Implications of senescence in cancer immunology

The concept of permanent and irreversible cell cycle arrest (senescence) was initially regarded as a defence mechanism against tumour progression. However, research has demonstrated that senescent cells can also contribute to cancer development and progression. The tumor-suppressing and tumor-promoting activities are primarily attributable to the set of factors (including chemokines, growth factors, cytokines, or metalloproteinases) that constitute the senescence-associated secretory phenotype (SASP). The cells can induce an antitumor immune response through these proinflammatory factors. However, the accumulation of senescent cells that have not been cleared by the immune system may favor a chronic inflammatory environment that favors tumor development and progression. In recent years, pharmacological interventions have been proposed to promote the elimination of senescent cells, inhibit SASP and/or enhance the immune response against senescent cells. These interventions include senolytic therapies, senomorphic therapies, nanotherapy and vaccines.

In light of the intricate and diverse functions observed in senescent cells and the SASP across various types of cancer, this Research Topic aims to showcase the latest advances and provide an update on this field. From one perspective, the objective is to ascertain how senescent cells can bolster the antitumor immune response, and how the accumulation of such cells can remodel the tumor microenvironment, thus facilitating tumor growth, immune evasion, tumor progression (including metastasis), and even potential resistance to treatment. Finally, other objective is to further explore new antitumor therapeutic strategies based on the elimination of senescent cells by modulating SASP and the immune response.

Submission of original research articles, reviews and mini-reviews, including, but not limited to, the topics listed below are welcome:

1. Mechanisms by which senescent cells induce an antitumor immune response.

2. Mechanisms by which senescent cells induce a chronic inflammatory response that favors tumor development and progression and/or affect the efficacy of antitumor treatments.

3. Mechanisms of SASP modulation to improve the efficacy of the immune response.

4. Therapeutic strategies against senescent cells or that modulate SASP and the immune response.

Please note that manuscripts consisting solely of bioinformatics or computational analysis of public genomic or transcriptomic databases which are not accompanied by robust and relevant validation (clinical cohort or biological validation in vitro or in vivo) are out of scope for this Research Topic.