Epigenetics and Cancer Therapy

A special issue of Life (ISSN 2075-1729). This special issue belongs to the section "Physiology and Pathology".

Deadline for manuscript submissions: 22 June 2024 | Viewed by 974

Special Issue Editors


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Guest Editor
Department of Public Health Medicine, UP Medical School, University of Pécs, Pécs, Hungary
Interests: cancer; lung cancer; MDR; genetics; genetic markers; drug transporters; chemotherapy; genotoxicology

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Guest Editor
Department of Public Health Medicine, UP Medical School, University of Pécs, Pécs, Hungary
Interests: genotoxicology; mutations; ecotoxicology; ecogenotoxilogy

Special Issue Information

Dear Colleagues,

Cancer is a heterogeneous disease and one of the leading causes of death worldwide, which is affected by genetic and epigenetic modulations in the regulation of cell division. One of the most serious obstacles in applied cancer therapy is the occurrence of multidrug resistance, which may evolve due to oncogene mutations, modifications in the tumor microenvironment, tumor diversification, target site mutations or epigenetic adjustment. The phenomenon of multidrug resistance may occur naturally but acquiring it during chemotherapy is more recurrent. Consequently, recent laboratory studies and clinical trials have analyzed remarkable drugs for targeted and personalized therapy; however, the given drug treatment becomes inefficient due to the development of multidrug resistance. Despite the emergence of new therapies, patients—mostly in advanced stages of the disease—are still being treated following a set protocol including surgery, radiation and chemotherapy or a combination of the above.

In this context, we present a Special Issue, with Dr. Luca Jaromi and Dr. Gellert Gerencser as Guest Editors, which will collate papers aimed at identifying genetic markers that influence the outcome of various cancer treatments, including chemotherapy agents, chemoradiotherapy and radiation techniques. We invite papers that underscore the sophisticated treatment approaches as well as the relationships between accumulation of various cancer therapeutic agents and expression levels of target genes, thereby contributing to a better understanding and more effective treatment of cancer or malignant tumours.

Dr. Luca Járomi
Dr. Gellért Gerencsér
Guest Editors

Manuscript Submission Information

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Keywords

  • epigenetics
  • cancer therapy
  • multidrug resistance (MDR)
  • accumulation
  • biomarkers

Published Papers (1 paper)

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Research

12 pages, 556 KiB  
Article
The Contribution of Tissue Inhibitor of Metalloproteinase-2 Genotypes to Breast Cancer Risk in Taiwan
by Yun-Chi Wang, Jie-Long He, Chung-Lin Tsai, Huey-En Tzeng, Wen-Shin Chang, Shih-Han Pan, Li-Hsiou Chen, Chen-Hsien Su, Jiunn-Cherng Lin, Chih-Chiang Hung, Da-Tian Bau and Chia-Wen Tsai
Life 2024, 14(1), 9; https://doi.org/10.3390/life14010009 - 20 Dec 2023
Cited by 1 | Viewed by 741
Abstract
Tissue inhibitor of metalloproteinase-2 (TIMP-2) is an endogenous inhibitor of matrix metalloproteinase-2 and is highly expressed in breast cancer (BC) cases at diagnosis. However, the genetic investigations for the association of TIMP-2 genotypes with BC risk are rather limited. In this study, contribution [...] Read more.
Tissue inhibitor of metalloproteinase-2 (TIMP-2) is an endogenous inhibitor of matrix metalloproteinase-2 and is highly expressed in breast cancer (BC) cases at diagnosis. However, the genetic investigations for the association of TIMP-2 genotypes with BC risk are rather limited. In this study, contribution of TIMP-2 rs8179090, rs4789936, rs2009196 and rs7342880 genotypes to BC risk was examined among Taiwan’s BC population. TIMP-2 genotypic profiles were revealed among 1232 BC cases and 1232 controls about their contribution to BC using a PCR-based RFLP methodology. The TIMP-2 rs8179090 homozygous variant CC genotype was significantly higher in BC cases than controls (odds ratio (OR) = 2.76, 95% confidence interval (95%CI) = 1.78–4.28, p = 0.0001). Allelic analysis showed that C allele carriers have increased risk for BC (OR = 1.39, 95%CI = 1.20–1.62, p = 0.0001). Genotypic together with allelic analysis showed that TIMP-2 rs4789936, rs2009196 or rs7342880 were not associated with BC risk. Stratification analysis showed that TIMP-2 rs8179090 genotypes were significantly associated with BC risk among younger (≤55) aged women, not among those of an elder (>55) age. Last, rs8179090 genotypes were also associated with triple negative BC. This study sheds light into the etiology of BC in Taiwanese women. Rs8179090 may be incorporated into polygenic risk scores and risk prediction models, which could aid in stratifying individuals for targeted breast cancer screening. Full article
(This article belongs to the Special Issue Epigenetics and Cancer Therapy)
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