Chemoresistance in Solid Tumours

A special issue of Cancers (ISSN 2072-6694).

Deadline for manuscript submissions: closed (25 August 2023) | Viewed by 2165

Special Issue Editors

Department of Gastroenterological Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama 700-8558, Japan
Interests: colorectal cancer; epithelial-mesenchymal transition (EMT); molecular imaging

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Guest Editor
1. Division of Surgical Oncology, Department of Surgery, University of California San Diego, La Jolla, CA 92037, USA
2. AntiCancer Inc., San Diego, CA 92111, USA
Interests: cancer research

Special Issue Information

Dear Colleagues, 

Current precision medicine for solid tumours comprises a combination of appropriate cytotoxic agents and molecularly targeted drugs for each molecular subtype. Since molecular subtypes provide appropriate therapeutic targets, various molecular subtypes have been explored by gene mutation, gene expression, and protein expression. However, this tumour heterogeneity is considered one of the main reasons for chemoresistance, since refractory solid tumours exhibit high tumour heterogeneity and cannot be eliminated by several anticancer drugs. Although the cancer stem cell theory has been accepted as a model that can resolve tumour heterogeneity, tumour heterogeneity remains unresolved because cancer cells have the plasticity to revert from non-cancer stem cells to cancer stem cells. In addition, the microenvironment is one of the factors contributing to chemotherapeutic resistance in solid tumours. For example, pancreatic cancer has a predominance of stroma and few cancer cells, but this stroma acts as a barrier to the reach of anticancer drugs and hinders the infiltration of cytotoxic lymphocytes. The prognosis for patients with highly advanced solid tumours remains poor because tumour heterogeneity, the plasticity inherent in cancer cells, and the contribution of the microenvironment to chemotherapy resistance remain unresolved.

Therefore, this Special Issue of Cancers will highlight new research articles and timely review articles on novel therapies to resolve chemotherapy resistance in solid tumours.

Dr. Shuya Yano
Dr. Robert M. Hoffman
Guest Editors

Manuscript Submission Information

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Keywords

  • solid tumours
  • heterogeneity
  • chemotherapeutic resistance

Published Papers (1 paper)

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Research

13 pages, 7020 KiB  
Article
Conventional Cancer Therapies Can Accelerate Malignant Potential of Cancer Cells by Activating Cancer-Associated Fibroblasts in Esophageal Cancer Models
by Satoshi Komoto, Kazuhiro Noma, Takuya Kato, Teruki Kobayashi, Noriyuki Nishiwaki, Toru Narusaka, Hiroaki Sato, Yuki Katsura, Hajime Kashima, Satoru Kikuchi, Toshiaki Ohara, Hiroshi Tazawa and Toshiyoshi Fujiwara
Cancers 2023, 15(11), 2971; https://doi.org/10.3390/cancers15112971 - 30 May 2023
Cited by 1 | Viewed by 1709
Abstract
Esophageal cancer is one of the most aggressive tumors, and the outcome remains poor. One contributing factor is the presence of tumors that are less responsive or have increased malignancy when treated with conventional chemotherapy, radiotherapy, or a combination of these. Cancer-associated fibroblasts [...] Read more.
Esophageal cancer is one of the most aggressive tumors, and the outcome remains poor. One contributing factor is the presence of tumors that are less responsive or have increased malignancy when treated with conventional chemotherapy, radiotherapy, or a combination of these. Cancer-associated fibroblasts (CAFs) play an important role in the tumor microenvironment. Focusing on conventional cancer therapies, we investigated how CAFs acquire therapeutic resistance and how they affect tumor malignancy. In this study, low-dose chemotherapy or radiotherapy-induced normal fibroblasts showed enhanced activation of CAFs markers, fibroblast activation protein, and α-smooth muscle actin, indicating the acquisition of malignancy in fibroblasts. Furthermore, CAFs activated by radiotherapy induce phenotypic changes in cancer cells, increasing their proliferation, migration, and invasion abilities. In in vivo peritoneal dissemination models, the total number of tumor nodules in the abdominal cavity was significantly increased in the co-inoculation group of cancer cells and resistant fibroblasts compared to that in the co-inoculation group of cancer cells and normal fibroblasts. In conclusion, we demonstrated that conventional cancer therapy causes anti-therapeutic effects via the activation of fibroblasts, resulting in CAFs. It is important to select or combine modalities of esophageal cancer treatment, recognizing that inappropriate radiotherapy and chemotherapy can lead to resistance in CAF-rich tumors. Full article
(This article belongs to the Special Issue Chemoresistance in Solid Tumours)
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