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Molecular Genetics of Tumor Heterogeneity
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Molecular Genetics of Tumor Heterogeneity

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

Deadline for manuscript submissions: closed (31 January 2021) | Viewed by 8354

Special Issue Editor

Prof. Dr. Pavel Sumazin

E-Mail Website
Guest Editor
Baylor College of Medicine, Houston, TX 77030, USA
Interests: computational biology; bioinformatics

Special Issue Information

Dear Colleagues,

Tumor heterogeneity is a major roadblock to the success of targeted cancer treatments. Recent work in this area suggests that treatments have variable effects on tumor subregions and subclones, suggesting that methods to target all tumor subclones are necessary for successful treatment. More research is needed in order to study the genetic, epigenetic, and cellular diversity of cancers and the influence of this diversity on existing and experimental cancer therapies. Moreover, methods to investigate tumor heterogeneity at the point of care, for each individual patient, are needed to supplement other efforts in personalized oncology. In order to advance the field, research progress and new methods and techniques will be required, including new computational models, biopsy techniques, and analysis methods, as well as large-scale studies of tumor heterogeneity. We seek to aggregate contributions that focus on technological and methodological advances related to improving our understanding of tumor heterogeneity, its effects on tumors and therapies, and the potential place of associated technologies within a personalized-oncology toolset.

Prof. Pavel Sumazin
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.

Published Papers (3 papers)

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Research

15 pages, 18186 KiB  
Article
Time-Resolved scRNA-Seq Tracks the Adaptation of a Sensitive MCL Cell Line to Ibrutinib Treatment
by Viktoria Fuhr, Ehsan Vafadarnejad, Oliver Dietrich, Panagiota Arampatzi, Angela Riedel, Antoine-Emmanuel Saliba, Andreas Rosenwald and Hilka Rauert-Wunderlich
Int. J. Mol. Sci. 2021, 22(5), 2276; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22052276 - 25 Feb 2021
Cited by 4 | Viewed by 3730
Abstract
Since the approval of ibrutinib for relapsed/refractory mantle cell lymphoma (MCL), the treatment of this rare mature B-cell neoplasm has taken a great leap forward. Despite promising efficacy of the Bruton tyrosine kinase inhibitor, resistance arises inevitably and the underlying mechanisms remain to [...] Read more.
Since the approval of ibrutinib for relapsed/refractory mantle cell lymphoma (MCL), the treatment of this rare mature B-cell neoplasm has taken a great leap forward. Despite promising efficacy of the Bruton tyrosine kinase inhibitor, resistance arises inevitably and the underlying mechanisms remain to be elucidated. Here, we aimed to decipher the response of a sensitive MCL cell line treated with ibrutinib using time-resolved single-cell RNA sequencing. The analysis uncovered five subpopulations and their individual responses to the treatment. The effects on the B cell receptor pathway, cell cycle, surface antigen expression, and metabolism were revealed by the computational analysis and were validated by molecular biological methods. The observed upregulation of B cell receptor signaling, crosstalk with the microenvironment, upregulation of CD52, and metabolic reprogramming towards dependence on oxidative phosphorylation favor resistance to ibrutinib treatment. Targeting these cellular responses provide new therapy options in MCL. Full article
(This article belongs to the Special Issue Molecular Genetics of Tumor Heterogeneity)
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12 pages, 2387 KiB  
Article
Unproductive Effects of ALK Gene Amplification and Copy Number Gain in Non-Small-Cell Lung Cancer. ALK Gene Amplification and Copy Gain in NSCLC
by Federica Zito Marino, Gerardo Botti, Gabriella Aquino, Stefano Ferrero, Gabriella Gaudioso, Alessandro Palleschi, Danilo Rocco, Rosario Salvi, Maria Carolina Micheli, Pietro Micheli, Alessandro Morabito, Gaetano Rocco, Antonio Giordano, Rossella De Cecio and Renato Franco
Int. J. Mol. Sci. 2020, 21(14), 4927; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms21144927 - 12 Jul 2020
Cited by 7 | Viewed by 2263
Abstract
Background: The Anaplastic Lymphoma Kinase (ALK) gene is known to be affected by several genetic alterations, such as rearrangement, amplification and point mutation. The main goal of this study was to comprehensively analyze ALK amplification (ALK-A) and ALK gene copy number [...] Read more.
Background: The Anaplastic Lymphoma Kinase (ALK) gene is known to be affected by several genetic alterations, such as rearrangement, amplification and point mutation. The main goal of this study was to comprehensively analyze ALK amplification (ALK-A) and ALK gene copy number gain (ALK-CNG) in a large cohort of non-small-cell lung cancer (NSCLC) patients in order to evaluate the effects on mRNA and protein expression. Methods: ALK locus number status was evaluated in 578 NSCLC cases by fluorescence in situ hybridization (FISH). In addition, ALK immunohistochemistry and ALK mRNA in situ hybridization were performed. Results: Out of 578 cases, 17 cases showed ALK-A. In addition, 14 cases presented ALK-CNG and 72 cases presented chromosome 2 polyploidy. None of those carrying ALK-A and -CNG showed either ALK immunohistochemical expression or ALK mRNA expression through in situ hybridization. We observed a high frequency of extra copies of the ALK gene. Conclusions: Our findings demonstrated that ALK-A is not involved in mRNA production and consequently is not involved in protein production; these findings support the hypothesis that ALK-A might not play a role in the pathogenesis of NSCLC, underlining the absence of a specific clinical application. Full article
(This article belongs to the Special Issue Molecular Genetics of Tumor Heterogeneity)
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12 pages, 1770 KiB  
Article
Genomic Biomarkers of Survival in Patients with Adenocarcinoma of the Uterine Cervix Receiving Chemoradiotherapy
by Ying-Chun Lin, Yu-Chia Chen, Rui-Yun Chen, Yi-Xuan Huang, Siang-Jyun Tu, Ji-An Liang, Yao-Ching Hung, Lian-Shung Yeh, Wei-Chun Chang, Wu-Chou Lin, Yin-Yi Chang, Shang-Wen Chen and Jan-Gowth Chang
Int. J. Mol. Sci. 2020, 21(11), 4117; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms21114117 - 09 Jun 2020
Cited by 2 | Viewed by 1968
Abstract
This study investigated the prognostic effects of genomic biomarkers for predicting chemoradiotherapy (CRT)-based treatment outcomes in patients with adenocarcinoma (AC) of the uterine cervix. In all, 21 patients receiving definitive CRT were included. In accordance with the International Federation of Gynecology and Obstetrics [...] Read more.
This study investigated the prognostic effects of genomic biomarkers for predicting chemoradiotherapy (CRT)-based treatment outcomes in patients with adenocarcinoma (AC) of the uterine cervix. In all, 21 patients receiving definitive CRT were included. In accordance with the International Federation of Gynecology and Obstetrics (FIGO) staging system, 5, 8, and 8 patients were classified as having stage IB3, II, and III disease, respectively. Pretreatment biomarkers were analyzed using tissue microarrays from biopsy specimens. Genomic alterations were examined by next-generation sequencing (NGS). The outcome endpoints were disease-free survival (DFS), distant metastasis-free survival (DMFS), and local relapse-free survival (LRFS). A Cox regression model was used to examine the prognostic effects of the biomarkers and clinical parameters. The presence of myeloid cell leukemia-1 (MCL1) gene amplification and a lower immunohistochemical (IHC) marker of tumor necrotic factor alpha (TNF-α) H-score were two prognostic factors for inferior DFS. The four-year DFS was 28% and 68% for patients with or without MCL1 copy number gain, respectively (p = 0.028). In addition, MCL1 amplification predicted poor DMFS. A lower tumor mutation number (TMN) calculated from nonsynonymous mutations was associated with lower LRFS. For patients with adenocarcinoma of the uterine cervix receiving definitive CRT, prognostic information can be supplemented by MCL1 amplification, the TMN, and the TNF-α H score. Full article
(This article belongs to the Special Issue Molecular Genetics of Tumor Heterogeneity)
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