well as histopathological data.Complete methylation was detected by methylation-specific PCR for both GATA-4 and GATA-5 in four cell lines (H358; DMS-53; A549; and H1299); all of which had no expression by reverse transcrip | 15585625 | [
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Hypermethylation of the GATA genes in lung cancer. | tion-PCR analysis. Demethylation with 5-aza-2'deoxycytidine restored expression in each case. GATA-6 was ubiquitously expressed in all of the six cell lines. GATA-4 bisulfite sequencing revealed complete methylation of the GATA-4 promoter in H358 cells; correlating well with its lack of expression at the mRNA level. Only a few CpG sites showed methylation by bisulfite sequencing within the GATA-4 promoter in a cell line that expressed the gene. In 63 cases of primary lung cancers; GATA-4 and GATA-5 promoter | 15585625 | [
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Hypermethylation of the GATA genes in lung cancer. | methylation was detected in (42 of 63) 67% and (26 of 63) 41%; respectively. GATA-6 remained unmethylated both in cell lines and primary tumors. Six autopsy specimens of normal lung tissue showed no aberrant promoter hypermethylation for the GATA genes. Correlation of concomitant GATA-4 and GATA-5 methylation with clinicopathological parameters only found a statistically significant increase in methylation frequency with increasing patient age (P < 0.001).These epigenetic changes in the GATA genes in lung | 15585625 | [
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Carbonic anhydrase IX in early-stage non-small cell lung cancer. | Tumor hypoxia is associated with poor prognosis and increased tumor aggressiveness. Carbonic anhydrase (CA) IX; an endogenous marker for tumor hypoxia; catalyzes the hydration of carbon dioxide into carbonic acid and contributes to the pH regulation of tumor cells. Therefore; CA IX might allow tumors to acclimate to a hypoxic microenvironment; promoting tumor cell proliferation. We hypothesized that CA IX expression is related to tumor cell proliferation and poor disease-free survival in patients with early | 15585626 | [
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Carbonic anhydrase IX in early-stage non-small cell lung cancer. | -stage non-small-cell lung cancer (NSCLC).CA IX expression was measured in 75 resected NSCLC tumors to assess prognostic implications for disease-free survival. The relationship of CA IX expression with microvessel density (MVD) and proliferation (Ki-67) index was assessed via colocalization analysis.All patients had operable NSCLC (stage I; 58; stage II; 17). CA IX expression was present in 54 (72%) of 75 patients and was associated with tumor necrosis (P < 0.05). CA IX-positive tumor areas showed greater | 15585626 | [
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Carbonic anhydrase IX in early-stage non-small cell lung cancer. | cell proliferation as measured by Ki-67 index (P < 0.05) and less MVD (P < 0.05) than did CA IX-negative areas in colocalization analysis. The percentage of CA IX-positive tumor cells was significantly related to postoperative recurrence and poor disease-free survival (P < 0.05). Ki-67 index and pathologic stage were also independent prognostic factors for worse disease-free survival (P < 0.05).CA IX expression of tumor cells may be an indicator for poor disease-free survival in early-stage NSCLC. | 15585626 | [
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Plasma glutathione S-Transferase P1-1 as a prognostic factor in patients with advanced non-Hodgkin's lymphoma (stages III and IV). | This study aims to investigate whether the plasma level of glutathione S-transferase P1-1 (GSTP1-1); which is a phase II detoxifying enzyme known to be a resistance factor for anticancer drugs; could be a prognostic factor of de novo non-Hodgkin lymphoma (NHL) in clinical stages (CSs) III and IV.Study population consisted of 80 NHL patients with no prior treatment: 12 patients were at CS I; 14 at CS II; 25 at CS III; and 29 at CS IV. All 54 patients at CS III or CS IV were treated with cyclophosphamide; dox | 15585627 | [
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Plasma glutathione S-Transferase P1-1 as a prognostic factor in patients with advanced non-Hodgkin's lymphoma (stages III and IV). | orubicin; vincristine; and prednisolone (CHOP). Plasma GSTP1-1 concentration was measured by ELISA. We stained lymph node tissues for GSTP1-1 using anti-GSTP1-1 monoclonal antibody 5F and quantitatively assessed the intensity of immunostaining by using the KS-400 image analyzing system.There was a significant stepwise increment of plasma GSTP1-1 concentration from CS I to CS IV (P < 0.05). Of the 54 patients with CS III or IV treated with CHOP; 28 (52%) had elevated plasma GSTP1-1 levels. Plasma GSTP1-1 con | 15585627 | [
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Plasma glutathione S-Transferase P1-1 as a prognostic factor in patients with advanced non-Hodgkin's lymphoma (stages III and IV). | centration tended to correlate with the intensity of GSTP1-1 expression in lymphoma tissues as assessed by immunostaining (P = 0.07). The CR rates in patients at CS III and CS IV treated by CHOP; 55.2% (14 of 26) and 16.0% (5 of 28) for the low and high plasma GSTP1-1 groups; respectively; were significantly different (P < 0.01). For these two groups; the median survival times were 64 and 25 months; respectively (P < 0.01); and the median times to progression were 58 and 12 months; respectively (P < 0.01). | 15585627 | [
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Plasma glutathione S-Transferase P1-1 as a prognostic factor in patients with advanced non-Hodgkin's lymphoma (stages III and IV). | There was no significant correlation between plasma GSTP1-1 concentrations and other NHL prognostic indicators in these patients as determined by univariate and multivariate analyses.These results showed that plasma GSTP1-1 is a useful prognostic factor for CS III and IV advanced NHL. Thus; it may be a promising strategy to treat NHL concomitantly with anticancer drugs and GSTP1-1-specific inhibitors. | 15585627 | [
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Preradiotherapy hemoglobin level but not microvessel density predicts locoregional control and survival in laryngeal cancer treated with primary radical radiotherapy. | To evaluate the roles of preradiotherapy hemoglobin level and microvessel density (MVD) as predictive factors for tumor control and survival in patients with laryngeal cancer treated with primary radiotherapy.Two hundred and fourteen patients with stage I-IV laryngeal cancer were included in the analysis. Patients were treated with once daily fractionated radiotherapy over 6.5 weeks or twice daily fractionated radiotherapy over 4.5 weeks up to total doses of 62 to 68 Gy. Preradiotherapy hemoglobin levels we | 15585628 | [
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] |
Preradiotherapy hemoglobin level but not microvessel density predicts locoregional control and survival in laryngeal cancer treated with primary radical radiotherapy. | re obtained from patient journals; and pretreatment tumor biopsies were stained with CD34 antibody for the counting of microvessels. The prognostic implication of preradiotherapy hemoglobin level and MVD on tumor control and survival was tested.Five-year locoregional control probability was 88.9% for patients with preradiotherapy hemoglobin levels >137.5 g/L (median) and 64.4% for patients with preradiotherapy hemoglobin levels <137.5 g/L (P = 0.01). The corresponding figures for disease-free survival were | 15585628 | [
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Preradiotherapy hemoglobin level but not microvessel density predicts locoregional control and survival in laryngeal cancer treated with primary radical radiotherapy. | 87.8 and 62.8% (P = 0.007); respectively; and for overall survival 58.1 and 40.3% (P < 0.001); respectively. In multivariate analysis; tumor stage and preradiotherapy hemoglobin level were significant prognostic factors for locoregional control and disease-free survival; whereas tumor stage; preradiotherapy hemoglobin-level; gender; and age were significant prognostic factors for overall survival. No correlation was found between MVD and tumor control and survival.Preradiotherapy hemoglobin level; but not M | 15585628 | [
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Preradiotherapy hemoglobin level but not microvessel density predicts locoregional control and survival in laryngeal cancer treated with primary radical radiotherapy. | VD; predicts locoregional control and survival in patients with laryngeal cancer treated with radiotherapy. | 15585628 | [
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Interplay of insulin-like growth factor-II, insulin-like growth factor-I, insulin-like growth factor-I receptor, COX-2, and matrix metalloproteinase-7, play key roles in the early stage of colorectal carcinogenesis. | The aim of this study was to characterize the relationship of insulin-like growth factor (IGF)-II expression with IGF-I; IGF-I receptor (IGF-IR); cyclooxygenase-2 (COX-2); and matrix metalloproteinase (MMP)-7 in early colorectal carcinogenesis.With the semiquantitative reverse transcriptase-PCR; 90 human colorectal tumor tissues (63 adenomas and 27 submucosal pT1 cancers) were analyzed for IGF-II; IGF-IR; IGF-I; COX-2; and MMP-7 expression. Ninety-nine adenoma tissues and 60 pT1 cancer tissues were also ana | 15585629 | [
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Interplay of insulin-like growth factor-II, insulin-like growth factor-I, insulin-like growth factor-I receptor, COX-2, and matrix metalloproteinase-7, play key roles in the early stage of colorectal carcinogenesis. | lyzed immunohistochemically for IGF-II expression. Loss of imprinting of the IGF-II gene was analyzed. Paired carcinoma and adenoma tissues obtained from a carcinoma in adenoma lesion was analyzed by a cDNA array.IGF-II mRNA expression was detected in 37.8% of the 90 colorectal tumor tissues. The frequency of IGF-II mRNA expression was significantly higher in pT1 cancer (70.4%) than in adenoma (23.8%). Immunohistochemical IGF-II expression was also more frequently detected in pT1 cancer (58.3%) than in aden | 15585629 | [
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Interplay of insulin-like growth factor-II, insulin-like growth factor-I, insulin-like growth factor-I receptor, COX-2, and matrix metalloproteinase-7, play key roles in the early stage of colorectal carcinogenesis. | oma (25.3%). Loss of imprinting of the IGF-II gene was observed in 15 (44.1%) of the 34 colorectal tumors in which IGF-II was overexpressed. IGF-II expression was positively correlated with the expression of IGF-IR and IGF-I. COX-2 and MMP-7 mRNA expression was detected in 42.2% and 77.8% of the tumor tissues; respectively; and both were positively correlated with IGF-I; IGF-II; and IGF-IR expression. IGF-II was the most differentially expressed gene between carcinoma and adenoma lesions.IGF-II; in conjunct | 15585629 | [
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Interplay of insulin-like growth factor-II, insulin-like growth factor-I, insulin-like growth factor-I receptor, COX-2, and matrix metalloproteinase-7, play key roles in the early stage of colorectal carcinogenesis. | ion with IGF-IR; IGF-I; COX-2; and MMP-7; seems to play a key role in the early stage of colorectal carcinogenesis. | 15585629 | [
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Gain of OGP, an estrogen-regulated oviduct-specific glycoprotein, is associated with the development of endometrial hyperplasia and endometrial cancer. | Lesions in the endometrium are difficult to differentially diagnose. The present study examined whether oviduct-specific glycoprotein is differentially expressed in normal; hyperplastic; and malignant endometrium.The expression of oviduct-specific glycoprotein was characterized by immunohistochemical methods with whole sections of endometrium from 90 women. An endometrial cancer tissue microarray with 200 cases of endometrial cancer was also assessed for oviduct-specific glycoprotein; estrogen receptor; and | 15585630 | [
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Gain of OGP, an estrogen-regulated oviduct-specific glycoprotein, is associated with the development of endometrial hyperplasia and endometrial cancer. | PTEN expression.In normal endometrium; there was focal oviduct-specific glycoprotein expression in the basalis layer; where the stem cells reside; in 10 of 15 cases. On average; atypical hyperplastic endometria stained more intensely than hyperplastic endometria (P = 0.017); whereas the percentage of positively stained cells was not significantly different. The mean staining indices (intensity x percentage of positive cells score) for hyperplasia and atypical hyperplastic were 4.7 and 5.5 and were signific | 15585630 | [
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Gain of OGP, an estrogen-regulated oviduct-specific glycoprotein, is associated with the development of endometrial hyperplasia and endometrial cancer. | antly higher than staining indices seen in normal cycling endometria or well-differentiated endometrioid endometrial carcinomas (P < 0.0001 and P < 0.001; respectively). The endometrial cancer tissue microarray showed that of 139 endometrioid endometrial carcinomas; 11 cases were strongly oviduct-specific glycoprotein positive; whereas the other 128 cases were negative or weakly positive. Analysis of Kaplan-Meier curves with log-rank statistics showed a trend toward significance; with strong oviduct-specifi | 15585630 | [
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Gain of OGP, an estrogen-regulated oviduct-specific glycoprotein, is associated with the development of endometrial hyperplasia and endometrial cancer. | c glycoprotein staining serving as a predictor of good prognosis (P = 0.1). There was a significant positive correlation between oviduct-specific glycoprotein staining and loss of PTEN in the cases of endometrial cancer (P = 0.004).Oviduct-specific glycoprotein may be a useful diagnostic adjunct to more accurately classify premalignant and early malignant change in the endometrium; improving on the current irreproducible histologic classification system. | 15585630 | [
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Increased angiogenesis and lymphangiogenesis in inflammatory versus noninflammatory breast cancer by real-time reverse transcriptase-PCR gene expression quantification. | Inflammatory breast cancer is a distinct and aggressive form of locally advanced breast cancer with unique clinical and pathological features. Recently; histologic evidence of intense angiogenesis was found in inflammatory breast cancer specimens. The aim of this study was to confirm the angiogenic phenotype of inflammatory breast cancer and to investigate its potential to induce lymphangiogenesis.Real-time quantitative reverse transcriptase-PCR was used to measure levels of mRNA of tumor angiogenesis and l | 15585631 | [
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Increased angiogenesis and lymphangiogenesis in inflammatory versus noninflammatory breast cancer by real-time reverse transcriptase-PCR gene expression quantification. | ymphangiogenesis-related factors [vascular endothelial growth factor (VEGF)-A; VEGF-C; VEGF-D; Flt-1; KDR; Flt-4; Ang-1; Ang-2; Tie-1; Tie-2; cyclooxygenase-2; fibroblast growth factor-2 (FGF-2); Egr-1; Prox-1; and LYVE-1] in tumor specimens of 16 inflammatory breast cancer and 20 noninflammatory breast cancer patients. Tissue microarray technology and immunohistochemistry were used to study differential protein expression of some of the angiogenic factors in inflammatory breast cancer and noninflammatory b | 15585631 | [
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Increased angiogenesis and lymphangiogenesis in inflammatory versus noninflammatory breast cancer by real-time reverse transcriptase-PCR gene expression quantification. | reast cancer. Active lymphangiogenesis was further assessed by measuring lymphatic endothelial cell proliferation.Inflammatory breast cancer specimens had significantly higher mRNA expression levels than noninflammatory breast cancer specimens of the following genes: KDR (P = 0.033); Ang-1; (P = 0.0001); Tie-1 (P = 0.001); Tie-2 (P = 0.001); FGF-2 (P = 0.002); VEGF-C (P = 0.001); VEGF-D (P = 0.012); Flt-4 (P = 0.001); Prox-1 (P = 0.005); and LYVE-1 (P = 0.013). High mRNA levels of FGF-2 and cyclooxygenase-2 | 15585631 | [
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Increased angiogenesis and lymphangiogenesis in inflammatory versus noninflammatory breast cancer by real-time reverse transcriptase-PCR gene expression quantification. | corresponded to increased protein expression by immunohistochemistry. Inflammatory breast cancer specimens contained significantly higher fractions of proliferating lymphatic endothelial cells than noninflammatory breast cancer specimens (P = 0.033).Using real-time quantitative reverse transcriptase-PCR and immunohistochemistry; we confirmed the intense angiogenic activity in inflammatory breast cancer and demonstrated the presence of active lymphangiogenesis in inflammatory breast cancer. This may help ex | 15585631 | [
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Increased angiogenesis and lymphangiogenesis in inflammatory versus noninflammatory breast cancer by real-time reverse transcriptase-PCR gene expression quantification. | plain the high metastatic potential of inflammatory breast cancer by lymphatic and hematogenous route. Both pathways are potential targets for the treatment of inflammatory breast cancer. | 15585631 | [
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c-erbB-2 related aggressiveness in breast cancer is hypoxia inducible factor-1alpha dependent. | c-erbB-2-positive breast carcinomas are highly aggressive tumors. In vitro data on breast cell lines showed that c-erbB-2 enhanced translational efficiency of hypoxia inducible factor-1alpha (HIF1alpha) production (Laughner et al.; Mol Cell Biol 2001;21:3995-4005). We investigated the clinical correlate of this observation to assess whether c-erbB-2 expression was related to HIF1alpha expression; angiogenesis; and prognosis. A series of 180 breast carcinomas of known c-erbB-2 status (90 c-erbB-2-positive an | 15585632 | [
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c-erbB-2 related aggressiveness in breast cancer is hypoxia inducible factor-1alpha dependent. | d 90 c-erbB-2-negative carcinomas) were stained immunohistochemically for HIF1alpha and CD31 endothelial cell antigen. c-erbB-2 positivity was clearly related to HIF1alpha protein expression and high angiogenesis. However; prognosis was decreased only in cases with simultaneous c-erbB-2 and HIF1alpha expression. If activation of c-erbB-2 in humans results in overexpression of HIF1alpha independently of conditions of hypoxia; as occur in experimental studies; this interaction may represent a main pathway con | 15585632 | [
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c-erbB-2 related aggressiveness in breast cancer is hypoxia inducible factor-1alpha dependent. | ferring clinical aggressiveness to c-erbB-2-positive breast tumors. | 15585632 | [
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Lack of impact of the loss of constitutive folate receptor alpha expression, achieved by RNA Interference, on the activity of the new generation antifolate pemetrexed in HeLa cells. | Pemetrexed [PMX (Alimta)] is a new generation antifolate with activity in a variety of solid tumors. It is an excellent substrate for most folate transporters; notably the reduced folate carrier (RFC) and folate receptor (FR)-alpha. The role of FR-alpha in PMX pharmacological activity is uncertain. Whereas high-level expression may enhance the activity of this agent; it is not clear what role constitutive levels of this transporter contribute to PMX activity. In this study; constitutive levels of FR-alpha e | 15585634 | [
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Lack of impact of the loss of constitutive folate receptor alpha expression, achieved by RNA Interference, on the activity of the new generation antifolate pemetrexed in HeLa cells. | xpression were abolished by small interfering RNA-induced silencing in HeLa cells and RFC-null HeLa R5 cells as confirmed by Northern blotting; immunohistochemistry; and cell surface binding. PMX growth inhibition was unchanged in HeLa and R5 cells in the absence of FR-alpha expression. Loss of FR-alpha expression did not decrease net accumulation of PMX in either wild-type or RFC-null HeLa cells. Likewise; folate pools in wild-type HeLa cells were not decreased by FR-alpha gene silencing and were negligibl | 15585634 | [
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Lack of impact of the loss of constitutive folate receptor alpha expression, achieved by RNA Interference, on the activity of the new generation antifolate pemetrexed in HeLa cells. | y affected in the RFC-null R5 subline grown with 5-formyltetrahydrofolate. FR-alpha surface binding in HeLa cells was shown to be greater than that in a variety of other human solid tumor cell lines. Hence; constitutively expressed FR-alpha in HeLa cells does not contribute to PMX activity in the presence or absence of RFC function. This is likely the case in many human solid tumor cell lines. | 15585634 | [
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Evaluation of combination chemotherapy: integration of nonlinear regression, curve shift, isobologram, and combination index analyses. | Isobologram and combination index (CI) analyses are the two most popular methods for evaluating drug interactions in combination cancer chemotherapy. As the commonly used CI-based software program uses linear regression; our first objective was to evaluate the effects of logarithmic data transformation on data analysis and conclusions. Monte-Carlo simulations were conducted with experimentally relevant parameter values to generate error-containing effect or concentration-effect data of single agents and com | 15585635 | [
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Evaluation of combination chemotherapy: integration of nonlinear regression, curve shift, isobologram, and combination index analyses. | binations. The simulated data were then analyzed with linear and nonlinear regression. The results showed that data transformation reduced the accuracy and precision of the regression-derived IC(50); curve shape parameter and CI values. Furthermore; as neither isobologram nor CI analyses provide output of concentration-effect curves for investigator evaluation; our second objective was to develop a method and the associated computer program/algorithm to (a) normalize drug concentrations in IC(50) equivalent | 15585635 | [
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Evaluation of combination chemotherapy: integration of nonlinear regression, curve shift, isobologram, and combination index analyses. | s and thereby enable simultaneous presentation of the curves for single agents and combinations in a single plot for visual inspection of potential curve shifts; (b) analyze concentration-effect data with nonlinear regression; and (c) use the curve shift analysis simultaneously with isobologram and CI analyses. The applicability of this method was shown with experimentally obtained data for single agent doxorubicin and suramin and their combinations in cultured tumor cells. In summary; this method; by incor | 15585635 | [
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Evaluation of combination chemotherapy: integration of nonlinear regression, curve shift, isobologram, and combination index analyses. | porating nonlinear regression and curve shift analysis; although retaining the attractive features of isobologram and CI analyses; reduced the potential errors introduced by logarithmic data transformation; enabled visual inspection of data variability and goodness of fit of regression analysis; and simultaneously provided information on the extent of drug interaction at different combination ratios/concentrations and at different effect levels. | 15585635 | [
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Detection of neuroblastoma cells in bone marrow and peripheral blood by different techniques: accuracy and relationship with clinical features of patients. | Detection of metastatic tumor cells in bone marrow (BM) and peripheral blood (PB) of children with neuroblastoma is crucial for prognosis and planning of therapy. Aims of this large descriptive repeated survey were to evaluate the diagnostic accuracy of different techniques in diagnostic samples obtained at several disease course time points and to correlate positive results with patient clinical features and outcome.BM aspirates; trephine biopsies; PB; and peripheral blood stem cell (PBSC) samples from Ita | 15585633 | [
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Detection of neuroblastoma cells in bone marrow and peripheral blood by different techniques: accuracy and relationship with clinical features of patients. | lian children with neuroblastoma were analyzed by morphological and histologic techniques; as well as by immunocytochemistry (IC) for disialoganglioside GD(2) and reverse transcription-PCRs (RT-PCRs) for tyrosine hydroxylase (TH) and pgp9.5 genes. The diagnostic odd ratio (DOR) was used to measure the accuracy of the different techniques.A total of 2;247 evaluations were done on 561 BM; 265 PB; and 69 PBSC samples from 247 patients. IC showed the best accuracy. Whereas TH RT-PCR accuracy was satisfactory; t | 15585633 | [
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Detection of neuroblastoma cells in bone marrow and peripheral blood by different techniques: accuracy and relationship with clinical features of patients. | hat of pgp9.5 was very low. Positive results obtained by IC in BM and PB samples at diagnosis from stage 1; 2; and 3 patients correlated with unfavourable outcome. No correlation was found between positive results obtained by IC or TH RT-PCR in BM; PB; and PBSC samples from stage 4 patients and their outcome.Because of its elevated diagnostic accuracy; IC may represent a useful adjunct to conventional morphological techniques; especially in view of its potential prognostic role in patients with localized di | 15585633 | [
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Detection of neuroblastoma cells in bone marrow and peripheral blood by different techniques: accuracy and relationship with clinical features of patients. | sease. Longitudinal multicenter studies are warranted to definitely establish the clinical usefulness of TH RT-PCR. | 15585633 | [
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Lack of microvessels in well-differentiated regions of human head and neck squamous cell carcinoma A253 associated with functional magnetic resonance imaging detectable hypoxia, limited drug delivery, and resistance to irinotecan therapy. | Combination chemotherapy with irinotecan (CPT-11; 50 mg/kg/week x 4 intravenously); followed 24 hour later by 5-fluorouracil (50 mg/kg/week x 4 intravenously); results in 10 and 100% cure rates of animals bearing human head and neck squamous cell carcinoma xenografts A253 and FaDu; respectively. A253 consists of 30% well-differentiated and avascular and 70% poorly differentiated regions with low microvessel density (10/x400); whereas FaDu is uniformly poorly differentiated with higher microvessel density (1 | 15585636 | [
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Lack of microvessels in well-differentiated regions of human head and neck squamous cell carcinoma A253 associated with functional magnetic resonance imaging detectable hypoxia, limited drug delivery, and resistance to irinotecan therapy. | 9/x400). Studies were carried out for determining the role of well-differentiated and avascular regions in drug resistance in A253 and detection of such regions with noninvasive functional magnetic resonance (fMR) imaging.Tumors were harvested for histopathologic evaluation and immunohistochemistry (CD31; CD34; differentiation marker: involucrin; hypoxia markers: carbonic anhydrase IX; pimonidazole; vascular endothelial factor (VEGF) and Ki67) immediately after fMR imaging following the 3rd dose of chemothe | 15585636 | [
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Lack of microvessels in well-differentiated regions of human head and neck squamous cell carcinoma A253 associated with functional magnetic resonance imaging detectable hypoxia, limited drug delivery, and resistance to irinotecan therapy. | rapy. High-performance liquid chromatography determination of intratumoral drug concentration of 7-ethyl-10-hydroxyl-camptothecin and autoradiography with (14)C-labeled CPT-11 was done 2 hours after CPT-11 administration.Although A253 xenografts showed three times higher concentration of 7-ethyl-10-hydroxyl-camptothecin; FaDu was more responsive to therapy. After therapy; A253 tumor consisted mostly (approximately 80%) of well-differentiated regions (positive for involucrin) lacking microvessels with a hypo | 15585636 | [
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Lack of microvessels in well-differentiated regions of human head and neck squamous cell carcinoma A253 associated with functional magnetic resonance imaging detectable hypoxia, limited drug delivery, and resistance to irinotecan therapy. | xic rim (positive for carbonic anhydrase IX and pimonidazole) containing few proliferating (Ki67 positive) poorly differentiated cells. Autoradiography revealed that well-differentiated A253 tumor regions showed 5-fold lower (14)C-labeled CPT-11 concentrations compared with poorly differentiated areas (P < 0.001). Blood oxygen level dependant fMR imaging was able to noninvasively distinguish the hypoxic and well-vascularized regions within the tumors.Avascular-differentiated regions in squamous cell carcino | 15585636 | [
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Lack of microvessels in well-differentiated regions of human head and neck squamous cell carcinoma A253 associated with functional magnetic resonance imaging detectable hypoxia, limited drug delivery, and resistance to irinotecan therapy. | ma offer sanctuary to some hypoxic but viable tumor cells (carbonic anhydrase IX and Ki67 positive) that escape therapy because of limited drug delivery. This study provides direct evidence that because of a specific histologic structure; avascular; well-differentiated hypoxic regions in tumors exhibit low drug uptake and represent a unique form of drug resistance. | 15585636 | [
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Inhibition of proliferation and induction of apoptosis by 25-hydroxyvitamin D3-3beta-(2)-Bromoacetate, a nontoxic and vitamin D receptor-alkylating analog of 25-hydroxyvitamin D3 in prostate cancer cells. | The 25-hydroxyvitamin D(3) (25-OH-D(3)) is a nontoxic and low-affinity vitamin D receptor (VDR)-binding metabolic precursor of 1;25-dihydroxyvitamin D(3) [1;25(OH)(2)D(3)]. We hypothesized that covalent attachment of a 25-OH-D(3) analog to the hormone-binding pocket of VDR might convert the latter into transcriptionally active holo-form; making 25-OH-D(3) biologically active. Furthermore; it might be possible to translate the nontoxic nature of 25-OH-D(3) into its analog. We showed earlier that 25-hydroxyvi | 15585637 | [
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Inhibition of proliferation and induction of apoptosis by 25-hydroxyvitamin D3-3beta-(2)-Bromoacetate, a nontoxic and vitamin D receptor-alkylating analog of 25-hydroxyvitamin D3 in prostate cancer cells. | tamin D(3)-3-bromoacetate (25-OH-D(3)-3-BE) alkylated the hormone-binding pocket of VDR. In this communication we describe that 10(-6) mol/L of 25-OH-D(3)-3-BE inhibited the growth of keratinocytes; LNCaP; and LAPC-4 androgen-sensitive and PC-3 and DU145 androgen-refractory prostate cancer cells; and PZ-HPV-7 immortalized normal prostate cells with similar or stronger efficacy as 1;25(OH)(2)D(3). But its effect was strongest in LNCaP; PC-3; LAPC-4; and DU145 cells. Furthermore; 25-OH-D(3)-3-BE was toxic to | 15585637 | [
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Inhibition of proliferation and induction of apoptosis by 25-hydroxyvitamin D3-3beta-(2)-Bromoacetate, a nontoxic and vitamin D receptor-alkylating analog of 25-hydroxyvitamin D3 in prostate cancer cells. | these prostate cancer cells and caused these cells to undergo apoptosis as shown by DNA-fragmentation and caspase-activation assays. In a reporter assay with COS-7 cells; transfected with a 1alpha;25-dihydroxyvitamin D(3)-24-hydroxylase (24-OHase)-construct and VDR-expression vector; 25-OH-D(3)-3-BE induced 24-OHase promoter activity. In a "pull down assay" with PC-3 cells; 25-OH-D(3)-3-BE induced strong interaction between VDR and general transcription factors; retinoid X receptor; and GRIP-1. Collectively | 15585637 | [
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Inhibition of proliferation and induction of apoptosis by 25-hydroxyvitamin D3-3beta-(2)-Bromoacetate, a nontoxic and vitamin D receptor-alkylating analog of 25-hydroxyvitamin D3 in prostate cancer cells. | ; these results strongly suggested that the cellular effects of 25-OH-D(3)-3-BE were manifested via 1;25(OH)(2)D(3)/VDR signaling pathway. A toxicity study in CD-1 mice showed that 166 microg/kg of 25-OH-D(3)-3-BE did not raise serum-calcium beyond vehicle control. Collectively; these results strongly suggested that 25-OH-D(3)-3-BE has a strong potential as a therapeutic agent for androgen-sensitive and androgen-refractory prostate cancer. | 15585637 | [
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Inhibition of cyclooxygenase (COX)-2 expression by Tet-inducible COX-2 antisense cDNA in hormone-refractory prostate cancer significantly slows tumor growth and improves efficacy of chemotherapeutic drugs. | Overexpression of the proinflammatory enzyme cyclooxygenase (COX)-2 is associated with the progression of various malignancies; the role of COX-2 in prostate cancer is less clear. The significance of COX-2 in prostate cancer growth and response to chemotherapy was investigated in an androgen-refractory prostate cancer cell line using a Tet-inducible antisense COX-2 expression system.An antisense COX-2 cDNA construct under the control of a doxycycline-inducible promoter was transfected into a prostate cancer | 15585639 | [
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Inhibition of cyclooxygenase (COX)-2 expression by Tet-inducible COX-2 antisense cDNA in hormone-refractory prostate cancer significantly slows tumor growth and improves efficacy of chemotherapeutic drugs. | cell line; PC-3ML. Modulations of cell growth; apoptosis; and chemosensitivity in the presence or absence of doxycycline were analyzed. Tumor incidence; growth rate; and response to two cytotoxic drugs; COL-3 [chemically modified tetracycline-3-(6-demethyl-6-deoxy-4-dedimethylamino-tetracycline)] and Taxotere (docetaxel); were investigated in tumor xenografts. Apoptotic incidences and tumor microvessel density in tumors were determined by immunohistochemistry.Conditional suppression of COX-2 in PC-3ML caus | 15585639 | [
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Inhibition of cyclooxygenase (COX)-2 expression by Tet-inducible COX-2 antisense cDNA in hormone-refractory prostate cancer significantly slows tumor growth and improves efficacy of chemotherapeutic drugs. | ed reduced cell proliferation; decreased levels of phosphorylated AKT; G(0)-G(1) arrest; and increased apoptosis and caspase-3 activity. Suppression of COX-2 increased Bax protein and decreased Bcl-x(L) protein in vitro. COX-2 antisense-expressing PC-3ML tumors showed a 57% growth delay compared with nontransfected or vector controls. Oral administration of COL-3 (40 mg/kg; oral gavage) or Taxotere (2.3 mg/kg; intraperitoneally; 3x per week) in tumor-bearing mice further slowed tumor growth (65% and approxi | 15585639 | [
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Inhibition of cyclooxygenase (COX)-2 expression by Tet-inducible COX-2 antisense cDNA in hormone-refractory prostate cancer significantly slows tumor growth and improves efficacy of chemotherapeutic drugs. | mately 94%; respectively). Compared with the control group; the occurrence of apoptosis in antisense COX-2 tumors was eight times higher; and the tumor microvessel density was three times lower.These results provide direct evidence that constitutive expression of COX-2 in prostate cancer has both angiogenic and cytoprotective functions. Suppression of tumor cell COX-2 is sufficient to enhance chemotherapy response in prostate cancer. | 15585639 | [
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Inhibition of SRC tyrosine kinase as treatment for human pancreatic cancer growing orthotopically in nude mice. | The Src family comprises a family of nonreceptor intracellular tyrosine kinases that mediate a variety of cellular pathways. Src kinases are overexpressed in a variety of human tumors; including cancer of the colon; breast; and pancreas; and they are an integral part of tumor cell signaling pathways associated with migration; proliferation; adhesion; and angiogenesis.We investigated whether the blockade of Src kinase by daily oral administration of the novel Src tyrosine kinase inhibitor AZM475271 [kindly p | 15585638 | [
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Inhibition of SRC tyrosine kinase as treatment for human pancreatic cancer growing orthotopically in nude mice. | rovided by AstraZeneca (Macclesfield; United Kingdom)]; alone or in combination with intraperitoneal gemcitabine; can inhibit growth and metastasis of orthotopically implanted human pancreatic carcinoma cells in nude mice.Treatment with AZM475271 alone reduced the primary pancreatic tumor volume by approximately 40%; whereas AZM475271 plus gemcitabine reduced tumor volume by 90%. Furthermore; treatment with AZM475271 and gemcitabine significantly reduced metastasis: none of eight animals who received the co | 15585638 | [
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Inhibition of SRC tyrosine kinase as treatment for human pancreatic cancer growing orthotopically in nude mice. | mbination treatment had lymph node or liver metastases; compared with five of five and three of five animals; respectively; in the control group (P = 0.001). Src inhibition by AZM475271 (alone or with gemcitabine) was associated with significantly reduced tumor cell proliferation; decreased tumor microvessel density; and increased apoptosis in vivo. Moreover; these effects were all significantly increased when gemcitabine was combined with AZM475271 compared with gemcitabine alone.Src inhibition by AZM47527 | 15585638 | [
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Inhibition of SRC tyrosine kinase as treatment for human pancreatic cancer growing orthotopically in nude mice. | 1; either alone or in combination with gemcitabine; demonstrated significant antitumor and antimetastatic activity in an orthotopic nude mouse model for human pancreatic cancer. The combination of AZM475271 with gemcitabine sensitized tumor cells to the cytotoxic effect of gemcitabine. | 15585638 | [
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Prognostic significance of tissue transglutaminase in drug resistant and metastatic breast cancer. | Drug resistance and metastasis pose major impediments in the successful treatment of cancer. We previously reported that multidrug-resistant breast cancer cells exhibit high levels of tissue transglutaminase (TG2; EC 2.3.2.13). Because the drug-resistant and metastatic phenotypes are thought to share some common pathways; we sought to determine whether metastatic breast cancer cells express high levels of TG2.The metastatic breast cancer cell line MDA-MB-231 and the sublines derived from it were tested for | 15585642 | [
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Prognostic significance of tissue transglutaminase in drug resistant and metastatic breast cancer. | TG2 expression. Similarly; several sublines derived from an immortal but normal breast epithelial cell line; MCF10A; representing various stages in breast cancer progression were studied for TG2 expression. The primary and nodal tumor samples from 30 patients with breast cancer were also studied for TG2 expression.The MDA-MB-231 cells expressed high basal levels of TG2. Two clones derived from this cell line; MDA231/cl.9 and MDA231/cl.16; showed a 10- to 15-fold difference in TG2 level. TG2-deficient MDA231 | 15585642 | [
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Prognostic significance of tissue transglutaminase in drug resistant and metastatic breast cancer. | /cl.9 cells exhibited higher sensitivity to doxorubicin and were less invasive than were the TG2-sufficient MDA231/cl.16 cells. The MCF10A-derived sublines had increased TG2 expression as they advanced from noninvasive to an invasive phenotype. Importantly; the metastatic lymph node tumors from patients with breast cancer showed significant higher levels of TG2 expression compared with the primary tumors from the same patients.TG2 expression is up-regulated in drug-resistant and metastatic breast cancer cel | 15585642 | [
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Prognostic significance of tissue transglutaminase in drug resistant and metastatic breast cancer. | ls; and it can serve as a valuable prognostic marker for these phenotypes. | 15585642 | [
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Pharmacokinetic model-predicted anticancer drug concentrations in human tumors. | In an era when molecular and targeted anticancer therapeutics is a major focus and when understanding drug dynamics in tumor is critical; it seems advantageous to be able to relate drug concentrations in tumors to corresponding biological end points. To that end; a novel method; based on physiologically based hybrid pharmacokinetic models; is presented to predict human tumor drug concentrations. Such models consist of a forcing function; describing the plasma drug concentration-time profile; which is linked | 15585640 | [
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Pharmacokinetic model-predicted anticancer drug concentrations in human tumors. | to a model describing drug disposition in tumors. The hybrid models are originally derived from preclinical data and then scaled to humans. Integral to the scale-up procedure is the ability to derive human forcing functions directly from clinical pharmacokinetic data. Three examples of this approach are presented based on preclinical investigations with carboplatin; topotecan; and temozolomide. Translation of these preclinical hybrid models to humans used a Monte Carlo simulation technique that accounted f | 15585640 | [
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Pharmacokinetic model-predicted anticancer drug concentrations in human tumors. | or intrasubject and intersubject variability. Different pharmacokinetic end points; such as the AUC tumor; were extracted from the simulated human tumor drug concentrations to show how the predicted drug concentrations might be used to select drug-dosing regimens. It is believed that this modeling strategy can be used as an aid in the drug development process by providing key insights into drug disposition in tumors and by offering a foundation to optimize drug regimen design. | 15585640 | [
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Inhibition of mTOR activity restores tamoxifen response in breast cancer cells with aberrant Akt Activity. | The Akt kinase is a serine/threonine protein kinase that has been implicated in mediating a variety of biological responses. Studies show that high Akt activity in breast carcinoma is associated with a poor pathophenotype; as well as hormone and chemotherapy resistance. Additionally; high Akt activity is associated with other features of poor prognosis. Thus; a chemotherapeutic agent directed specifically toward tumors with high Akt activity could prove extremely potent in treating those breast tumors with | 15585641 | [
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Inhibition of mTOR activity restores tamoxifen response in breast cancer cells with aberrant Akt Activity. | the most aggressive phenotypes. Several studies have demonstrated that rapamycin; which inhibits mammalian target of rapamycin (mTOR); a downstream target of Akt; sensitizes certain resistant cancer cells to chemotherapeutic agents. This study evaluated the efficacy of mTOR inhibition in the treatment of tamoxifen-resistant breast carcinoma characterized by high Akt activity. We found that MCF-7 breast cancer cell lines expressing a constitutively active Akt are able to proliferate under reduced estrogen co | 15585641 | [
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Inhibition of mTOR activity restores tamoxifen response in breast cancer cells with aberrant Akt Activity. | nditions and are resistant to the growth inhibitory effects of tamoxifen; both in vitro as well as in vivo in xenograft models. Cotreatment with the mTOR inhibitor rapamycin in vitro; or the ester of rapamycin; CCI-779 (Wyeth) in vivo; inhibited mTOR activity and restored sensitivity to tamoxifen; suggesting that Akt-induced tamoxifen resistance is mediated in part by signaling through the mTOR pathway. Although the mechanism underlying the synergism remains to be understood; the results were associated wit | 15585641 | [
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Inhibition of mTOR activity restores tamoxifen response in breast cancer cells with aberrant Akt Activity. | h rapamycin's ability to block transcriptional activity mediated by estrogen receptor alpha; as assessed by reporter gene assays with estrogen-responsive element luciferase. These data corroborate prior findings indicating that Akt activation induces resistance to tamoxifen in breast cancer cells. Importantly; these data indicate a novel mechanism for tamoxifen resistance and suggest that blockage of the phosphatidylinositol 3'-kinase/Akt signaling pathway by mTOR inhibition effectively restores the suscept | 15585641 | [
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Inhibition of mTOR activity restores tamoxifen response in breast cancer cells with aberrant Akt Activity. | ibility of these cells to tamoxifen. These data may have implication for future clinical studies of mTOR inhibition in breast carcinoma. | 15585641 | [
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Enhanced tumor cell radiosensitivity and abrogation of G2 and S phase arrest by the Hsp90 inhibitor 17-(dimethylaminoethylamino)-17-demethoxygeldanamycin. | Because of the potential for affecting multiple signaling pathways; inhibition of Hsp90 may provide a strategy for enhancing tumor cell radiosensitivity. Therefore; we have investigated the effects of the orally bioavailable Hsp90 inhibitor 17-(dimethylaminoethylamino)-17-demethoxygeldanamycin (17-DMAG) on the radiosensitivity of human tumor cells in vitro and grown as tumor xenografts.The effect of 17-DMAG on the levels of three proteins (Raf-1; ErbB2; and Akt) previously implicated in the regulation of ra | 15585643 | [
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Enhanced tumor cell radiosensitivity and abrogation of G2 and S phase arrest by the Hsp90 inhibitor 17-(dimethylaminoethylamino)-17-demethoxygeldanamycin. | diosensitivity was determined in three human solid tumor cell lines. A clonogenic assay was then used to evaluate cell survival after exposure to 17-DMAG followed by irradiation. For mechanistic insight; the G(2)- and S-phase checkpoints were evaluated in 17-DMAG-treated cells. Finally; the effect of in vivo administration of 17-DMAG in combination with radiation on the growth rate of xenograft tumors was determined.17-DMAG exposure reduced the levels of the three radiosensitivity-associated proteins in a c | 15585643 | [
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Enhanced tumor cell radiosensitivity and abrogation of G2 and S phase arrest by the Hsp90 inhibitor 17-(dimethylaminoethylamino)-17-demethoxygeldanamycin. | ell line-specific manner with ErbB2 being the most susceptible. Corresponding concentrations of 17-DMAG enhanced the radiosensitivity of each of the tumor cell lines. This sensitization seemed to be the result of a 17-DMAG-mediated abrogation of the G(2)- and S-phase cell cycle checkpoints. The oral administration of 17-DMAG to mice bearing tumor xenografts followed by irradiation resulted in a greater than additive increase in tumor growth delay.These data indicate that 17-DMAG enhances the in vitro and in | 15585643 | [
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Enhanced tumor cell radiosensitivity and abrogation of G2 and S phase arrest by the Hsp90 inhibitor 17-(dimethylaminoethylamino)-17-demethoxygeldanamycin. | vivo radiosensitivity of human tumor cells. The mechanism responsible seems to involve the abrogation of radiation-induced G(2)- and S-phase arrest. | 15585643 | [
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pRb2/p130 decreases sensitivity to apoptosis induced by camptothecin and doxorubicin but not by taxol. | In addition to their original function as cell cycle regulators; retinoblastoma (Rb) family members were recently reported to modulate the sensitivity of cancer cells to chemotherapeutic agents. The purpose of this study is to investigate the possible role of pRb2/p130 in the sensitivity of ovarian cancer to camptothecin; doxorubicin; and taxol.pRb2/p130 was overexpressed in the CAOV-3 ovarian cancer cell line; and the effect of pRb2/p130 overexpression on sensitivity to apoptosis trigged by IC(50) doses of | 15585644 | [
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pRb2/p130 decreases sensitivity to apoptosis induced by camptothecin and doxorubicin but not by taxol. | different drugs was evaluated by various methods; including 3-(4;5-dimethylthiazol-2-yl)-2;5-diphenyltetrazolium bromide assay; flow cytometry; and Western blot analyses.The results reported in this study support the conclusion that overexpression of pRb2/p130 in the CAOV-3 ovarian cancer cell line lacking wild-type p53 is able to inhibit apoptosis triggered by camptothecin and doxorubicin through the c-Jun NH(2)-terminal kinase signaling transduction pathway. Conversely; taxol-induced cell death is not in | 15585644 | [
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pRb2/p130 decreases sensitivity to apoptosis induced by camptothecin and doxorubicin but not by taxol. | fluenced by the pRb2/p130 protein level.A careful analysis of pRb2/p130 expression in tumor specimens could help to identify the best clinical protocol to be used for each patient; improving efficacy and tolerance and therefore offering additional progress in the treatment of advanced ovarian cancer. | 15585644 | [
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Histone deacetylase inhibitor trichostatin A represses estrogen receptor alpha-dependent transcription and promotes proteasomal degradation of cyclin D1 in human breast carcinoma cell lines. | Estrogen receptor alpha (ERalpha)-positive breast cancer cell lines are up to 10 times more sensitive than ERalpha-negative cell lines to the antiproliferative activity of the histone deacetylase inhibitor trichostatin A (TSA). The purpose of the study was to investigate the mechanisms underlying this differential response.In the ERalpha-positive MCF-7 cell line; TSA repressed ERalpha and cyclin D1 transcription and induced ubiquitin dependent proteasomal degradation of cyclin D1; leading primarily to G(1)- | 15585645 | [
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Histone deacetylase inhibitor trichostatin A represses estrogen receptor alpha-dependent transcription and promotes proteasomal degradation of cyclin D1 in human breast carcinoma cell lines. | S-phase cell cycle arrest. By contrast; cyclin D1 degradation was enhanced but its transcription unaffected by TSA in the ERalpha-negative MDA-MB-231 cell line; which arrested in G(2)-M phase. Cyclin D1 degradation involved Skp2/p45; a regulatory component of the Skp1/Cullin/F-box complex; silencing SKP2 gene expression by RNA interference stabilized cyclin D1 and abrogated the cyclin D1 down-regulation response to TSA.Tamoxifen has been shown to inhibit ERalpha-mediated cyclin D1 transcription; and acquire | 15585645 | [
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Histone deacetylase inhibitor trichostatin A represses estrogen receptor alpha-dependent transcription and promotes proteasomal degradation of cyclin D1 in human breast carcinoma cell lines. | d resistance to tamoxifen is associated with a shift to ERalpha-independent cyclin D1 up-regulation. Taken together; our data show that TSA effectively induces cyclin D1 down-regulation through both ERalpha-dependent and ERalpha-independent mechanisms; providing an important new strategy for combating resistance to antiestrogens. | 15585645 | [
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The selective cyclooxygenase-2 inhibitor nimesulide prevents Helicobacter pylori-associated gastric cancer development in a mouse model. | Helicobacter pylori infection can lead to gastric cancer; and cyclooxygenase-2 (COX-2) is overexpressed in the stomach during H. pylori infection. Therefore; we investigated whether nonsteroidal anti-inflammatory drugs might protect against this form of cancer. Specifically; we examined the chemopreventive effect of the COX-2 inhibitor nimesulide on H. pylori-associated gastric carcinogenesis in mice.C57BL/6 mice were treated with the carcinogen N-methyl-N-nitrosourea (MNU) and/or H. pylori. To determine th | 15585646 | [
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The selective cyclooxygenase-2 inhibitor nimesulide prevents Helicobacter pylori-associated gastric cancer development in a mouse model. | e effect of COX-2 inhibition; nimesulide was mixed with feed pellets and administered for the duration of the experiment. All of the mice were sacrificed 50 weeks after the start of the experiment. Histopathology; immunohistochemistry; and Western blotting for COX-2; Bax and Bcl-2 were performed in stomach tissues. In vitro experiments with the human gastric cancer cell line AGS were also performed to identify mechanisms underlying cancer chemoprevention by nimesulide.Gastric tumors developed in 68.8% of mi | 15585646 | [
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The selective cyclooxygenase-2 inhibitor nimesulide prevents Helicobacter pylori-associated gastric cancer development in a mouse model. | ce that were given both MNU and H. pylori; whereas less than 10% developed gastric tumors when given either MNU or H. pylori alone. These findings indicate that H. pylori promotes carcinogen-induced gastric tumorigenesis. In mice treated with both MNU and H. pylori; nimesulide administration substantially reduced H. pylori-associated gastric tumorigenesis; whereas substantial inductions of apoptosis were observed. In vitro studies demonstrated that nimesulide and H. pylori when combined acted synergisticall | 15585646 | [
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The selective cyclooxygenase-2 inhibitor nimesulide prevents Helicobacter pylori-associated gastric cancer development in a mouse model. | y to induce more apoptosis than either alone.Our data show that nimesulide prevents H. pylori-associated gastric carcinogenesis; and suggest that COX-2 may be a target for chemoprevention of gastric cancer. | 15585646 | [
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Increased Fas expression reduces the metastatic potential of human osteosarcoma cells. | The process of metastasis requires the single tumor cell that seeds the metastatic clone to complete a complex series of steps. Identifying factors responsible for these steps is essential in developing and improving targeted therapy for metastasis. Resistance to receptor-mediated cell death; such as the Fas/Fas ligand pathway; is one mechanism commonly exploited by metastatic cell populations.LM7; a subline of the SAOS human osteosarcoma cell line with low Fas expression; was selected for its high metastat | 15585647 | [
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Increased Fas expression reduces the metastatic potential of human osteosarcoma cells. | ic potential in an experimental nude mouse model. When transfected with the full-length Fas gene (LM7-Fas); these cells expressed higher levels of Fas than the parental LM7 cells or LM7-neo control-transfected cells. These cells were also more sensitive to Fas-induced cell death than controls. When injected intravenously into nude mice; the LM7-Fas cell line produced a significantly lower incidence of tumor nodules than control cell lines. Lung weight and tumor nodule size were also decreased in those mice | 15585647 | [
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Increased Fas expression reduces the metastatic potential of human osteosarcoma cells. | injected with LM7-Fas. Levels of Fas were quantified in osteosarcoma lung nodules from 17 patients. Eight samples were Fas negative; whereas the remaining 9 were only weakly positive compared with normal human liver (positive control).Our results demonstrate that altering Fas expression can impact the metastatic potential of osteosarcoma cells. We conclude that the increase of Fas on the surface of the LM7 osteosarcoma cells increased their sensitivity to Fas-induced cell death in the microenvironment of th | 15585647 | [
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Increased Fas expression reduces the metastatic potential of human osteosarcoma cells. | e lung; where Fas ligand is constitutively expressed. Thus; loss of Fas expression is one mechanism by which osteosarcoma cells may evade host resistance mechanisms in the lung; increasing metastatic potential. Fas may therefore be a new therapeutic target for osteosarcoma. | 15585647 | [
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Clonal evidence for the transduction of CD34+ cells with lymphomyeloid differentiation potential and self-renewal capacity in the SCID-X1 gene therapy trial. | Immune function has been restored in 9 of 10 children with X-linked severe combined immunodeficiency by gamma c gene transfer in CD34+ cells. The distribution of both T-cell receptor (TCR) V beta family usage and TCR V beta complementarity-determining region 3 (CDR3) length revealed a broadly diversified T-cell repertoire. Retroviral integration site analysis in T cells demonstrated a high number of distinct insertion sites; indicating polyclonality of genetically corrected cell clones; in all patients. Det | 15585650 | [
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Clonal evidence for the transduction of CD34+ cells with lymphomyeloid differentiation potential and self-renewal capacity in the SCID-X1 gene therapy trial. | ection of gamma c transgene expression on patients' mature myeloid cells has prompted us to investigate the nature of the most immature transduced hematopoietic precursor cells. Insertion sites shared by T and B lymphocytes as well as highly purified granulocytes and monocytes demonstrate the correction of common multipotent progenitor cells. Moreover; our data show that differentiated leukocytes share the same exact insertion sites with CD34+ cells that we obtained 8 months later and that were able to gene | 15585650 | [
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Clonal evidence for the transduction of CD34+ cells with lymphomyeloid differentiation potential and self-renewal capacity in the SCID-X1 gene therapy trial. | rate long-term culture-initiating cells (LTC-ICs). This finding demonstrates the initial transduction of very primitive multipotent progenitor cells with self-renewal capacity. These results provide a first evidence in the setting of a clinical trial that CD34+ cells maintain both lymphomyeloid potential as well as self-renewal capacity after ex vivo manipulation. | 15585650 | [
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] |
RNAi-induced down-regulation of FLT3 expression in AML cell lines increases sensitivity to MLN518. | FMS-like tyrosine kinase 3 (FLT3) is a receptor tyrosine kinase that is constitutively activated in approximately 30% of acute myelogenous leukemia (AML) patients and appears to confer an adverse prognosis. Thus; development of inhibitors and/or antibodies that specifically target FLT3 has been of substantial interest. In this regard; phase 1 and 2 trials involving FLT3 inhibitors have recently reported FLT3 inhibition and leukemic blast reduction in some patients. Despite this; issues such as specificity a | 15585651 | [
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] |
RNAi-induced down-regulation of FLT3 expression in AML cell lines increases sensitivity to MLN518. | nd resistance need to be addressed. Consequently; the development of alternative approaches for targeting FLT3 would be of great consequence. In the present report; we demonstrate that FLT3 siRNA effectively down-regulates FLT3 expression in Ba/F3 cells transfected with FLT3 containing an activating internal tandem duplication (ITD) in the juxtamembrane domain and FLT3-ITD-positive Molm-14 human leukemia cells. Treatment with the FLT3 siRNA results in growth inhibition and apoptosis of these cells. Furtherm | 15585651 | [
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RNAi-induced down-regulation of FLT3 expression in AML cell lines increases sensitivity to MLN518. | ore; siRNA-induced down-regulation of FLT3 increased the sensitivity of both cell lines to treatment with the FLT3 inhibitor MLN518. This illustrates the potential benefit of combined therapeutic approaches. | 15585651 | [
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Plag1 and Plagl2 are oncogenes that induce acute myeloid leukemia in cooperation with Cbfb-MYH11. | Recurrent chromosomal rearrangements are associated with the development of acute myeloid leukemia (AML). The frequent inversion of chromosome 16 creates the CBFB-MYH11 fusion gene that encodes the fusion protein CBFbeta-SMMHC. This fusion protein inhibits the core-binding factor (CBF); resulting in a block of hematopoietic differentiation; and induces leukemia upon the acquisition of additional mutations. A recent genetic screen identified Plag1 and Plagl2 as CBF beta-SMMHC candidate cooperating proteins. | 15585652 | [
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Plag1 and Plagl2 are oncogenes that induce acute myeloid leukemia in cooperation with Cbfb-MYH11. | In this study; we demonstrate that Plag1 and Plagl2 independently cooperate with CBF beta-SMMHC in vivo to efficiently trigger leukemia with short latency in the mouse. In addition; Plag1 and Plagl2 increased proliferation by inducing G1 to S transition that resulted in the expansion of hematopoietic progenitors and increased cell renewal in vitro. Finally; PLAG1 and PLAGL2 expression was increased in 20% of human AML samples. Interestingly; PLAGL2 was preferentially increased in samples with chromosome 16 | 15585652 | [
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Plag1 and Plagl2 are oncogenes that induce acute myeloid leukemia in cooperation with Cbfb-MYH11. | inversion; suggesting that PLAG1 and PLAGL2 may also contribute to human AML. Overall; this study shows that Plag1 and Plagl2 are novel leukemia oncogenes that act by expanding hematopoietic progenitors expressing CbF beta-SMMHC. | 15585652 | [
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