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Results for “Radiosensitivity”

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At least 631 records · Page 35Linked to original sources

PubMed1992

Low pH does not affect the dose response for 5'-amino-5'-deoxythymidine modulation of IdUrd DNA incorporation and radiosensitization in a human bladder cancer cell line.

We report that coincubation of 647V cells for one cell cycle with low concentrations (30 microM) of 5'-amino-5'-deoxythymidine increased IdUrd DNA incorporation and radiosensitivity at low extracellular pH (pHe 6.8) in a fashion similar to treatment at normal pHe. IdUrd DNA incorporation is inhibited by high (300 microM) 5'-AdThd concentrations at both normal and low pHe (7.4 and 6.8), resulting in no significant radiosensitization. These results at low pHe were not anticipated based on previously published studies of 5'-AdThd modulation of thymidine kinase (TK) activity and nucleoside cellular uptake. Our results suggest that regulation of intracellular pH (pHi) during the course of one cell cycle negates the 5'-AdThd dose-dependent modulation of TK activity demonstrated previously. Flow cytometric measurement of pHi in 647V cells showed that normal pHi (pH 7.4) was maintained in 647V cells over a 12- to 24-h exposure to low pHe (pH 6.8). Thus the concomitant use of IdUrd and high concentrations of 5'-AdThd (> 30 microM) is unlikely to result in selective in vivo radiosensitization of human tumors under conditions which are intermittently or chronically acidic. However, low concentrations of 5'-AdThd may prove to be an effective in vivo modulator of IdUrd radiosensitization of human tumors under both normal and acidic conditions.

Cell Cycle↗

PubMed1992

[Synthesis and radiosensitizing activity of nitro-arylimino-diethyl-sodium thiosulfate and nitro phenylalanine derivatives].

A series of compounds was synthesized, these compounds were tested for Hela-S3 cells in vitro for radiosensitizing activity. Five of them are 2,2'-(arylimino)-diethyl-sodium thiosulfate and two of them are phenylalanine derivatives. Most of them showed various degrees of radiosensitizing activity. Among them, SER of L07 was 1.89 at 3 mmol, and had low cytotoxicity to Hela-S3 cells, ID50 was 18.8 mmol. The relationship between radiosensitizing effects and chemical structure was discussed. It offers a base for further exploration of selectively hypoxic cell radiosensitizers.

HeLa Cells↗

PubMed2004

[Radiosensitization by pentoxifylline in human hepatoma cell line HepG2 and its mechanism].

OBJECTIVE: To investigate the radiosensitization by pentoxifylline (PTX) in human hepatoma cell line HepG2 and its possible mechanism. METHODS: MTT assay was used to evaluate the cytotoxicity of PTX and clonogenic assay employed to observe its effects on the radiosensitivity of the cells quantified by calculating the sensitive enhancement ratio (SER). Flow cytometry was performed to observe the changes in the cell cycle of HepG2 cells in response to X-ray irradiation and the effect of PTX intervention. RESULTS: The cytotoxicity of PTX increased in a dose-dependent manner following a 24-hour treatment, with the optimal dose range of 1-5 mmol/L. A sub-toxic dose of PTX at 2 mmol/L was used in the subsequent experiments. PTX significantly reduced the clonogenic activity and enhanced the radiosensitivity of HepG2 cells with a SER of 1.3+/-0.16 at the dose of 2 mmol/L. Irradiation resulted in cell cycle arrest at G2 phase in HepG2 cells, and the percentages of HepG2 cells in G2-M phase were 32.15% and 19.52% respectively after exposure to 6 Gy radiation alone and to 6 Gy plus 2 mmol/L PTX at 20 h, demonstrating the effectiveness of PTX in resolving radiation-induced G2 arrest. CONCLUSION: Radiosensitization by PTX is possibly associated with the abrogation of G2 arrest in HepG2 cells following radiation exposure.

Carcinoma, Hepatocellular↗

PubMed2004

[Radiosensitivity detected by "comet" assay in two human tumor cell lines].

OBJECTIVE: To evaluate the value of the "comet" assay in detecting the radiosensitivity in human tumor cell lines. METHODS: The radiation-induced primary DNA damage and repair were detected by the comet assay in CNE-1 and 973 cell lines. The tail moment was used as the end point, to quantitate the primary DNA damage and subsequent repair ability. The cell-survival curve was plotted by the classical colony assay, to detect the D(0) value and Dq value. The results from the above two assays were compared. RESULTS: 1. With the increment of irradiation doses, under the same experimental condition, the radiation-induced primary DNA damage was more severe in CNE-1 cells than in 973 cells (P < 0.01). From the cell-survival curves, the D(0) value was 1.631 and 1.822 in CNE-1 and CNE-1 973 cells respectively, indicating that CNE-1 cells were more sensitive to irradiation than 973 cells. The radiosensitivity detected by comet assay and by colony assay in the two cell lines tended to be consistent. 2. The half-repair time of 973 and CNE-1 cell line was 33 min and 41 min detected by comet assay, which indicats that the ability of DNA damage and repair in CNE-1 cells was weaker than in 973 cells. The Dq value of the cell survival curve was 2.152 for 973 and 0.626 for CNE-1 cell line detected by the colony assay, which indicates that the sublethal damage repair in 973 cells being much faster than in CNE-1 cells. The repair ability reflected by the results in the two cell lines was consistent. CONCLUSION: The radiosensitivities reflected by the results of the primary DNA damage and repair detected by both comet assay and colony assay in CNE-1 and 973 cells are consistent. It suggests that comet assay is a good method for detecting the radiosensitivity of tumor cells.

Adenocarcinoma↗

PubMed2004

Experimental evidence on possibility to radiosensitize aggressive tumors by porphyrins.

Two murine experimental tumor models of different aggressiveness (murine Ehrlich ascitic carcinoma and MH-22A hepatoma) were used to investigate the radiosensitization by porphyrins. Data obtained clearly indicate that hematoporphyrin dimethyl ether, photofrin and hematoporphyrin derivative exert some radiosensitizing properties which are in clear correlation with purity of the compound. Of interest to note, that just aggressive Ehrlich ascitic carcinoma was radiosensitized to gamma-radiation, whereas no signs of radiosensitization were observed in MH-22A hepatoma tumor. Data obtained support the idea, that dicarboxylic porphyrins, being ligands of peripheral benzodiazepine receptors (responsible for proliferation and highly expressed in aggressive tumors) might induce several sublethal injuries in the cell which further work in concert with ionizing radiation producing synergistic interaction of two antiproliferative factors.

Animals↗

PubMed2005

Radiosensitization, after a combined treatment of survivin siRNA and irradiation, is correlated with the activation of caspases 3 and 7 in a wt-p53 sarcoma cell line, but not in a mt-p53 sarcoma cell line.

Survivin, a member of the inhibitor-of-apoptosis family is an essential protein for regular mitosis and is involved in an anti-apoptotic pathway. In some studies, an association between survivin expression and radiosensitivity has been described for tumor cells, but the relationship between p53 and survivin regarding radioresistance remains to be clarified. In order to increase the effect of irradiation on two sarcoma cell lines, A-204 with wt-p53 and US 8-93 with mt-p53, siRNA was applied to knock down survivin expression. The effects of combined treatment of siRNA treatment and irradiation were investigated by clonogenic survival assay, measurement of activity of caspases 3 and 7, Western blot hybridization for survivin and p53, and morphological analysis of apoptosis. Survivin knock down caused radiosensitization in the cell line A-204 (wt-p53) with an enhancement factor of 1.8 at 2 Gy (p=0.05) and 2.5 at 4 Gy (p=0.02), respectively. No radiosensitization was found in the cell line US 8-93 (mt-p53), when clonogenic survival was analyzed. These findings were supported by an increase in activity (up to 5.2-fold) of caspases 3 and 7 in cell line A-204 (wt-p53), but not in cell line US 8-93 (mt-p53) after a combined treatment of siRNA and irradiation. Our findings suggest that the wt-p53-caspase pathway is of importance for the radiosensitization induced by targeting survivin, which may have an impact on future gene therapeutical treatments.

Apoptosis↗

PubMed2003

[Study on mutation of ATM/PI3K region in NPC cell lines with different radiosensitivity].

To try to elucidate the relationship between the radiosensitivity of NPC cell lines and ATM gene, this study was designed to investigate the mutation of ATM/PI3K region in NPC cell lines with different radiosensitivity. Two NPC cell lines of CNE1 and CNE2 with different radiosensitivities were established. Reverse transcriptase polymerase chain reaction (RT-PCR) was used to get a 546bp fragment (8578nt-9123nt) of ATM cDNA, containing the PI-3 kinase domain (8753-8815bp). Direct sequencing of RT-PCR product was applied to determine the mutations in the gene. The sequence of the 546bp fragment is identical to the sequence of ATM gene published in GenBank, that is, there are no any mutations on the fragment of ATM/PI3K we examined either in CNE1 or in CNE2. It indicates that there may be no correlations between the mutation of ATM/PI3K and the variation of radiosensitivity in NPC cell lines CNE1, CNE2.

English Abstract↗

PubMed2005

Chromosomal radiosensitivity in breast cancer patients: influence of age of onset of the disease.

The age dependency of onset of the disease on chromosomal radiosensitivity of an unselected group of breast cancer patients (n=100) was investigated and compared to a group of healthy women (n=100). The chromosomal radiosensitivity was assessed with the G2 and the G0 micro-nucleus (MN) assay. For the G2 assay lymphocytes were irradiated in vitro with a dose of 0.4 Gy 60Co gamma-rays after 70 h incubation and chromatid breaks were scored in 50 metaphases. For the G0 MN assay lymphocytes were exposed in vitro to 3.5 Gy 60Co gamma-rays at low dose rate (LDR). 72 h post-irradiation cultures were arrested and micronuclei were scored in 1000 binucleate cells. The results demonstrated that the group of breast cancer patients was more radiosensitive than a population of healthy women and this with both the G2 and the G0 MN assay. Analyses of the G2 and MN response in different age groups of the breast cancer patients revealed no significant differences in mean G2 and MN scores and suggest that the age of onset of the disease has no effect on chromosomal radiosensitivity in unselected breast cancer patients. Correlations with different clinical parameters were also investigated.

Adenocarcinoma↗

PubMed2005

Thalidomide radiosensitizes tumors through early changes in the tumor microenvironment.

PURPOSE: The aim of this work was to study changes in the tumor microenvironment early after an antiangiogenic treatment using thalidomide (a promising angiogenesis inhibitor in a variety of cancers), with special focus on a possible "normalization" of the tumor vasculature that could be exploited to improve radiotherapy. EXPERIMENTAL DESIGN: Tumor oxygenation, perfusion, permeability, interstitial fluid pressure (IFP), and radiation sensitivity were studied in an FSAII tumor model. Mice were treated by daily i.p. injection of thalidomide at a dose of 200 mg/kg. Measurements of the partial pressure of oxygen (pO(2)) were carried out using electron paramagnetic resonance oximetry. Three complementary techniques were used to assess the blood flow inside the tumor: dynamic contrast-enhanced magnetic resonance imaging, Patent Blue staining, and laser Doppler imaging. IFP was measured by a "wick-in-needle" technique. RESULTS: Our results show that thalidomide induces tumor reoxygenation within 2 days. This reoxygenation is correlated with a reduction in IFP and an increase in perfusion. These changes can be attributed to extensive vascular remodeling that we observed using CD31 labeling. CONCLUSIONS: In summary, the microenvironmental changes induced by thalidomide were sufficient to radiosensitize tumors. The fact that thalidomide radiosensitization was not observed in vitro, and that in vivo radiosensitization occurred in a narrow time window, lead us to believe that initial vascular normalization by thalidomide accounts for tumor radiosensitization.

Angiogenesis Inhibitors↗

PubMed2005

Radiation-induced DNA-damage and gene expression profiles in human lung cancer cells with different radiosensitivity.

BACKGROUND: Measurements of DNA double strand breaks and their subsequent repair after in vitro irradiation has been suggested to be an alternative way of monitoring radiotherapeutic response. METHODS: In the present study, the DNA repair kinetics (using a neutral version of the Comet assay) up to 45 min after a single dose of 2 Gy was studied as well as the gene expression profiles, before and 45 min after the irradiation, in two human lung cancer cell lines with different radiosensitivity (U-1285 and U-1810). RESULTS: Immediately after the irradiation, both cell lines responded with increased levels of DNA damage. However, the induced damage was slightly higher in U-1810 (known to be radioresistant) than in U-1285 (known to be radiosensitive), and the latter cell line also seemed to have a slightly more efficient DNA-repair. The two different lung cancer cell lines were highly heterogeneous in gene expression, both before and after the irradiation, and there was no obvious relationship between the Comet data and the microarray data. CONCLUSION: Given the fact that U-1810 has been classified as radioresistant and U-1285 as radiosensitive in clonogenic assays, the results of the present study indicate that radiation-induced DNA double strand breaks and DNA-repair efficiency are poor indicators of the intrinsic radiosensitivity of human lung cancer cells irradiated with a single dose in vitro.

Biomarkers, Tumor↗

PubMedDate not supplied

Thalidomide radiosensitization of normal murine hematopoietic but not squamous cell carcinoma or multiple myeloma tumor cell lines.

BACKGROUND: Thalidomide (TL), due to its antiangiogenic effects, has been postulated to be a potential radiosensitizer of multiple myeloma and squamous tumors in vivo. MATERIALS AND METHODS: To determine whether TL was a radiosensitizer, 32D cl 3 cells (hematopoietic progenitor) as well as SCC-VII (squamous cell carcinoma), OPM1 or OPM2 (multiple myeloma) tumor cells were irradiated to doses ranging from 0 to 8 Gy and then plated in 0, 50 or 150 microM TL in each of three protocols: i) 1 hour before irradiation; ii) 1 hour before irradiation and also in medium following irradiation; or iii) placed in TL containing medium following irradiation. RESULTS: Using 150 microM TL (which did not stimulate cell growth) the 32D cl 3 cells had increased radiation sensitivity compared to the control irradiated cells. In contrast, the SCC-VII, OPMI or OPM2 cells showed no detectable radiosensitization when incubated in TL before, during or after irradiation compared to the control irradiated cells. CONCLUSION: These results demonstrated that TL may be a selective radiosensitizer.

Animals↗

PubMedDate not supplied

GL331, a topoisomerase II inhibitor, induces radiosensitization of human glioma cells.

BACKGROUND: GL331 is a topoisomerase II inhibitor and its effects on cultured human T98G glioma cells were investigated in this study. The effects of combined GL331 and radiation treatment on human T98G glioma cells were also examined. MATERIALS AND METHODS: The glioma cells were treated with GL331 and the clonogenic assay was used to study its cytotoxicity effects. A combination treatment, using either concomitant irradiation at the beginning or end of the GL331 treatment (designated as the RT-GL331 and GL331-RT protocols, respectively), was used to investigate the radiosensitization effects of GL331. The levels of radiosensitization of various protocols were evaluated by the dose-enhancement ratio and Isobologram analysis. The cell cycle distribution of the glioma cells treated with various protocols was explored using flow-activated cell sorter (FACS) analysis. RESULTS: The clonogenic assay demonstrated that GL331 exerts cytotoxic effects on the glioma cells in a concentration- and time-dependent manner (p < 0.001). The combination treatments, RT-GL331 and GL331-RT, increased the dose-enhancement ratio, with a higher ratio for the RT-GL331 protocol. Isobologram analysis revealed sub-additive glioma cell cytotoxicity for the GL331-RT protocol; in contrast, mainly supra-additive effects were demonstrated for the RT-GL331 protocol. FACS analysis revealed that GL331 and radiation caused the glioma cells to accumulate in the G2/M-phase of the cell cycle and combination of these two treatments as the RT-GL331 protocol further increased the G2/M fraction of the glioma cells. CONCLUSION: The induction of GL331 radiosensitization was sequence-dependent, with stronger cytotoxic effects on the gliomas noted where radiation was delivered concomitantly with the beginning of GL331 treatment. Such radiosensitization effects might be, at least partly, related to the increased cell accumulation in the G2/M-phase.

Cell Death↗

PubMed2005

Correlation of HER1/EGFR expression and degree of radiosensitizing effect of the HER1/EGFR-tyrosine kinase inhibitor erlotinib.

Epidermal growth factor receptor (HER1/EGFR)-mediated signal transduction pathways are important in cellular response to ionizing radiation. High HER1/EGFR expression on cancer cells may contribute to radioresistance. In this pre-clinical study, we evaluated the radiosensitizing effect of erlotinib, a small molecule HER1/EGFR inhibitor in three human cancer cell lines with different HER1/EGFR expression--A431 (very high expression), H157 (moderate expression) and H460 (low expression). Our results demonstrated that A431 was the most radioresistant, while H460 was the most radiosensitive. However, A431 cells were the most sensitive to erlotinib (IC50 = 300 nM) and H460 cells the most resistant (IC50 = 8 microM). H157 had intermediate sensitivity to radiation and erlotinib (IC50 = 3 microM). With 300 nM erlotinib, the radiation dose enhancement ratios (DER) were 1.40, 1.17 and 1.04 in A431, H157 and H460, respectively. Treatment with erlotinib for 24 hr at 300 nM increased G1 arrest by 18.6, 2.0 and 4.8% in A431, H157 and H460, respectively. Erlotinib-induced apoptosis was augmented by radiation in A431 cells only. In conclusion, high HER1/EGFR expression may result in a high degree of radiosensitization with erlotinib combined with radiation. The extent of erlotinib-induced radiosensitization was proportional to HER1/EGFR expression, as well as autophosphorylation of the human epidermal growth factor receptor (HER1/EGFR).

Apoptosis↗

PubMed2006

[Correlation of growth hormone receptor expression to preoperative radiosensitivity of rectal cancer patients].

BACKGROUND & OBJECTIVE: Growth hormone (GH) could activate pathways involved in DNA repair process by binding to growth hormone receptor (GHR), which is thought as one of the mechanisms of radioprotection. This study was to evaluate the correlation of GHR expression to radiosensitivity of rectal cancer. METHODS: The expression of GHR in biopsy specimens from 98 rectal cancer patients before preoperative irradiation and postoperative specimens was detected by immunohistochemistry (IHC) and reverse transcription-polymerase chain reaction (RT-PCR). Radiosensitivity was evaluated according to Rectal Cancer Regression Grading. RESULTS: IHC revealed that GHR overexpression was positively correlated to poor response to radiotherapy (P<0.001, rs=0.399); RT-PCR also showed that radiosensitivity was significantly higher in GHR mRNA-negative group than in GHR mRNA-positive group (P<0.001, rs=0.398). Compared with the biopsy specimens before preoperative irradiation, the paired postoperative specimens showed significantly increased GHR expression in residual cancer cells (P<0.001). CONCLUSION: Detection of GHR expression before preoperative irradiation may predict radiosensitivity of rectal cancer.

Adult↗

PubMed2006

[Correlations of biomolecular markers, such as P53 protein and vascular endothelial growth factor, to radiosensitivity of nasopharyngeal carcinoma].

BACKGROUND & OBJECTIVE: About 20%-40% nasopharyngeal carcinoma (NPC) patients, who are in the same staging group, receiving the same treatment modality and radiotherapy dose, relapse in the irradiated fields within 5 years. This is mainly due to the differences in internal radiosensitivity. This study was to analyze the proliferation, apoptosis, angiogenesis, and lymphogenesis of tumor cells, and to explore the correlation of these factors to radiosensitivity. METHODS: P53 protein, vascular endothelial growth factor (VEGF) protein, survivin protein, VEGF-C protein, Ki67 protein, and microvascular density (MVD) of 60 biopsy samples from radiosensitive group and 60 from radio-resistant group were detected by immunohistochemistry, respectively. Their correlations to clinical characteristics were analyzed. RESULTS: The positive rates of P53, VEGF, survivin, VEGF-C, Ki67 were 65.0%, 57.5%, 60.8%, 42.5%, 57.5%, respectively. The positive rates of P53 and VEGF, and MVD in the radio-sensitive group and in the radio-resistant group were (25.97+/-21.26)%, (18.50+/-19.86)%, 32.65+/-19.61 and (37.85+/-28.67)%, (30.83+/-23.94)%, 41.95+/-16.97, respectively (P<0.05). The positive rates of Survivin, VEGF-C, and Ki67 between the two groups had no statistic difference (P>0.05). The correlations between P53, VEGF, and MVD were obvious. CONCLUSION: P53 protein, VEGF protein and MVD might be biomolecular markers for evaluating the internal radiosensitivity of NPC patients.

Adult↗

PubMed2003

A new paradigm for the treatment of high-risk prostate cancer: radiosensitization with docetaxel.

Survival and biochemical outcome of patients with localized, high-risk prostate cancer treated with definitive three-dimensional conformal radiation therapy (3-D CRT) with or without hormonal therapy are poor. Other therapeutic strategies are needed to improve outcome in these poor-prognostic-group patients. One such strategy involves the use of chemotherapeutic agents to radiosensitize the effects of local 3-D CRT. Very few investigators have tested this novel concept of chemotherapeutic radiosensitization. Two studies evaluated the combination of estramustine phosphate and vinblastine (EV) with radiation therapy (RT). In both studies, the combination of EV and RT resulted in moderate to severe acute and late toxicity. A recently completed, phase I trial evaluated the maximally tolerated dose (MTD) of weekly docetaxel that could be concurrently delivered with 3-D CRT (70.2 Gy) in men with high-risk prostate cancer. The MTD of concurrent weekly docetaxel with 3-D CRT was determined to be 20 mg/m(2), and this combination was shown to be safe and well tolerated. This was the first trial to evaluate taxane radiosensitization in prostate cancer. Other phase I/II studies are needed to further assess chemotherapeutic radiosensitization in localized, high-risk prostate cancer.

Journal Article↗

PubMed2005

Normal tissue radiosensitivity: prediction on deterministic or stochastic basis?

For the same standardized physical radiation dose there is considerable variation, among different patients, of the magnitude of early and late normal tissue reactions. Technical and clinical factors account for about one third only of these variations. Genetic or epigenetic differences between patients account for the greater proportion of interpatient radiosensitivity differences. Attempts have been made to correlate differences in the tissue radiosensitivity with the in vitro radiosensitivity of fibroblasts or lymphocytes as well as with other biological cellular processes related to cell death (mainly DNA repair and chromosomal aberrations). Apart from some genetic diseases such as ataxia telangiectasia, there were positive results in some studies that could not be reproduced in others. It is now realized that for normal tissue radiation-induced morbidity (a) cell kill is not the only factor, (b) interaction with a large number of gene products, such as IL-2, IL-6, TGF-beta, is involved, and (c) radiosensitivity differences can reflect genetic differences. Polymorphism in a wide range of genes can now be demonstrated and analyzed as a source of variations in the radiation response. cDNA microarray procedures can also allow simultaneous measurement, in the same sample, of thousands of genes and thus avoiding basing the investigation on a restricted number of genes. Preliminary results could show retrospectively a correlation between late normal tissue reactions and expression of certain genes. Using cDNA microarray before radiotherapy to predict the occurrence of serious late reactions is still under consideration. Theoretically, an efficient predictor procedure may serve in (a) detection of hypersensitive patients before submitting them to highly toxic radiotherapy regimes such as whole body irradiation, (b) detection of hypersensitive patients in clinical situations where radiotherapy can be effectively replaced by other modalities, and (c) selection of patients for elaborate radiotherapy techniques involving dose escalation to high levels.

Dose Fractionation, Radiation↗

PubMed2006

Enhancing radiosensitivity of Hela cells by combining transfection of bcl-2 c-myc ASODNs.

Previous studies have detected bcl2 and c-myc upregulated in Hela cells. In this study, we investigated the effect on apoptosis of Hela cells by combining transfection of bcl2 and c-myc antisense oligonucleotides(ASODNs), and to explore the relationship between combining gene transfection and radiosensitivity of Hela cells, furthermore, to seek a new method to enhance the radiosensitivity of tumor cells. ASODNs of bcl2 and c-myc coated with cationic liposomes were designed and synthesized and transfected to Hela cells. The expressions of BCL2 and C-MYC were assessed by immunohistochemistry (IHC) staining and flow cytometry (FCM), and the induced-apoptosis phenomenon of Hela cells transfected with bcl2 ASODN or c-myc ASODN was observed by Giemsa Staining, DNA Ladder and FCM. Irradiation was performed on ASODNs transfected cells, then the radiosensitivity, biological reaction and cell proliferation of the transfected cells were investigated by cellular clone formation analysis, MTT assay and FCM. Both bcl2 and c-myc ASODNs could partially inhibit the growth of Hela cells by reducing the expression of bcl2 and c-myc (p < 0.05). The apoptosis rate of Hela cells treated with bcl2 ASODN was 6.60 +/- 0.70%, c-myc ASODN 10.29 +/- 0.66%, bcl2 + c-myc ASODNs 11.83 +/- 0.57 %, which were much higher than that of control 1.79 +/- 0.19%(p < 0.05). The sensitivity enhancement ratio(SER) of Hela cells transfected with bcl2 ASODN,c-myc ASODN and bcl2 + c-myc ASODNs was 1.20, 1.53 and 2.18 respectively. Combining transfection of bcl2 and c-myc ASODN could more effectively induce apoptosis of Hela cells, which subsequently enhanced radiosensitivity of Hela cells. Furthermore, combining transfection ASODNs of apoptosis-inhibiting genes or oncogenes followed radiotherapy to malignant tumor cells might be a new potential strategy.

Analysis of Variance↗