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 4063

Special Issue Editor


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Guest Editor
1. Department of Pathology, Ohio State University, Columbus, OH 43210, USA.
2. OSUCCC James, OSU Wexner Medical Center, Columbus, OH 43210, USA.
Interests: senescence; chemokines; tumor immune microenvironment

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:

  1. Molecular targets, mechanisms, and markers of therapy-induced senescence;
  2. The role of therapy-induced senescence in cancer progression, therapeutic response, and therapy-adverse events;
  3. The influence of tumor senescence on the tumor microenvironment;
  4. Use of senolytic agents in cancer therapy.

Dr. Anna E. Vilgelm
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Cancers is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2900 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

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

Published Papers (1 paper)

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Review

15 pages, 1152 KiB  
Review
Senescence in HBV-, HCV- and NAFLD- Mediated Hepatocellular Carcinoma and Senotherapeutics: Current Evidence and Future Perspective
by Vassilis G. Giannakoulis, Peter Dubovan, Eleni Papoutsi, Agapi Kataki and John Koskinas
Cancers 2021, 13(18), 4732; https://doi.org/10.3390/cancers13184732 - 21 Sep 2021
Cited by 12 | Viewed by 3463
Abstract
Cell senescence constitutes a physiological process that serves as protection from malignant transformation of cells. However, recent scientific discoveries also identify cell senescence as pivotal in hepatocellular cancer (HCC) biology. The review herein aimed to accumulate evidence on senescence as a mediator of [...] Read more.
Cell senescence constitutes a physiological process that serves as protection from malignant transformation of cells. However, recent scientific discoveries also identify cell senescence as pivotal in hepatocellular cancer (HCC) biology. The review herein aimed to accumulate evidence on senescence as a mediator of HCC occurrence in hepatitis B (HBV), C (HCV) virus infections, and non-alcoholic fatty liver disease (NAFLD). In HBV infection, the carcinogenic HBV X protein frequently mutates during chronic infection, and subsequently exhibits different effects on senescence. In HCV infection, senescent non-functional T-cells do not effectively clear pre-malignant hepatocytes. Furthermore, the HCV Core protein inhibits the occurrence of normal stress-induced hepatocyte senescence, allowing damaged cells to maintain their proliferative potential. In NAFLD-mediated HCC, current data point towards the gut microbiome and hepatic stellate cell senescence. Additionally, senescence contributes in the development of resistance in targeted therapies, such as sorafenib. Finally, the promising role of senotherapeutics in HCC was also explored. Overall, although we may still be at a primitive stage in fully unraveling the role of senescence in cancer, it seems that understanding and harnessing senescence may have the potential to revolutionize the way we treat hepatocellular cancer. Full article
(This article belongs to the Special Issue Senescent Cells and Cancer Therapy)
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