Senescent Cells and Cancer Therapy
A special issue of Cancers (ISSN 2072-6694). This special issue belongs to the section "Cancer Therapy".
Deadline for manuscript submissions: closed (1 March 2022) | Viewed by 4429
Special Issue Editor
Special Issue Information
Dear Colleagues,
Senescence is a natural stress response mechanism characterized by stable cell cycle arrest and secretion of pro-inflammatory factors, stromal components, and other molecules, known as senescence-associated secretory phenotype (SASP). Many types of cancer treatments, including radiation, chemotherapy, and targeted therapies, can leave behind senescent tumor cells. Paradoxically, therapy-induced senescence (TIS) and SASP can have both tumor-promoting and tumor-suppressing properties depending on the cellular context and inducing stimuli. For instance, TIS halts tumor cell proliferation. However, senescent cells can sometimes escape growth arrest leading to post-therapy tumor recurrence. Similarly, inflammatory mediators secreted by senescent cells can facilitate tumor immuno-surveillance. On the other hand, SASP can facilitate tumor infiltration with immune cell subsets that promote tumor growth and metastasis. Moreover, TIS and SASP have been linked with therapy side effects. Therefore, while induction of senescence may benefit patients in the short term, prompt removal of senescent cells may present a path toward improved treatment outcome.
For this Special Issue entitled Senescent Cells and Cancer Therapy, we invite original research and reviews manuscripts on the topics of therapy-induced senescence including, but not limited to:
- Molecular targets, mechanisms, and markers of therapy-induced senescence;
- The role of therapy-induced senescence in cancer progression, therapeutic response, and therapy-adverse events;
- The influence of tumor senescence on the tumor microenvironment;
- Use of senolytic agents in cancer therapy.
Dr. Anna E. Vilgelm
Guest Editor
Manuscript Submission Information
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Keywords
- Senescent cells
- Senescence-associated secretory phenotype (SASP)
- Tissue remodeling
- Tumor microenvironment
- Cytokines, pro-inflammatory factors
- Immune surveillance
- Inflammation
- Tumor relapse
- Cancer therapy
- Therapy-induced senescence
- DNA damage
- p16
- p21
- p53
- NFκB
- Senotherapy
- Senolytic
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