ArticleJournal of translational medicine2012
Enhanced antitumoral efficacy and immune response following conditionally replicative adenovirus containing constitutive HSF1 delivery to rodent tumors.
Article in Journal of translational medicine, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 15 citations in OpenAlex.
- HSF1 is involved in immunotherapeutic response through regulating APOJ/STAT3-mediated PD-L1 expression in hepatocellular carcinoma.Cancer biology & therapy · 2023Article
- Step-by-Step Immune Activation for Suicide Gene Therapy Reinforcement.International journal of molecular sciences · 2021Review
- Immuno-Oncolytic Viruses: Emerging Options in the Treatment of Colorectal Cancer.Molecular diagnosis & therapy · 2021Review
- Checkpoint Inhibitors for Non-Small Cell Lung Cancer Among Older Adults.Current oncology reports · 2017Review
- Metabolic control of the proteotoxic stress response: implications in diabetes mellitus and neurodegenerative disorders.Cellular and molecular life sciences : CMLS · 2016Review
- Antitumour responses induced by a cell-based Reovirus vaccine in murine lung and melanoma models.BMC cancer · 2016Article
- In situ vaccination: Cancer immunotherapy both personalized and off-the-shelf.Molecular oncology · 2015Review
- Oncolytic viruses as therapeutic cancer vaccines.Molecular cancer · 2013Review
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Authors and funding
12 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundOncolytic adenoviruses are promising as anticancer agents but have limited clinical responses. Our previous study showed that heat shock transcription factor 1 (HSF1) overexpression could increase the anti-tumor efficacy of E1B55kD deleted oncolytic adenovirus through increasing the viral burst. Due to the important roles of heat shock proteins (HSPs) in eliciting innate and adaptive immunity, we reasoned that besides increasing the viral burst, HSF1 may also play a role in increasing tumor specific immune response.
methodsIn the present study, intra-dermal murine models of melanoma (B16) and colorectal carcinoma (CT26) were treated with E1B55kD deleted oncolytic adenovirus Adel55 or Adel55 incorporated with cHSF1, HSF1i, HSP70, or HSP90 by intra-tumoral injection. Tumors were surgically excised 72 h post injection and animals were analyzed for tumor resistance and survival rate.
resultsApproximately 95% of animals in the Adel55-cHSF1 treated group showed sustained resistance upon re-challenge with autologous tumor cells, but not in PBS, Adel55, or Adel55-HSF1i treated groups. Only 50-65% animals in the Adel55-HSP70 and Adel55-HSP90 treated group showed tumor resistance. Tumor resistance was associated with development of tumor type specific cellular immune responses. Adel55-cHSF1 treatment also showed higher efficacy in diminishing progression of the secondary tumor focus than Adel55-HSP70 or Adel55-HSP90 treatment.
conclusionsBesides by increasing its burst in tumor cells, cHSF1 could also augment the potential of E1B55kD deleted oncolytic adenovirus by increasing the tumor-specific immune response, which is beneficial to prevent tumor recurrence. cHSF1 is a better gene for neoadjuvant immunotherapy than other heat shock protein genes.
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