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Cancers
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Carcinogenesis
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Carcinogenesis

A special issue of Cancers (ISSN 2072-6694). This special issue belongs to the section "Cancer Pathophysiology".

Deadline for manuscript submissions: closed (30 April 2021) | Viewed by 25552

Special Issue Editor

Dr. Yoko Matsuda

E-Mail Website
Guest Editor
Oncology Pathology, Department of Pathology and Host-Defense, Faculty of Medicine, Kagawa University, 1750-1 Ikenobe, Miki-cho, Kita-gun, Kagawa 761-0793, Japan
Interests: pancreatic cancer; pathology; telomere; telomerase; aging; carcinogenesis; stem cell; neoadjuvant therapy

Special Issue Information

Dear colleagues,

Carcinogenesis is the process which forms cancer cells. Various changes in the gene, epigenome, chromosome, cell mitosis, metabolism, and oxidative stress are involved as part of the steps of carcinogenesis. Various hypotheses for carcinogenesis have been proposed; multistep carcinogenesis, cancer stem cell, and clonal evolution. Animal models of carcinogenesis using chemical carcinogens have provided a lot of insights; however, little is known about the changes, mechanisms, and causes of carcinogenesis in humans. It is important to understand carcinogenesis steps in humans to develop methods for early detection and prevention of cancers.

The purpose of this Special Issue is to explore the expanding field of molecular and biological mechanisms of carcinogenesis as well as the clinical relevance of carcinogenesis. This Special Issue welcomes both original research articles and reviews until April 30, 2021.

Dr. Yoko Matsuda
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

  • carcinogenesis
  • pathology
  • genome
  • epigenome

Published Papers (5 papers)

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Review

17 pages, 1293 KiB  
Review
Mitochondrial Metabolism in Carcinogenesis and Cancer Therapy
by Hadia Moindjie, Sylvie Rodrigues-Ferreira and Clara Nahmias
Cancers 2021, 13(13), 3311; https://doi.org/10.3390/cancers13133311 - 1 Jul 2021
Cited by 31 | Viewed by 8660
Abstract
Carcinogenesis is a multi-step process that refers to transformation of a normal cell into a tumoral neoplastic cell. The mechanisms that promote tumor initiation, promotion and progression are varied, complex and remain to be understood. Studies have highlighted the involvement of oncogenic mutations, [...] Read more.
Carcinogenesis is a multi-step process that refers to transformation of a normal cell into a tumoral neoplastic cell. The mechanisms that promote tumor initiation, promotion and progression are varied, complex and remain to be understood. Studies have highlighted the involvement of oncogenic mutations, genomic instability and epigenetic alterations as well as metabolic reprogramming, in different processes of oncogenesis. However, the underlying mechanisms still have to be clarified. Mitochondria are central organelles at the crossroad of various energetic metabolisms. In addition to their pivotal roles in bioenergetic metabolism, they control redox homeostasis, biosynthesis of macromolecules and apoptotic signals, all of which are linked to carcinogenesis. In the present review, we discuss how mitochondria contribute to the initiation of carcinogenesis through gene mutations and production of oncometabolites, and how they promote tumor progression through the control of metabolic reprogramming and mitochondrial dynamics. Finally, we present mitochondrial metabolism as a promising target for the development of novel therapeutic strategies. Full article
(This article belongs to the Special Issue Carcinogenesis)
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17 pages, 2254 KiB  
Review
Relationship between Lung Carcinogenesis and Chronic Inflammation in Rodents
by Yuko Nakano-Narusawa, Masanao Yokohira, Keiko Yamakawa, Juanjuan Ye, Misa Tanimoto, Linxuan Wu, Yuri Mukai, Katsumi Imaida and Yoko Matsuda
Cancers 2021, 13(12), 2910; https://doi.org/10.3390/cancers13122910 - 10 Jun 2021
Cited by 11 | Viewed by 3263
Abstract
Lung cancer remains the leading cause of cancer-related deaths, with an estimated 1.76 million deaths reported in 2018. Numerous studies have focused on the prevention and treatment of lung cancer using rodent models. Various chemicals, including tobacco-derived agents induce lung cancer and pre-cancerous [...] Read more.
Lung cancer remains the leading cause of cancer-related deaths, with an estimated 1.76 million deaths reported in 2018. Numerous studies have focused on the prevention and treatment of lung cancer using rodent models. Various chemicals, including tobacco-derived agents induce lung cancer and pre-cancerous lesions in rodents. In recent years, transgenic engineered rodents, in particular, those generated with a focus on the well-known gene mutations in human lung cancer (KRAS, EGFR, and p53 mutations) have been widely studied. Animal studies have revealed that chronic inflammation significantly enhances lung carcinogenesis, and inhibition of inflammation suppresses cancer progression. Moreover, the reduction in tumor size by suppression of inflammation in animal experiments suggests that chronic inflammation influences the promotion of tumorigenesis. Here, we review rodent lung tumor models induced by various chemical carcinogens, including tobacco-related carcinogens, and transgenics, and discuss the roles of chronic inflammation in lung carcinogenesis. Full article
(This article belongs to the Special Issue Carcinogenesis)
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27 pages, 366 KiB  
Review
Virus-Driven Carcinogenesis
by Yuichiro Hatano, Takayasu Ideta, Akihiro Hirata, Kayoko Hatano, Hiroyuki Tomita, Hideshi Okada, Masahito Shimizu, Takuji Tanaka and Akira Hara
Cancers 2021, 13(11), 2625; https://doi.org/10.3390/cancers13112625 - 27 May 2021
Cited by 34 | Viewed by 5096
Abstract
Cancer arises from the accumulation of genetic and epigenetic alterations. Even in the era of precision oncology, carcinogens contributing to neoplastic process are still an important focus of research. Comprehensive genomic analyses have revealed various combinations of base substitutions, referred to as the [...] Read more.
Cancer arises from the accumulation of genetic and epigenetic alterations. Even in the era of precision oncology, carcinogens contributing to neoplastic process are still an important focus of research. Comprehensive genomic analyses have revealed various combinations of base substitutions, referred to as the mutational signatures, in cancer. Each mutational signature is believed to arise from specific DNA damage and repair processes, including carcinogens. However, as a type of carcinogen, tumor viruses increase the cancer risk by alternative mechanisms, including insertional mutagenesis, viral oncogenes, and immunosuppression. In this review, we summarize virus-driven carcinogenesis to provide a framework for the control of malignant cell proliferation. We first provide a brief overview of oncogenic viruses and describe their implication in virus-related tumors. Next, we describe tumor viruses (HPV, Human papilloma virus; HBV, Hepatitis B virus; HCV, Hepatitis C virus; EBV, Epstein–Barr virus; Kaposi sarcoma herpesvirus; MCV, Merkel cell polyoma virus; HTLV-1, Human T-cell lymphotropic virus, type-1) and tumor virus-related cancers. Lastly, we introduce emerging tumor virus candidates, human cytomegalovirus (CMV), human herpesvirus-6 (HHV-6) and adeno-associated virus-2 (AAV-2). We expect this review to be a hub in a complex network of data for virus-associated carcinogenesis. Full article
(This article belongs to the Special Issue Carcinogenesis)
21 pages, 2539 KiB  
Review
Carcinogenesis of Triple-Negative Breast Cancer and Sex Steroid Hormones
by Naoko Honma, Yoko Matsuda and Tetuo Mikami
Cancers 2021, 13(11), 2588; https://doi.org/10.3390/cancers13112588 - 25 May 2021
Cited by 9 | Viewed by 4758
Abstract
Triple-negative breast cancer (TNBC) lacks an effective treatment target and is usually associated with a poor clinical outcome; however, hormone unresponsiveness, which is the most important biological characteristic of TNBC, only means the lack of nuclear estrogenic signaling through the classical estrogen receptor [...] Read more.
Triple-negative breast cancer (TNBC) lacks an effective treatment target and is usually associated with a poor clinical outcome; however, hormone unresponsiveness, which is the most important biological characteristic of TNBC, only means the lack of nuclear estrogenic signaling through the classical estrogen receptor (ER), ER-α. Several sex steroid receptors other than ER-α: androgen receptor (AR), second ER, ER-β, and non-nuclear receptors represented by G-protein-coupled estrogen receptor (GPER), are frequently expressed in TNBC and their biological and clinical importance has been suggested by a large number of studies. Despite the structural similarity between each sex steroid hormone (androgens and estrogens) or each receptor (AR and ER-β), and similarity in the signaling mechanisms of these hormones, most studies or reviews focused on one of these receptors, and rarely reviewed them in a comprehensive way. Considering the coexistence of these hormones and their receptors in TNBC in a clinical setting, a comprehensive viewpoint would be important to correctly understand the association between the carcinogenic mechanism or pathobiology of TNBC and sex steroid hormones. In this review, the carcinogenic or pathobiological role of sex steroid hormones in TNBC is considered, focusing on the common and divergent features of the action of these hormones. Full article
(This article belongs to the Special Issue Carcinogenesis)
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9 pages, 977 KiB  
Review
Pathological Changes in Pancreatic Carcinogenesis: A Review
by Keiko Yamakawa, Juanjuan Ye, Yuko Nakano-Narusawa and Yoko Matsuda
Cancers 2021, 13(4), 686; https://doi.org/10.3390/cancers13040686 - 8 Feb 2021
Cited by 2 | Viewed by 2378
Abstract
Despite advances in diagnostics and therapeutics, the prognosis of pancreatic cancer remains dismal. Because of a lack of early diagnostic methods, aggressive local progression, and high incidence of distant metastasis, most pancreatic cancers are inoperable; therefore, the characteristics of early pancreatic cancer have [...] Read more.
Despite advances in diagnostics and therapeutics, the prognosis of pancreatic cancer remains dismal. Because of a lack of early diagnostic methods, aggressive local progression, and high incidence of distant metastasis, most pancreatic cancers are inoperable; therefore, the characteristics of early pancreatic cancer have not been well understood. Autopsy studies revealed the characteristics of prediagnostic pancreatic malignancies, including precancerous lesions, early stage pancreatic cancer, and pancreatic cancer without clinical symptoms (occult cancers). Animal models using hamsters and genetically engineered mice have focused on mechanisms of carcinogenesis, thereby providing insights into risk factors and prevention and serving as a preclinical test for the development of novel diagnostic and treatment modalities. In this review, we have summarized pathological changes in the pancreas of humans and experimental animals during carcinogenesis. Full article
(This article belongs to the Special Issue Carcinogenesis)
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