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Special Issue "Molecular Pathology of Lung and Thoracic Cancers"

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: 31 August 2019.

Special Issue Editor

Guest Editor
Dr. Ayumu Taguchi

Translational Molecular Pathology, The University of Texas MD Anderson Cancer Center, 2130 W. Holcomb Blvd., Houston, TX 77030, USA
Website | E-Mail
Interests: biomarker; lung cancer; gastrointestinal cancer; proteomics; microRNA; exosome

Special Issue Information

Dear Colleagues,

Lung cancer is the most common type of thoracic cancer, making the most lethal cancer worldwide. Despite improvements in early detection, surgical treatment, systemic therapy, and radiotherapy, most patients with thoracic cancer are diagnosed at an advanced stage and have a poor prognosis.

Recent advances in molecular profiling technologies have dramatically deepened our understanding of cancer biology, and opened up novel approaches to detect molecular alteration as biomarkers in DNA, RNA, microRNA/long non-coding RNA, proteins, metabolites, exosomes, and circulating tumor cells, using a variety of biospecimens, such as tissue, blood, urine, sputum, and saliva. Molecular biomarkers can be used in multiple clinical settings, including risk assessment, screening, early detection, differential diagnosis, determination of prognosis, therapy selection, prediction of response/toxicity to treatment, and monitoring of reccurence/progression, and have potential to bring about a paradigm shift in current practice and improvement of lung cancer survival.

The scope of this Special Issue is to attract original research as well as review articles describing all aspects of tissue- or biofluid-based molecular biomarkers of lung cancer and other types of thoracic cancer, including thymic tumors and mesothelioma. Potential topics include but are not limited to the following: discovery and/or validation of diagnostic, prognostic, and therapeutic molecular biomarkers; method development for data acquisition and analysis; statistical and bioinformatic approaches to biomarker discovery and development of omics-based signatures; and integration and development of biomarker model.

Dr. Ayumu Taguchi
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 papers will be 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. The Article Processing Charge (APC) for publication in this open access journal is 1800 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

  • lung cancer
  • thoracic cancer
  • precision medicine
  • molecular biomarkers
  • molecular pathology
  • liquid biopsy
  • DNA mutation
  • DNA methylation
  • genome-wide association studies
  • single nucleotide polymorphism
  • gene expression
  • in situ hybridization
  • microRNA
  • long non-coding RNA
  • protein
  • immunohistochemistry
  • post-translational modifications
  • autoantibody
  • cytokine/chemokine
  • metabolite
  • exosome
  • circulating tumor cells
  • genomics
  • epigenomics
  • transcriptomics
  • proteomics
  • metabolomics
  • cell lines
  • mouse models

Published Papers (4 papers)

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Research

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Open AccessArticle
Male-Specific Long Noncoding RNA TTTY15 Inhibits Non-Small Cell Lung Cancer Proliferation and Metastasis via TBX4
Int. J. Mol. Sci. 2019, 20(14), 3473; https://doi.org/10.3390/ijms20143473
Received: 19 June 2019 / Revised: 11 July 2019 / Accepted: 13 July 2019 / Published: 15 July 2019
PDF Full-text (2315 KB) | HTML Full-text | XML Full-text | Supplementary Files
Abstract
Gender affects cancer susceptibility. Currently, there are only a few studies on Y chromosome-linked long noncoding RNAs (lncRNAs), and the potential association between lncRNAs and cancers in males has not been fully elucidated. Here, we examined the expression of testis-specific transcript Y-linked 15 [...] Read more.
Gender affects cancer susceptibility. Currently, there are only a few studies on Y chromosome-linked long noncoding RNAs (lncRNAs), and the potential association between lncRNAs and cancers in males has not been fully elucidated. Here, we examined the expression of testis-specific transcript Y-linked 15 (TTTY15) in 37 males with non-small cell lung cancer (NSCLC), and performed circular chromosome conformation capture with next-generation sequencing to determine the genomic interaction regions of the TTTY15 gene. Our results showed that the expression levels of TTTY15 were lower in NSCLC tissues. Lower TTTY15 expression levels were associated with Tumor-Node-Metastasis (TNM) stage. A TTTY15 knockdown promoted malignant transformation of NSCLC cells. Based on the bioinformatics analysis of circular chromosome conformation capture data, we found that T-box transcription factor 4 (TBX4) may be a potential target gene of TTTY15. The RNA immunoprecipitation and chromatin immunoprecipitation results showed that TTTY15 may interact with DNA (cytosine-5)-methyltransferase 3A (DNMT3A), and the TTTY15 knockdown increased the binding of DNMT3A to the TBX4 promoter. We concluded that low TTTY15 expression correlates with worse prognosis among patients with NSCLC. TTTY15 promotes TBX4 expression via DNMT3A-mediated regulation. The identification of lncRNAs encoded by male-specific genes may help to identify potential targets for NSCLC therapy. Full article
(This article belongs to the Special Issue Molecular Pathology of Lung and Thoracic Cancers)
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Graphical abstract

Open AccessArticle
Oncogenic Effect of the Novel Fusion Gene VAPA-Rab31 in Lung Adenocarcinoma
Int. J. Mol. Sci. 2019, 20(9), 2309; https://doi.org/10.3390/ijms20092309
Received: 25 April 2019 / Revised: 8 May 2019 / Accepted: 8 May 2019 / Published: 10 May 2019
PDF Full-text (3466 KB) | HTML Full-text | XML Full-text | Supplementary Files
Abstract
Fusion genes have been identified as oncogenes in several solid tumors including lung, colorectal, and stomach cancers. Here, we characterized the fusion gene, VAPA-Rab31, discovered from RNA-sequencing data of a patient with lung adenocarcinoma who did not harbor activating mutations in EGFR [...] Read more.
Fusion genes have been identified as oncogenes in several solid tumors including lung, colorectal, and stomach cancers. Here, we characterized the fusion gene, VAPA-Rab31, discovered from RNA-sequencing data of a patient with lung adenocarcinoma who did not harbor activating mutations in EGFR, KRAS and ALK. This fusion gene encodes a protein comprising the N-terminal region of vesicle-associated membrane protein (VAMP)-associated protein A (VAPA) fused to the C-terminal region of Ras-related protein 31 (Rab31). Exogenous expression of VAPA-Rab31 in immortalized normal bronchial epithelial cells demonstrated the potential transforming effects of this fusion gene, including increased colony formation and cell proliferation in vitro. Also, enhanced tumorigenicity upon VAPA-Rab31 was confirmed in vivo using a mouse xenograft model. Metastatic tumors were also detected in the liver and lungs of xenografted mice. Overexpression of VAPA-Rab31 upregulated anti-apoptotic protein Bcl-2 and phosphorylated CREB both in cells and xenograft tumors. Reduced apoptosis and increased phosphorylation of CREB and Erk were observed in VAPA-Rab31-overexpressing cells after bortezomib treatment. Elevated Bcl-2 level via activated CREB contributed to the resistance to the bortezomib-induced apoptosis. Our data suggest the oncogenic function of the novel fusion gene VAPA-Rab31 via upregulated Bcl-2 and activated CREB in lung cancer. Full article
(This article belongs to the Special Issue Molecular Pathology of Lung and Thoracic Cancers)
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Figure 1

Open AccessArticle
Epigenetic Suppression of the T-box Subfamily 2 (TBX2) in Human Non-Small Cell Lung Cancer
Int. J. Mol. Sci. 2019, 20(5), 1159; https://doi.org/10.3390/ijms20051159
Received: 21 January 2019 / Revised: 15 February 2019 / Accepted: 18 February 2019 / Published: 7 March 2019
Cited by 1 | PDF Full-text (3539 KB) | HTML Full-text | XML Full-text | Supplementary Files
Abstract
(1) The TBX2 subfamily of transcription factors (TBXs 2, 3, 4 and 5) are markedly down-regulated in human non-small cell lung cancer (NSCLC) and exert tumor suppressor effects in lung malignancy. Yet, mechanisms underlying suppressed expression of the TBX2 subfamily in [...] Read more.
(1) The TBX2 subfamily of transcription factors (TBXs 2, 3, 4 and 5) are markedly down-regulated in human non-small cell lung cancer (NSCLC) and exert tumor suppressor effects in lung malignancy. Yet, mechanisms underlying suppressed expression of the TBX2 subfamily in NSCLC are elusive. Here, we interrogated probable epigenetic mechanisms in suppressed expression of the TBX2 subfamily in human NSCLC. (2) TBX2 subfamily gene expression and methylation levels in NSCLC and normal lung tissues were surveyed using publicly available RNA-sequence and genome-wide methylation datasets. Methylation β-values of the four genes were statistically compared between NSCLCs and normal lung tissues, correlated with gene expression levels, and interrogated with clinicopathological variables. Expression and methylation levels of TBXs were quantified in NSCLC cells using real-time PCR and methylation-specific PCR assays, respectively. Effects of the DNA methyltransferase inhibitor 5-azacytidine (Aza) on TBX2 subfamily expression were assessed in NSCLC cells. Impact of TBX2 subfamily expression on Aza-treated cells was evaluated by RNA interference. (3) All four TBXs were significantly hypermethylated in NSCLCs relative to normal lung tissues (p < 0.05). Methylation β-values of the genes, with exception of TBX2, were significantly inversely correlated with corresponding mRNA expression levels (p < 0.05). We found no statistically significant differences in hypermethylation levels of the TBX2 subfamily by clinicopathological features including stage and tobacco history. Expression levels of the TBX genes were overall suppressed in NSCLC cells relative to normal alveolar cells. Members of the subfamily were significantly hypermethylated in all tested NSCLC cell lines relative to normal alveolar cells. Treatment with Aza induced the expression of the TBX2 subfamily concomitant with NSCLC cell growth inhibition. Further, simultaneous knockdown of the four TBX genes markedly reduced anti-growth effects of Aza in NSCLC cells. (4) Our study sheds light on new epigenetic profiles in the molecular pathogenesis of human NSCLC. Full article
(This article belongs to the Special Issue Molecular Pathology of Lung and Thoracic Cancers)
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Review

Jump to: Research

Open AccessReview
The Roles of MicroRNA in Lung Cancer
Int. J. Mol. Sci. 2019, 20(7), 1611; https://doi.org/10.3390/ijms20071611
Received: 30 November 2018 / Revised: 11 March 2019 / Accepted: 26 March 2019 / Published: 31 March 2019
Cited by 1 | PDF Full-text (840 KB) | HTML Full-text | XML Full-text
Abstract
Lung cancer is the most devastating malignancy in the world. Beyond genetic research, epigenomic studies—especially investigations of microRNAs—have grown rapidly in quantity and quality in the past decade. This has enriched our understanding about basic cancer biology and lit up the opportunities for [...] Read more.
Lung cancer is the most devastating malignancy in the world. Beyond genetic research, epigenomic studies—especially investigations of microRNAs—have grown rapidly in quantity and quality in the past decade. This has enriched our understanding about basic cancer biology and lit up the opportunities for potential therapeutic development. In this review, we summarize the involvement of microRNAs in lung cancer carcinogenesis and behavior, by illustrating the relationship to each cancer hallmark capability, and in addition, we briefly describe the clinical applications of microRNAs in lung cancer diagnosis and prognosis. Finally, we discuss the potential therapeutic use of microRNAs in lung cancer. Full article
(This article belongs to the Special Issue Molecular Pathology of Lung and Thoracic Cancers)
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Figure 1

Int. J. Mol. Sci. EISSN 1422-0067 Published by MDPI AG, Basel, Switzerland RSS E-Mail Table of Contents Alert
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