Synthetic engineered bacteria for cancer therapy

Gong, Tong; Wu, Jinhui

doi:10.1080/17425247.2023.2241367

Cited by 1 publication

(1 citation statement)

References 185 publications

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“…Thus, these nanoparticles can act as surrogates of CAR T cells, bypassing the complexity of ACT production and thereby representing a more efficacious and cheaper off-the shelf tool. Similar tumor targeting payload delivery systems could also be considered such as protein/peptide-based delivery systems [ 84 , 85 ], DNA origami [ 86 ], oncoviruses [ 87 , 88 ], and bacteriotherapy [ 89 ]. Although each approach has its limitation, new synthetic biology and molecular engineering tools are likely to overcome obstacles related to each modality in the near future.…”

Section: Direct (Primary) Versus Indirect (Secondary) Cancer Cell Kil...mentioning

confidence: 99%

Shifting the paradigm: engaging multicellular networks for cancer therapy

Hu,

Ascierto,

Cesano

et al. 2024

J Transl Med

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Most anti-cancer modalities are designed to directly kill cancer cells deploying mechanisms of action (MOAs) centered on the presence of a precise target on cancer cells. The efficacy of these approaches is limited because the rapidly evolving genetics of neoplasia swiftly circumvents the MOA generating therapy-resistant cancer cell clones. Other modalities engage endogenous anti-cancer mechanisms by activating the multi-cellular network (MCN) surrounding neoplastic cells in the tumor microenvironment (TME). These modalities hold a better chance of success because they activate numerous types of immune effector cells that deploy distinct cytotoxic MOAs. This in turn decreases the chance of developing treatment-resistance. Engagement of the MCN can be attained through activation of immune effector cells that in turn kill cancer cells or when direct cancer killing is complemented by the production of proinflammatory factors that secondarily recruit and activate immune effector cells. For instance, adoptive cell therapy (ACT) supplements cancer cell killing with the release of homeostatic and pro-inflammatory cytokines by the immune cells and damage associated molecular patterns (DAMPs) by dying cancer cells. The latter phenomenon, referred to as immunogenic cell death (ICD), results in an exponential escalation of anti-cancer MOAs at the tumor site. Other approaches can also induce exponential cancer killing by engaging the MCN of the TME through the release of DAMPs and additional pro-inflammatory factors by dying cancer cells. In this commentary, we will review the basic principles that support emerging paradigms likely to significantly improve the efficacy of anti-cancer therapy.

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