Oops, you're using an old version of your browser so some of the features on this page may not be displaying properly.

MINIMAL Requirements: Google Chrome 24+Mozilla Firefox 20+Internet Explorer 11Opera 15–18Apple Safari 7SeaMonkey 2.15-2.23

Poster Display

52P - MUC1 targeted immunotherapy with an oncolytic adenovirus coding for a bispecific T cell engager

Date

08 Dec 2022

Session

Poster Display

Presenters

Saru Basnet

Citation

Annals of Oncology (2022) 16 (suppl_1): 100101-100101. 10.1016/iotech/iotech100101

Authors

S. Basnet1, J.M. Santos2, D.C.A. Quixabeira3, J. Clubb3, S. Grönberg-Vähä-Koskela1, S. Pakola3, T. Kudling1, C. Heiniö3, R. Havunen2, V. Cervera-Carrascon2, S. Sorsa2, M. Anttila3, A. Kanerva4, A. Hemminki2

Author affiliations

  • 1 Cancer Gene Therapy Group (CGTG),University of Helsinki, Helsinki/FI
  • 2 TILT Biotherapeutics Ltd, Helsinki/FI
  • 3 University of Helsinki, Helsinki/FI
  • 4 Helsinki University Hospital, Helsinki/FI

Resources

Login to get immediate access to this content.

If you do not have an ESMO account, please create one for free.

Abstract 52P

Background

Bispecific T cell engager (BsTe) is a fusion recombinant protein comprised of two single–chain variable fragments with dual specificity for a tumor–associated antigen (TAA) and T cell receptor (usually CD3ε). Immunotherapy with BsTe has shown efficacy in patients with hematologic malignancies and uveal melanoma. However, the antitumor efficacy of BsTe in most solid tumors has been limited due to their short serum half-life and insufficient tumor concentration. We designed a novel serotype 5/3 oncolytic adenovirus encoding for a BsTe cross-linking Mucin1 (MUC1) to CD3, Ad5/3–E2F–d24–aMUC1aCD3. The BsTe (aMUC1aCD3) is designed for the treatment of human solid tumors, where the BsTe links CD3 molecules on the surface of T cells and MUC1 on the target cancer cells.

Methods

Cell viability assays were used to assess the oncolytic potential of the novel Ad5/3–E2F–d24–aMUC1aCD3 construct. The functionality of virus-derived aMUC1aCD3 was evaluated in vitro using T cell activation, proliferation and cancer cell killing assays. The efficacy of the aMUC1aCD3 coding virus was investigated in vivo using a humanized MUC1 expressing lung cancer xenograft mouse model.

Results

The addition of aMUC1aCD3 transgenes did not compromise virus replication capacity. When Ad5/3–E2F–d24–aMUC1aCD3 is combined with allogenic T cells, rapid tumor cell lysis upon infection was observed using different cancer cell lines. TILT-321 infected cells secreted functional aMUC1aCD3 engagers as evidenced by increased T cell activity and competitive binding to MUC1+ cells. Ad5/3–E2F–d24–aMUC1aCD3 treatment also led to effective anti–tumor efficacy in vivo in a human MUC1 expressing lung cancer xenograft model. This response was associated with increased intratumoral T cell activation mediated by the aMUC1aCD3-armed adenovirus.

Conclusions

This study provides proof-of-concept for an effective strategy to overcome some of the limitations of recombinant BsTe delivery in the treatment of solid tumors. The proposed technology could be beneficial for the treatment of solid tumors preferentially those expressing MUC1.

Legal entity responsible for the study

The authors.

Funding

Ida-Montin Foundation, Orion Foundation, Minerva Foundation, Jane and Aatos Erkko Foundation.

Disclosure

J.M. Santos, V. Cervera-Carrascon, S.Sorsa: Financial Interests, Institutional, Full or part-time Employment: TILT Biotherapeutics Ltd; Financial Interests, Personal, Stocks/Shares: TILT Biotherapeutics Ltd. R. Havunen: Financial Interests, Institutional, Full or part-time Employment: TILT Biotherapeutics Ltd. All other authors have declared no conflicts of interest.

This site uses cookies. Some of these cookies are essential, while others help us improve your experience by providing insights into how the site is being used.

For more detailed information on the cookies we use, please check our Privacy Policy.

Customise settings
  • Necessary cookies enable core functionality. The website cannot function properly without these cookies, and you can only disable them by changing your browser preferences.