SEARCH · PubMed Health

Results for “ONCOLYSIS”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 19 recordsLinked to original sources

PubMedDate not supplied

Differential susceptibility of pediatric sarcoma cells to oncolysis by conditionally replication-competent herpes simplex viruses.

PURPOSE: Attenuated viruses derived from herpes simplex virus (HSV) type 1 that kill tumor cells (oncolysis) are currently in clinical trials for selected cancers, primarily carcinomas and gliomas. The authors sought to determine if pediatric sarcoma cells are also sensitive to HSV-mediated oncolysis. MATERIALS AND METHODS: The authors tested a panel of ten cell lines derived from rhabdomyosarcoma, osteosarcoma, Ewing sarcoma, and a secondary malignant fibrous histiocytoma for survival after exposure to attenuated HSV vectors. The viruses used included NV1020, haploid for the neurovirulence gene, and G207, deleted for both and ribonucleotide reductase but expressing the beta-galactosidase reporter gene. G207 transduction was determined by measuring beta-galactosidase expression. RESULTS: Sarcoma cells differed in their sensitivity to viral oncolysis but were relatively consistent by histologic type. Rhabdomyosarcoma and malignant fibrous histiocytoma cells were most sensitive while osteosarcoma cells were intermediately sensitive to oncolysis by both HSV recombinants. Although Ewing sarcoma cells showed efficient viral entry and gene transfer, these cells were the least susceptible to oncolysis by HSV. CONCLUSIONS: Conditionally replication-competent HSV-derived vectors may be useful for the treatment of rhabdomyosarcoma and osteosarcoma, but may not be as efficacious for treating Ewing sarcoma until the mechanism of resistance is defined and circumvented.

Cell Survival↗

PubMed2002

Ewing sarcoma family of tumors express adenovirus receptors and are susceptible to adenovirus-mediated oncolysis.

PURPOSE: Attenuated viruses derived from adenoviruses (Ad) that kill tumor cells (oncolysis) are currently in clinical trials for selected cancers. Some cancers have proven resistant to Ad infection due to low expression of viral receptors. The authors sought to determine whether members of the Ewing sarcoma family of tumors (ESFTs) express Ad receptors and are sensitive to Ad-mediated oncolysis. METHODS: Using flow cytometry, the authors tested a panel of cell lines derived from ESFTs for expression of both the Ad receptor, coxsackie-adenovirus receptor (CAR), and the cellular mediator of Ad uptake, alpha(v)-integrins, as well as for Ad-mediated gene transduction. Cell survival assays were used to assess the sensitivity to Ad-mediated oncolysis. Immunohistochemistry was used to assess CAR expression in primary tumors. mRNA levels of CAR in cell lines and tumor samples were also queried from a cDNA expression database. RESULTS: The ESFT cell lines expressed CAR and alpha(v)-integrins, showed high levels of gene transduction, and were highly sensitive to viral oncolysis. Primary tumor samples were positive for CAR expression by immunohistochemistry. Microarray analysis confirmed CAR expression in ESFT cell lines and tumors. CONCLUSIONS: Ewing sarcoma cells express the Ad receptors and are sensitive to Ad oncolysis. Treatment of Ewing sarcoma using conditionally replicative adenoviruses should be explored.

Adenoviridae↗

PubMed2001

Fiber knob modifications overcome low, heterogeneous expression of the coxsackievirus-adenovirus receptor that limits adenovirus gene transfer and oncolysis for human rhabdomyosarcoma cells.

Exploiting the lytic life cycle of viruses has gained recent attention as an anticancer strategy (oncolysis). To explore the utility of adenovirus (Ad)-mediated oncolysis for rhabdomyosarcoma (RMS), we tested RMS cell lines for Ad gene transduction and infection. RMS cells were variably transduced by Ad. Compared with control cells, RMS cells were less sensitive or even resistant to oncolysis by wild-type virus. RMS cells expressed the Ad internalization receptors, alpha(v) integrins, but had low or undetectable expression of the major attachment receptor, coxsackievirus-Ad receptor (CAR). Mutant Ads with ablated CAR binding exhibited only 5-20% of transgene expression in RMS cells seen with a wild-type vector, suggesting that residual or heterogeneous CAR expression mediated the little transduction that was detectable. Immunohistochemical analysis of archived clinical specimens showed little detectable CAR expression in five embryonal and eight alveolar RMS tumors. Stable transduction of the cDNA for CAR enabled both efficient Ad gene transfer and oncolysis for otherwise resistant RMS cells, suggesting that poor CAR expression is the limiting feature. Gene transfer to RMS cells was increased >2 logs using Ads engineered with modified fiber knobs containing either an integrin-binding RGD peptide or a polylysine peptide in the exposed HI loop. The RGD modification enabled increased oncolysis for RMS cells by a conditionally replicative Ad, Ad delta24RGD, harboring a retinoblastoma-binding mutation in the E1A gene. Thus, the development of replication-competent vectors targeted to cell surface receptors other than CAR is critical to advance the use of Ad for treating RMS.

Adenoviridae↗

PubMed2004

Interferon resistance promotes oncolysis by influenza virus NS1-deletion mutants.

NS1 protein of influenza virus is a virulence factor that counteracts Type I interferon (IFN)-mediated antiviral response by the host. A recombinant influenza A virus that lacks the NS1 protein only replicates efficiently in systems that contain defective IFN pathways. We demonstrate that the conditional replication properties of NS1-modified influenza A virus mutants can be exploited for the virus-mediated oncolysis of IFN-resistant tumor cells. IFN resistance in analyzed tumor cell lines correlated with a reduced expression of STAT1. Addition of exogenous IFNalpha or supernatant of virus-infected endothelial cells inhibited viral oncolysis in IFN-sensitive but not in IFN-resistant cell lines. The oncolytic potential of NS1-modified influenza A virus mutants could be exploited in vivo in a SCID mouse model of a subcutaneously-implanted human IFN-resistant melanoma. The data indicate that IFN-resistant tumors are a suitable target for oncolysis induced by NS1-modified influenza virus mutants. STAT1 might serve as a marker to identify these IFN-resistant tumors.

Animals↗

PubMed1997

The effect of ganciclovir on herpes simplex virus-mediated oncolysis.

Entry of herpes simplex virus (HSV) into tumor cells results in viral gene expression followed by cellular lysis. Attenuated HSVs selectively destroy tumors with sparing of surrounding normal tissue. HSV encodes a thymidine kinase (TK) that converts ganciclovir to a toxic metabolite. This metabolite may be transferred between cells and lead to the death of neighboring uninfected cells, termed bystanders. We sought to determine if HSV-mediated oncolysis is enhanced by ganciclovir treatment. In addition, we examined bystander killing in cocultures of TK transfectants and parental cells. hrR3, an attenuated HSV, expresses TK. The 50% lethal dose of hrR3 for a rat gliosarcoma (9L) and three human colorectal carcinomas (HT29, KM12C6, and KM12L4) was determined. Cells were infected with a 50% lethal dose of hrR3, followed by treatment with ganciclovir, and then cell survival was quantitated. In separate experiments 9L and HT29 cells were transfected with TK. Parental cells and TK transfectants were cocultured in various ratios, in the presence of ganciclovir, and cell survival was quantitated. hrR3-mediated oncolysis was enhanced by ganciclovir in the gliosarcoma but not in the three colorectal carcinomas. Cocultures of both 9L and HT29 parental cells with their corresponding TK transfectants demonstrated bystander killing. The mortality of 9L cocultures was 54% greater than that predicted for exclusive killing of transfectants. HT29 mortality was 8% greater than predicted. The ability of ganciclovir to augment hrR3-mediated oncolysis varies significantly between tumor cells lines. The extent of ganciclovir-mediated killing of neighboring nontransduced parental cells similarly varies. Consideration should be given to these factors in the design of gene therapy strategies using HSV vectors as oncolytic agents.

Animals↗

PubMed2006

Paclitaxel and vincristine potentiate adenoviral oncolysis that is associated with cell cycle and apoptosis modulation, whereas they differentially affect the viral life cycle in non-small-cell lung cancer cells.

Chemotherapy, including microtubule (MT)-interacting agents, can enhance the tumor-eradicating activity of replication-competent adenoviruses. The purpose of this study was to obtain more insight into the mechanism underlying this enhancement that may be exploited for the development of improved therapy. Two MT-interacting agents with opposite activity, paclitaxel (PTX) that stabilizes and vincristine (VCR) that destabilizes MTs, were found to synergistically enhance adenoviral oncolysis in non-small-cell lung cancer (NSCLC) cells. To explore the possibility that these drugs affect the viral life cycle by modulating adenoviral gene expression, we used a quantitative reverse transcription-polymerase chain reaction assay and found that PTX, but not VCR, increased the expression of E1A13S, ADP and Penton genes, which correlated with an increase in viral particle assembly and release. Next, the effect of combined treatment on cell-cycle progression was studied. Both drugs suppressed adenovirus-induced S-phase arrest and instead caused G2/M arrest, which was accompanied by an increase in apoptotic cells. Taken together, the enhancement of oncolysis by MT-interacting drugs appears not to require specific MT transport or scaffold functions. Our findings suggest that MT-interacting drug-induced cellular signals that modulate cell-cycle arrest and apoptosis are primarily on the basis of their oncolysis-enhancing activity.

Adenoviridae↗

PubMed2003

Virotherapeutics: conditionally replicative adenoviruses for viral oncolysis.

Viral oncolysis, or virotherapy, is an endeavor to use viruses as therapeutic agents in an effort to exploit their highly evolved qualities of host cell killing and simultaneous multiplication and spread. This review describes the concept of oncolytic adenoviruses, also called conditionally replicative adenoviruses (CRAds), and recent developments--inspired by early clinical results--that aim at the optimization of CRAd efficacy. Molecular strategies applied for the development of oncolytic adenoviruses include (i) the genetic manipulation of the expression and/or function of key regulatory viral proteins in order to restrict viral replication and spread to tumor cells, (ii) the engineering of the adenoviral capsid for efficient and tumor-targeted infection, and (iii) the incorporation of heterologous genes to facilitate combination therapies or tracking of the virus. Initial clinical trials have provided proof-of-concept for adenoviral oncolysis in patients and a favorable safety profile for oncolytic adenoviruses has been demonstrated. In conclusion, adenoviral oncolysis, with its distinct therapeutic mechanism, shows remarkable therapeutic potential. Advanced generations of virotherapeutics are currently in development.

Adenoviridae↗

PubMed2000

Oncolysis of diffuse hepatocellular carcinoma by intravascular administration of a replication-competent, genetically engineered herpesvirus.

Herpes simplex virus type 1 (HSV-1) replication within tumors can mediate tumor regression (oncolysis). The genetically engineered, HSV-1 mutant rRp450 does not express viral ribonucleotide reductase and is therefore replication conditional. During the course of infection, rRp450 expresses the cytochrome P450 transgene and HSV-1 thymidine kinase gene, thereby enabling it to bioactivate the prodrugs cyclophosphamide and ganciclovir, respectively. rRp450 replication in hepatocellular carcinoma (HCC) cells is cytotoxic and liberates progeny virion that infect adjacent tumor cells. rRp450-mediated oncolysis is enhanced in the presence of cyclophosphamide, whereas it is inhibited in the presence of ganciclovir. As a consequence of defective viral ribonucleotide reductase expression, the yield of rRp450 progeny virions from infection of HCC cells is 3 to 4 log orders greater than that from infection of normal hepatocytes. This is associated with dramatic tumor reduction of diffuse HCC after a single intravascular administration of rRp450. rRp450 holds the promise of the dual therapeutic benefit of selective oncolysis and P450 transgene delivery.

Animals↗

PubMed2006

Exploiting hypoxia in solid tumors to achieve oncolysis.

Chemo- and radio-resistant cancer cells within solid tumors undermine the effectiveness of these approaches to achieving oncolysis. These resistant cells and clusters of cells typically thrive at low oxygen tensions and are reliant on anaerobic metabolic pathways that churn out lactate. This hypoxic state is one that can be exploited and in this paper a novel method is advanced involving tumor cell infiltration by bifidobacterium species which should bring about prodigious lactate synthesis; concomitant blocking of its enzymatic degradation by urea as well as export (from the cell) by use of quercetin; depletion of ATP using exogenous thyroid; and compromised oxidative catabolism of free fatty acids and amino acids via oral intake of l-hydroxycitrate, melatonin and nontoxic NDGA. This "anaerobic pathway cocktail", it is hypothesized, will bring about a profound reduction in intracellular pH and a compromised state of cellular energetics sufficient to effect oncolysis.

Adenosine Triphosphate↗

PubMed2006

Oncolysis of pancreatic tumour cells by a gamma34.5-deleted HSV-1 does not rely upon Ras-activation, but on the PI 3-kinase pathway.

The ability of viruses to selectively target, replicate within, and destroy tumour cells without deleterious effects in normal cells (oncolysis), makes the use of viruses as an attractive tool for cancer treatment. Pancreatic adenocarcinoma, being insensitive to traditional therapy and having a rather poor prognosis, represents a suitable target to evaluate viral oncolysis as a novel therapeutic approach. Herpes simplex virus (HSV) has been reported to produce an oncolytic effect in cells overexpressing Ras. As Ras signalling is frequently aberrant in pancreatic cancer, we compared four pancreatic cell lines (which differ in the presence of mutated or wild-type ras) for their ability to support growth of gamma34.5-replication attenuated HSV-1 (R3616). Our data show that permissiveness to viral replication is neither associated with enhanced Ras signalling nor with defective PKR activity. By contrast, we provide evidence that disregulation of the PI 3-kinase signalling pathway allows conditionally replication-defective R3616 virus to overcome the cellular antiviral activity.

Adenocarcinoma↗

PubMed2007

Acquired resistance to reoviral oncolysis in Ras-transformed fibrosarcoma cells.

Reovirus shows considerable potential as an oncolytic agent for Ras-activated tumors and is currently in clinical trials. Here we ask whether such tumor cell lines can acquire resistance to reoviral oncolysis. We challenged human HT1080 fibrosarcoma cells that carry a Ras mutation by prolonged exposure to reovirus, thereby yielding highly virus-resistant HTR1 cells. These cells are persistently infected with reovirus, exhibit high Ras activity and retain the original Ras gene mutation, showing that resistance to reovirus can be displayed in cells with active Ras. The HTR1 cells also exhibit reduced cellular cathepsin B activity, which normally contributes to viral entry and activation. Persistently infected HTR1 cells were not tumorigenic in vivo, whereas immunologically cured virus-free HTR1 cells were highly tumorigenic. Thus, acquisition of resistance to reovirus may constrain therapeutic strategies. To determine whether reoviral resistance is associated with a general reduction in apoptotic potential, we challenged the HTR1 cells with apoptotic inducers and E1B-defective adenovirus, resulting in significant apoptosis and cell death following both approaches. Therefore, even if resistance to reoviral oncolysis should arise in tumor cells in vivo, other therapeutic strategies may nevertheless remain effective.

Base Sequence↗

PubMed2004

Reovirus oncolysis: the Ras/RalGEF/p38 pathway dictates host cell permissiveness to reovirus infection.

Reovirus is a benign human virus that was recently found to have oncolytic properties and is currently in clinical trials as a potential cancer therapy. We have previously demonstrated that activation of Ras signaling, a common event in cancer, renders cells susceptible to reovirus oncolysis. In this study, we investigate which elements downstream of Ras are important in reovirus infection. By using a panel of NIH 3T3 cells transformed with activated Ras mutated in the effector-binding domain, we found that only the RasV12G37 mutant, which was unable to signal to Raf or phosphatidylinositol 3-kinase but retained signaling capability to guanine nucleotide-exchange factors (GEFs) for the small G protein, Ral (known as RalGEFs), was permissive to reovirus. Expression of the activated mutant of the RalGEF, Rlf, also allowed reovirus replication. Specific inhibition of the Ral pathway by using dominant-negative RalA rendered normally permissive H-Ras cells (cells expressing activated Ras) resistant to reovirus. To further identify elements downstream of RalGEF that promote reovirus infection, we used chemical inhibitors of the downstream signaling elements p38 and JNK. We found that reovirus infection was blocked in the presence of the p38 inhibitor but not the JNK inhibitor. Together, these results implicate a Ras/RalGEF/p38 pathway in the regulation of reovirus replication and oncolysis.

3T3 Cells↗

PubMed1996

Treatment of a human breast cancer xenograft with an adenovirus vector containing an interferon gene results in rapid regression due to viral oncolysis and gene therapy.

Treatment of a human breast cancer cell line (MDA-MB-435) in nude mice with a recombinant adenovirus containing the human interferon (IFN) consensus gene, IFN-con1 (ad5/IFN), resulted in tumor regression in 100% of the animals. Tumor regression occurred when virus was injected either within 24 hr of tumor cell implantation or with established tumors. However, regression of the tumor was also observed in controls in which either the wild-type virus or a recombinant virus containing the luciferase gene was used, although tumor growth was not completely suppressed. Tumor regression was accompanied by a decrease in p53 expression. Two other tumors, the human myelogenous leukemic cell line K562 and the hamster melanoma tumor RPMI 1846, also responded to treatment but only with ad5/IFN. In the case of K562 tumors, there was complete regression of the tumor, and tumors derived from RPMI 1846 showed partial regression. We propose that the complete regression of the breast cancer with the recombinant virus ad5/IFN was the result of two events: viral oncolysis in which tumor cells are being selectively lysed by the replication-competent virus and the enhanced effect of expression of the IFN-con1 gene. K562 and RPMI 1846 tumors regressed only as a result of IFN gene therapy. This was confirmed by in vitro analysis. Our results indicate that a combination of viral oncolysis with a virus of low pathogenicity, itself resistant to the effects of IFN and IFN gene therapy, might be a fruitful approach to the treatment of a variety of different tumors, in particular breast cancers.

Adenoviruses, Human↗

PubMed2002

Toward a new generation of conditionally replicating adenoviruses: pairing tumor selectivity with maximal oncolysis.

Conditionally replicating adenoviruses (CRADs) represent a promising new platform for the treatment of cancer. CRADs have been demonstrated to kill tumor cells when other therapies fail, indicating that their antitumor properties are complementary to, and distinct from, those of standard treatments such as chemotherapy and radiation. In clinic trials CRADs have shown encouraging results, demonstrating mild side effects when administered at high doses and via different routes, including intratumorally, intraperitoneally, and intravenously. Tumor-selective replication has been detected, although as a single agent the efficacy appears to be limited. Interestingly, combined treatment with radiation or chemotherapy has been found to enhance CRAD efficacy considerably. To date, the molecular mechanisms underlying adenovirus-mediated oncolysis, and the way in which chemotherapy enhances oncolysis, are not well understood. A fuller knowledge of these processes will open up new strategies to improve the cell-killing potential of CRADs. Here, we discuss several possibilities that may lead to CRADs with enhanced oncolytic activity. These approaches include strategies to functionally couple tumor targeting and optimal oncolytic activity, and ways to further increase tumor cell disruption at later stages of infection to facilitate the spreading of virus throughout the tumor mass. In addition, improved methods to evaluate the efficacy of these agents in animal models, and in the clinic, will be required to systematically test and optimize CRAD efficacy, also taking into account the influence of tumor characteristics and the administration route.

Adenoviruses, Human↗

PubMed1987

Viral oncolysis in the A2G mouse revisited: monoclonal antibody-mediated tumor rejection.

A2G mice can be immunized against the Ehrlich ascites tumor (EAT) by influenza virus oncolysis or with influenza virus oncolysates. To facilitate studies of the cellular antigens immunopotentiated by viral oncolysis, monoclonal antibodies (mAbs) against EAT cells were produced from postoncolytic EAT-immune A2G mice. Reciprocal competitive binding on EAT cells was used to classify the mAbs into epitope-related groups. One mAb, 198.9, could fully protect A2G mice against EAT cell challenge, could rescue A2G mice from an established EAT, and could mediate lysis of EAT cells in vivo. mAb 198.9 provides a new tool for studying the biochemical characteristics and immunological properties of a cellular antigen centrally involved in this model.

Animals↗

PubMed2005

Conditionally replicative adenovirus expressing degradation-resistant p53 for enhanced oncolysis of human cancer cells overexpressing murine double minute 2.

Conditionally replicative adenoviruses (CRAd) are under investigation as anticancer agents. Previously, we found that the CRAd AdDelta24-p53, expressing the p53 tumor suppressor protein from its genome, more effectively killed most human cancer cells than did its parent AdDelta24. However, a minority of cancer cell lines poorly responded to the oncolysis-enhancing effect of p53. Here we show that refractory cell lines expressed high levels of the major negative p53 regulator murine double minute 2 (MDM2). To obviate MDM2-mediated inactivation of CRAd-encoded p53, we constructed the new CRAd AdDelta24-p53(14/19) encoding a p53 variant incapable of binding to MDM2. AdDelta24-p53(14/19) was approximately 10 times more effective than AdDelta24-p53 in killing cancer cell lines with high levels of human MDM2, but not cells with low MDM2. This finding supports the notion that exogenous expression of functional p53 augments the anticancer efficacy of CRAds. In addition, it confirms that high MDM2 expression is a molecular determinant of resistance against oncolysis enhancement by exogenous wild-type p53. Moreover, it shows that efficacy enhancement by restoration of functional p53 can also be accomplished in cancer cells expressing a p53 inhibitor. This further expands the utility of CRAds expressing functional p53 variants for effective virotherapy of cancer and thus their possible contribution to the advancement of individualized molecular medicine.

Adenoviridae↗

PubMed1998

Marker gene transfer and oncolysis of human Y79 retinoblastoma cells mediated by herpes simplex virus mutants.

Three different herpes simplex virus (HSV) mutants, designated hrR3, MGH-1 and R3616, were used to infect Y79 retinoblastoma cells grown in suspension. Two parameters were assayed: (a) vector-mediated gene expression, measured by histochemical staining of a transferred LacZ transgene, and (b) virus-mediated oncolysis, determined by the inability of infected cells to exclude trypan blue dye. The tested HSV mutants were found to infect cells grown in suspension at a relatively low multiplicity of infection (MOI = 0.01) and were capable of transferring the LacZ gene as early as 2 days after infection. Furthermore, differences in oncolytic activity were observed amongst the tested viruses: MGH-1 and R3616 exhibited 50% cell kill at a MOI of 0.1 over a period of 6 days, whereas hrR3-mediated oncolysis appeared less efficient. These studies provide a rationale for further exploitation of oncolytic herpes viruses as a potential treatment of intraocular tumors.

Cell Death↗

PubMed2005

Virus-mediated oncolysis of thyroid cancer by a replication-selective adenovirus driven by a thyroglobulin promoter-enhancer region.

CONTEXT: Currently, there is no effective treatment for iodine-resistant thyroid cancers. OBJECTIVE: As a new approach to treatment, the efficacy of replication-selective, human thyroglobulin (TG) enhancer and promoter-driven, adenovirus (AdhTGEP)-mediated oncolysis was investigated using two well-differentiated thyroid cancer cell lines, XTC (TG positive) and FTC-133 (TG negative), and other control tumor and nontumor cell lines (all TG negative). DESIGN: A cohort study design was used. SETTING: The study setting was laboratory bench-top experiments. SUBJECTS/PARTICIPANTS: In vitro TG-expressing and nonexpressing thyroid cell culture lines, nonthyroid tumor cell lines, as well as preclinical thyroid tumor-bearing mice were studied. INTERVENTION: Adenoviral infection of cell lines was determined by immunohistochemistry, selective replication by one-step growth assays, and cytotoxicity by 3-(4,5-dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2-(4-sulphophenyl)-2H-tetrozolium (MTS) assay. In vivo tumor growth inhibition was determined by a single intratumoral injection of 1 x 10(9) plaque-forming units AdhTGEP, AdLacZ (control virus), or PBS to 50- to 75-mm(3) tumors. XTC cells showed intense immunohistochemical staining, whereas FTC-133 and all other control cell lines showed minimal staining for viral infection with AdhTGEP. MAIN OUTCOME MEASURES: Cell survival and tumor growth inhibition after adenoviral infection were the main outcome measures. RESULTS: One-step growth assays showed at least a more than 60-fold titer of AdhTGEP in XTC than in FTC-133 cells. Cytotoxicity assays showed approximately 68% cell kill in XTC and minimal cell kill in FTC-133 and all other control cell lines at a multiplicity of infection of 250. There was significant in vivo growth inhibition of AdhTGEP-treated XTC tumors (67 +/- 49 mm(3)) compared with AdLacZ-treated XTC (228 +/- 45 mm(3); P < 0.01), PBS-treated XTC (372 +/- 70 mm(3); P < 0.001), or AdhTGEP-treated FTC-133 tumors (598 +/- 168 mm(3)). CONCLUSION: Replication-selective virus-mediated oncolysis is a potential therapy for recurrent, well-differentiated, TG-secreting thyroid cancer that is unresponsive to standard treatment.

Adenoviridae↗