Synergistic cytotoxic effects of recombinant human adenovirus p53 and radiation at various time points in A549 lung adenocarcinoma cells

Ma, Jie-Tao; Han, Cheng-Bo; Zhao, Jing; Wei, Jing; Zhou, Yang; Huang, Le-Tian; Zou, Huawei

doi:10.3892/ol.2012.747

Cited by 7 publications

(8 citation statements)

References 17 publications

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“…The wild-type p53 gene (wt-p53) influences cell survival and the response to radiation-induced DNA damage. The studies (Hirao et al 2000; Ma et al 2012) found activated p53 transcription promotes can lead to cell cycle arrest, DNA repair, tumor cell apoptosis, and even killing effect on tumor cells. A previous study (Kandioler et al 2002) suggested that patients were less sensitive to RT if the function of wt-p53 lost, and RT combined with rAd-p53 may increase the sensitivity in vivo and in vitro studies (Shiomitsu et al 2008; Gudkov and Komarova 2003; Cuddihy and Bristow 2004).…”

Section: Discussionmentioning

confidence: 99%

Recombinant human adenovirus-p53 therapy for the treatment of nasopharyngeal carcinoma: a meta-analysis

Cheng

Chen

2016

SpringerPlus

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To compare clinical curative effects and toxicity of recombinant human adenovirus-p53 injection (rAd-p53, Gendicine) combining chemoradiotherapy (CRT)/radiotherapy (RT) with those obtained with CRT/RT alone in nasopharyngeal carcinoma (NPC). We searched all the eligible studies from the Pubmed, Cochran Library, Embase, Web of science, Wanfang database and Chinese National Knowledge Infrastructure (CNKI). A total of twelve studies including 566 participants met the criteria to perform a meta-analysis. The results indicated the complete remission (CR) and overall response (OR) in the combination therapy group were significantly improved compared with the CRT/RT group (CR:RR = 2.03, 95% CI 1.66–2.48, p < 0.00001; OR:RR = 1.23, 95% CI 1.13–1.33, p < 0.00001), and patients who received the combination therapy showed significantly prolonged 1- and 2-year overall survival (OS), 2 year disease-free survival (DFS) rate and 2 year recurrence-free survival (RFS) rate (1 year OS:RR = 1.08, 95% CI 1.00–1.17, p = 0.04; 2 year OS:RR = 1.12, 95% CI 1.00–1.26, p = 0.04; 2 year DFS:RR = 1.41, 95% CI 1.09–1.83, p = 0.008; 2 year RFS:RR = 1.16, 95% CI 1.03–1.31, p = 0.02), but there was no significance in 3 year OS rate and 2 year distant metastases-free survival (DMFS) rate (3 year OS:RR = 1.28, 95% CI 1.00–1.62, p = 0.05; 2 year DMFS:RR = 1.05, 95% CI 0.89–1.24, p = 0.55). Furthermore, CRT/RT combined with rAd-p53 could not aggravate the myelosuppression versus CRT/RT alone (RR = 0.79, 95% CI 0.51–1.23, p = 0.30). The results demonstrated CRT/RT combined with rAd-p53 can result in enhanced survival and better clinical responses of patients with NPC. Therefore, rAd-p53 has great potential as an effective therapy for NPC.

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Section: Discussionmentioning

confidence: 99%

Recombinant human adenovirus-p53 therapy for the treatment of nasopharyngeal carcinoma: a meta-analysis

Cheng

Chen

2016

SpringerPlus

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“…76,94 These enhancements are achieved primarily as a result of p53-mediated autophagy and apoptosis. 74,119,120,123,124,128,[166][167][168][169][170] In addition to synergistic effects on chemo-or radiotherapy, Gendicine could be used to augment immunotherapy. Ad-p53 gene therapy enhanced LAK immunotherapy in the treatment of HNC.…”

Section: Enhancing Other Therapiesmentioning

confidence: 99%

The First Approved Gene Therapy Product for Cancer Ad-p53(Gendicine): 12 Years in the Clinic

et al. 2018

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Gendicine (recombinant human p53 adenovirus), developed by Shenzhen SiBiono GeneTech Co. Ltd., was approved in 2003 by the China Food and Drug Administration (CFDA) as a first-in-class gene therapy product to treat head and neck cancer, and entered the commercial market in 2004. Gendicine is a biological therapy that is delivered via minimally invasive intratumoral injection, as well as by intracavity or intravascular infusion. The wild-type (wt) p53 protein expressed by Gendicine-transduced cells is a tumor suppressor that is activated by cellular stress, and mediates cell-cycle arrest and DNA repair, or induces apoptosis, senescence, and/or autophagy, depending upon cellular stress conditions. Based on 12 years of commercial use in >30,000 patients, and >30 published clinical studies, Gendicine has exhibited an exemplary safety record, and when combined with chemotherapy and radiotherapy has demonstrated significantly higher response rates than for standard therapies alone. In addition to head and neck cancer, Gendicine has been successfully applied to treat various other cancer types and different stages of disease. Thirteen published studies that include long-term survival data showed that Gendicine combination regimens yield progression-free survival times that are significantly longer than standard therapies alone. Although the p53 gene is mutated in >50% of all human cancers, p53 mutation status did not significantly influence efficacy outcomes and long-term survival rate for Ad-p53-treated patients. To date, Shenzhen SiBiono GeneTech has manufactured 41 batches of Gendicine in compliance with CFDA QC/QA requirements, and 169,571 vials (1.0 × 10 vector particles per vial) have been used to treat patients. No serious adverse events have been reported, except for vector-associated transient fever, which occurred in 50-60% of patients and persisted for only a few hours. The manufacturing accomplishments and clinical experience with Gendicine, as well as the understanding of its cellular mechanisms of action and implications, could provide valuable insights for the international gene therapy community and add valuable data to promote further developments and advancements in the gene therapy field.

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“…P53 is one of the most popular genes which has been studied extensively in the field of tumour biology [7][8][9]. While it was not until 1997 did we discover its sibling -p63.…”

Section: Introductionmentioning

confidence: 99%

Effect of exogenous p51a gene on the growth and chemo sensitivity of human lung adenocarcinoma cell lines

Shen

Wang

Zhang

2018

Artificial Cells, Nanomedicine, and Biotechnology

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Exogenous p51A gene can increase its expression in A549 and NCI-H1299 cells, suppress cell growth and induce cell apoptosis. Moreover, it can also cooperate with chemotherapy and reduce the dose and side-effect. p51A gene can suppress tumours in spite of p53 status and p21 gene might be involved. It might become a new promising therapeutic gene of tumours, which will make up for the limitation of p53 gene therapy.

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Synergistic cytotoxic effects of recombinant human adenovirus p53 and radiation at various time points in A549 lung adenocarcinoma cells

Cited by 7 publications

References 17 publications

Recombinant human adenovirus-p53 therapy for the treatment of nasopharyngeal carcinoma: a meta-analysis

Recombinant human adenovirus-p53 therapy for the treatment of nasopharyngeal carcinoma: a meta-analysis

The First Approved Gene Therapy Product for Cancer Ad-p53(Gendicine): 12 Years in the Clinic

Effect of exogenous p51a gene on the growth and chemo sensitivity of human lung adenocarcinoma cell lines

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