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Cancer Biology: From Genetic Aspects to Treatment
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Cancer Biology: From Genetic Aspects to Treatment

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Oncology".

Deadline for manuscript submissions: 31 October 2024 | Viewed by 3450

Special Issue Editor

Dr. Silvia Cantara

E-Mail Website
Guest Editor
Department of Medical, Surgical and Neurological Sciences, University of Siena, 53100 Siena, Italy
Interests: cancer biology; endocrinology; molecular biology; genetics; cellular biology

Special Issue Information

Dear Colleagues,

Cancer is a complex disease characterized by the uncontrolled proliferation and dissemination of aberrant cells throughout the human body. This pathological condition stems from alterations in the fundamental genetic code encoded within our DNA. Predominantly, these alterations manifest within specific DNA segments referred to as genes.

The expanding frontiers of scientific knowledge have propelled molecular biology to play a pivotal role within contemporary oncological research. This prominence arises from its capacity to unveil mechanisms underpinning cellular growth and differentiation, novel diagnostic indicators, and therapeutic focal points. Thus, molecular biology has emerged as the fulcrum of progressive advancements in the field of oncology, offering possibilities for the development of efficacious therapeutic interventions.

This Special Issue of IJMS, ‘Cancer Biology: From Genetic Aspects to Treatment’, led by Dr. Silvia Cantara, aims to focus on new insights, novel developments and discoveries, current challenges, and future perspectives in the field of cancer biology.

We cordially invite you to submit your papers to this Special Issue.

Dr. Silvia Cantara
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. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. 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

  • cancer biology
  • cancer biomarker
  • cancer progression
  • cancer metastasis
  • genetic of cancer

Published Papers (4 papers)

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Research

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15 pages, 6377 KiB  
Article
Effects of Reduced Extracellular Sodium Concentrations on Cisplatin Treatment in Human Tumor Cells: The Role of Autophagy
by Laura Naldi, Benedetta Fibbi, Cecilia Anceschi, Patrizia Nardini, Daniele Guasti, Alessandro Peri and Giada Marroncini
Int. J. Mol. Sci. 2024, 25(8), 4377; https://doi.org/10.3390/ijms25084377 - 16 Apr 2024
Viewed by 430
Abstract
Hyponatremia is the prevalent electrolyte imbalance in cancer patients, and it is associated with a worse outcome. Notably, emerging clinical evidence suggests that hyponatremia adversely influences the response to anticancer treatments. Therefore, this study aims to investigate how reduced extracellular [Na+] [...] Read more.
Hyponatremia is the prevalent electrolyte imbalance in cancer patients, and it is associated with a worse outcome. Notably, emerging clinical evidence suggests that hyponatremia adversely influences the response to anticancer treatments. Therefore, this study aims to investigate how reduced extracellular [Na+] affects the responsiveness of different cancer cell lines (from human colon adenocarcinoma, neuroblastoma, and small cell lung cancer) to cisplatin and the underlying potential mechanisms. Cisplatin dose–response curves revealed higher IC50 in low [Na+] than normal [Na+]. Accordingly, cisplatin treatment was less effective in counteracting the proliferation and migration of tumor cells when cultured in low [Na+], as demonstrated by colony formation and invasion assays. In addition, the expression analysis of proteins involved in autophagosome–lysosome formation and the visualization of lysosomal areas by electron microscopy revealed that one of the main mechanisms involved in chemoresistance to cisplatin is the promotion of autophagy. In conclusion, our data first demonstrate that the antitumoral effect of cisplatin is markedly reduced in low [Na+] and that autophagy is an important mechanism of drug escape. This study indicates the role of hyponatremia in cisplatin chemoresistance and reinforces the recommendation to correct this electrolyte alteration in cancer patients. Full article
(This article belongs to the Special Issue Cancer Biology: From Genetic Aspects to Treatment)
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17 pages, 4786 KiB  
Article
Disrupting Poly(ADP-ribosyl)ating Pathway Creates Premalignant Conditions in Mammalian Liver
by Yaroslava Karpova, David J. Orlicky, Edward E. Schmidt and Alexei V. Tulin
Int. J. Mol. Sci. 2023, 24(24), 17205; https://doi.org/10.3390/ijms242417205 - 6 Dec 2023
Viewed by 1061
Abstract
Hepatocellular carcinoma (HCC) is a major global health concern, representing one of the leading causes of cancer-related deaths. Despite various treatment options, the prognosis for HCC patients remains poor, emphasizing the need for a deeper understanding of the factors contributing to HCC development. [...] Read more.
Hepatocellular carcinoma (HCC) is a major global health concern, representing one of the leading causes of cancer-related deaths. Despite various treatment options, the prognosis for HCC patients remains poor, emphasizing the need for a deeper understanding of the factors contributing to HCC development. This study investigates the role of poly(ADP-ribosyl)ation in hepatocyte maturation and its impact on hepatobiliary carcinogenesis. A conditional Parg knockout mouse model was employed, utilizing Cre recombinase under the albumin promoter to target Parg depletion specifically in hepatocytes. The disruption of the poly(ADP-ribosyl)ating pathway in hepatocytes affects the early postnatal liver development. The inability of hepatocytes to finish the late maturation step that occurs early after birth causes intensive apoptosis and acute inflammation, resulting in hypertrophic liver tissue with enlarged hepatocytes. Regeneration nodes with proliferative hepatocytes eventually replace the liver tissue and successfully fulfill the liver function. However, early developmental changes predispose these types of liver to develop pathologies, including with a malignant nature, later in life. In a chemically induced liver cancer model, Parg-depleted livers displayed a higher tendency for hepatocellular carcinoma development. This study underscores the critical role of the poly(ADP-ribosyl)ating pathway in hepatocyte maturation and highlights its involvement in liver pathologies and hepatobiliary carcinogenesis. Understanding these processes may provide valuable insights into liver biology and liver-related diseases, including cancer. Full article
(This article belongs to the Special Issue Cancer Biology: From Genetic Aspects to Treatment)
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Review

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18 pages, 615 KiB  
Review
Exploring Potential Biomarkers in Oesophageal Cancer: A Comprehensive Analysis
by Adrianna Romanowicz, Marta Lukaszewicz-Zajac and Barbara Mroczko
Int. J. Mol. Sci. 2024, 25(8), 4253; https://doi.org/10.3390/ijms25084253 - 11 Apr 2024
Viewed by 520
Abstract
Oesophageal cancer (OC) is the sixth leading cause of cancer-related death worldwide. OC is highly aggressive, primarily due to its late stage of diagnosis and poor prognosis for patients’ survival. Therefore, the establishment of new biomarkers that will be measured with non-invasive techniques [...] Read more.
Oesophageal cancer (OC) is the sixth leading cause of cancer-related death worldwide. OC is highly aggressive, primarily due to its late stage of diagnosis and poor prognosis for patients’ survival. Therefore, the establishment of new biomarkers that will be measured with non-invasive techniques at low cost is a critical issue in improving the diagnosis of OC. In this review, we summarize several original studies concerning the potential significance of selected chemokines and their receptors, including inflammatory proteins such as interleukin-6 (IL-6) and C-reactive protein (CRP), hematopoietic growth factors (HGFs), claudins (CLDNs), matrix metalloproteinases (MMPs) and their tissue inhibitors (TIMPs), adamalysines (ADAMs), as well as DNA- and RNA-based biomarkers, in OC. The presented results indicate the significant correlation between the CXCL12, CXCR4, CXCL8/CXCR2, M-CSF, MMP-2, MMP-9 ADAM17, ADAMTS-6, and CLDN7 levels and tumor stage, as well as the clinicopathological parameters of OC, such as the presence of lymph node and/or distant metastases. CXCL12, CXCL8/CXCR2, IL-6, TIMP-2, ADAM9, and ADAMTS-6 were prognostic factors for the overall survival of OC patients. Furthermore, IL-6, CXCR4, CXCL8, and MMP-9 indicate higher diagnostic utility based on the area under the ROC curve (AUC) than well-established OC tumor markers, whereas CLDN18.2 can be used in novel targeted therapies for OC patients. Full article
(This article belongs to the Special Issue Cancer Biology: From Genetic Aspects to Treatment)
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Other

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8 pages, 514 KiB  
Hypothesis
Alpha Satellite DNA in Targeted Drug Therapy for Prostate Cancer
by Isidoro Feliciello and Đurđica Ugarković
Int. J. Mol. Sci. 2023, 24(21), 15585; https://doi.org/10.3390/ijms242115585 - 25 Oct 2023
Viewed by 975
Abstract
Prostate cancer is the most common solid cancer in men and, despite the development of many new therapies, metastatic castration-resistant prostate cancer still remains a deadly disease. Therefore, novel concepts for the treatment of metastatic prostate cancer are needed. In our opinion, the [...] Read more.
Prostate cancer is the most common solid cancer in men and, despite the development of many new therapies, metastatic castration-resistant prostate cancer still remains a deadly disease. Therefore, novel concepts for the treatment of metastatic prostate cancer are needed. In our opinion, the role of the non-coding part of the genome, satellite DNA in particular, has been underestimated in relation to diseases such as cancer. Here, we hypothesise that this part of the genome should be considered as a potential target for the development of new drugs. Specifically, we propose a novel concept directed at the possible treatment of metastatic prostate cancer that is mostly based on epigenetics. Namely, metastatic prostate cancer is characterized by the strongly induced transcription of alpha satellite DNA located in pericentromeric heterochromatin and, according to our hypothesis, the stable controlled transcription of satellite DNA might be important in terms of the control of disease development. This can be primarily achieved through the epigenetic regulation of pericentromeric heterochromatin by using specific enzymes as well as their activators/inhibitors that could act as potential anti-prostate cancer drugs. We believe that our concept is innovative and should be considered in the potential treatment of prostate cancer in combination with other more conventional therapies. Full article
(This article belongs to the Special Issue Cancer Biology: From Genetic Aspects to Treatment)
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