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The Role of Genetic and Epigenetic Aberrations in Cancer

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

Deadline for manuscript submissions: closed (16 November 2022) | Viewed by 5678

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Special Issue Editor

Dr. Matthias Wirth

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Guest Editor

Department of Hematology, Oncology and Tumor Immunology, Charité-Universitätsmedizin Berlin, Campus Benjamin Franklin, 12203 Berlin, Germany
Interests: functional genomics; therapy resistance; pancreatic cancer; multiple myeloma; cancer transcriptome variations; epigenetics; precision medicine

Special Issue Information

Dear Colleagues,

In recent decades, the combination of various high-throughput technologies and functional studies have identified and validated signaling pathways that are dysregulated in certain tumor types. Oncogenic mutations, genetic rearrangements, and epigenetic alterations leading to remodeled transcriptional activity and altered protein expression contribute to the malignant behavior of tumor cells. Genome-wide profiles of different tumor entities have revealed that similar mutations originally attributed to only one entity are also present in tumors at other anatomical sites. The identification of biomarkers and therapeutic targets have shown unprecedented efficacy in some cancers and marginal success in others. Thus, identifying patient subgroups that respond to molecular targeted therapies and elucidating primary resistance mechanisms by integrating molecular profiling and histopathological characteristics are important components to increase treatment efficacy and provide more precise therapeutic options.

In this Special Issue, original research articles and reviews are welcome. Research areas may include (but are not limited to) the following: biomarker identification, therapeutic efficacy in molecular subgroups, resistance mechanisms (primary and secondary), and epigenetic and genetic events contributing to tumorigenesis.

I look forward to receiving your contributions.

Dr. Matthias Wirth
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

molecular profiling
epigenetic alterations
cancer modeling
oncogenic signaling
targeted therapy
biomarker-driven therapy
treatment resistance (primary/secondary)

Published Papers (2 papers)

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Research

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21 pages, 4170 KiB

Open AccessArticle

Epigenetic Silencing of LRP2 Is Associated with Dedifferentiation and Poor Survival in Multiple Solid Tumor Types

by Martin Q. Rasmussen, Gitte Tindbæk, Morten Muhlig Nielsen, Camilla Merrild, Torben Steiniche, Jakob Skou Pedersen, Søren K. Moestrup, Søren E. Degn and Mette Madsen

Cancers 2023, 15(6), 1830; https://0-doi-org.brum.beds.ac.uk/10.3390/cancers15061830 - 17 Mar 2023

Cited by 1 | Viewed by 2166

Abstract

More than 80% of human cancers originate in epithelial tissues. Loss of epithelial cell characteristics are hallmarks of tumor development. Receptor-mediated endocytosis is a key function of absorptive epithelial cells with importance for cellular and organismal homeostasis. LRP2 (megalin) is the largest known endocytic membrane receptor and is essential for endocytosis of various ligands in specialized epithelia, including the proximal tubules of the kidney, the thyroid gland, and breast glandular epithelium. However, the role and regulation of LRP2 in cancers that arise from these tissues has not been delineated. Here, we examined the expression of LRP2 across 33 cancer types in The Cancer Genome Atlas. As expected, the highest levels of LRP2 were found in cancer types that arise from LRP2-expressing absorptive epithelial cells. However, in a subset of tumors from these cancer types, we observed epigenetic silencing of LRP2. LRP2 expression showed a strong inverse correlation to methylation of a specific CpG site (cg02361027) in the first intron of the LRP2 gene. Interestingly, low expression of LRP2 was associated with poor patient outcome in clear cell renal cell carcinoma, papillary renal cell carcinoma, mesothelioma, papillary thyroid carcinoma, and invasive breast carcinoma. Furthermore, loss of LRP2 expression was associated with dedifferentiated histological and molecular subtypes of these cancers. These observations now motivate further studies on the functional role of LRP2 in tumors of epithelial origin and the potential use of LRP2 as a cancer biomarker. Full article

(This article belongs to the Special Issue The Role of Genetic and Epigenetic Aberrations in Cancer)

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Review

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18 pages, 1107 KiB

Open AccessReview

Genetic Clonality as the Hallmark Driving Evolution of Non-Small Cell Lung Cancer

by Marcin Nicoś and Paweł Krawczyk

Cancers 2022, 14(7), 1813; https://0-doi-org.brum.beds.ac.uk/10.3390/cancers14071813 - 02 Apr 2022

Cited by 4 | Viewed by 3049

Abstract

Data indicate that many driver alterations from the primary tumor of non-small cell lung cancer (NSCLC) are predominantly shared across all metastases; however, disseminating cells may also acquire a new genetic landscape across their journey. By comparing the constituent subclonal mutations between pairs of primary and metastatic samples, it is possible to derive the ancestral relationships between tumor clones, rather than between tumor samples. Current treatment strategies mostly rely on the theory that metastases are genetically similar to the primary lesions from which they arise. However, intratumor heterogeneity (ITH) affects accurate diagnosis and treatment decisions and it is considered the main hallmark of anticancer therapy failure. Understanding the genetic changes that drive the metastatic process is critical for improving the treatment strategies of this deadly condition. Application of next generation sequencing (NGS) techniques has already created knowledge about tumorigenesis and cancer evolution; however, further NGS implementation may also allow to reconstruct phylogenetic clonal lineages and clonal expansion. In this review, we discuss how the clonality of genetic alterations influence the seeding of primary and metastatic lesions of NSCLC. We highlight that wide genetic analyses may reveal the phylogenetic trajectories of NSCLC evolution, and may pave the way to better management of follow-up and treatment. Full article

(This article belongs to the Special Issue The Role of Genetic and Epigenetic Aberrations in Cancer)

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