Special Issue "Molecular Profiling of Lung Cancer"

A special issue of Cancers (ISSN 2072-6694).

Deadline for manuscript submissions: 31 March 2019

Special Issue Editor

Guest Editor
Dr. Kentaro Inamura

Division of Pathology, The Cancer Institute, Japanese Foundation for Cancer Research, 3-8-31 Ariake, Koto-ku, Tokyo 135-8550, Japan
Website | E-Mail
Interests: molecular/surgical pathology; lung cancer; urological (kidney, prostate, urinary bladder) cancer; colorectal cancer; microRNA; non-coding RNA

Special Issue Information

Dear Colleagues,

High-throughput technologies have enabled the molecular profiling of lung cancer, allowing for refined risk assessments, as well as the development of non-invasive screening methods or therapeutic interventions for lung cancer. The objective of this Special Issue is to publish the latest findings in the molecular profiling/signatures of lung cancer aimed toward clinical implementation.

Topics of this Special Issue include, but are not limited to:

  • Molecular profiling/signatures that can classify lung cancers into specific subtypes with different clinical outcomes or sensitivities to specific treatments (e.g., molecular-targeted therapy, immune checkpoint inhibitor, neoadjuvant chemotherapy, and so forth). Molecular characteristics related to sensitivity to immunotherapy are of interest.
  • Molecular profiling/characterization of specific lung cancer subtypes: Adenocarcinoma with specific driver mutations may develop, progress, or metastasize via specific molecular pathways.
  • Molecular profiling/signatures that allow the determination of useful biomarkers for liquid biopsy. Liquid biopsy is an emerging and promising non-invasive screening method.
  • Molecular profiling/signatures that allow the determination of key molecules in specific pathways (e.g., downstream pathway of multiple classes of growth factor receptors).
  • Molecular profiling/signatures that allow the determination of biomarkers for specific clinicopathological characteristics (e.g., clinical outcomes).
  • Molecular profiling/signatures that allow the determination of biomarkers for acquired resistance to specific drugs (e.g., tyrosine kinase inhibitors, immune checkpoint inhibitors, and so forth).
  • Molecular profiling/signatures of the normal-looking lung tissue surrounding the lung cancer (field cancerization).

Target topics (examples are described above) are comprehensive and will give a thorough view of the increasing knowledge of molecular profiling/signatures of lung cancer.

Dr. Kentaro Inamura
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. Cancers is an international peer-reviewed open access monthly 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.

Published Papers (4 papers)

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Research

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Open AccessArticle Liquid Biopsies in Lung Cancer: Four Emerging Technologies and Potential Clinical Applications
Cancers 2019, 11(3), 331; https://doi.org/10.3390/cancers11030331
Received: 1 February 2019 / Accepted: 28 February 2019 / Published: 7 March 2019
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Abstract
Background: Liquid biopsies offer a promising alternative to tissue samples, providing non-invasive diagnostic approaches or serial monitoring of disease evolution. However, certain challenges remain, and the full potential of liquid biopsies has yet to be reached. Here we report several methodological approaches to [...] Read more.
Background: Liquid biopsies offer a promising alternative to tissue samples, providing non-invasive diagnostic approaches or serial monitoring of disease evolution. However, certain challenges remain, and the full potential of liquid biopsies has yet to be reached. Here we report several methodological approaches to interrogate liquid biopsies using circulating tumour cell (CTC) enumeration and characterisation, transcriptomics, Raman spectroscopy, and copy number instability (CNI) scores using blood samples of lung cancer (LC) patients. Methods: We choose LC; since it still is the most common cause of cancer-related mortality worldwide, and therefore there is a need for development of new non-invasive diagnostic/prognostic technologies. Changes in gene expression were assessed using RNA-seq, and in CTCs using ImageStream, an imaging flow-cytometer. CNI scores, from paired tissue/ctDNA were also explored. Raman spectroscopy was used to provide chemical fingerprints of plasma samples. Results: CTCs were detected in all LC patients (n = 10). We observed a significant increase in CTC levels in LC patients (n = 10) compared to controls (n = 21). A similar CNI was noted in the tissue and plasma of 2 patients, where higher CNI scores corresponded with poorer outcome. Significant changes in Raman spectra (carotenoid concentrations) were noted in LC patients (n = 20) compared to controls (n = 10). RNA-seq revealed differential expression of 21 genes between LC cases and controls in both LC tissue and blood samples. Conclusions: Liquid biopsies can potentially provide a more comprehensive picture of the disease compared to a single tissue biopsy. CTC enumeration is feasible and sensitive for LC patients. Molecular profiling of CTCs is also possible from total blood. CNI scores and Raman spectra require further investigation. Further work is being undertaken to explore these methods of detection in a larger LC cohort. Full article
(This article belongs to the Special Issue Molecular Profiling of Lung Cancer)
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Open AccessArticle Transfer of Extracellular Vesicle-Associated-RNAs Induces Drug Resistance in ALK-Translocated Lung Adenocarcinoma
Cancers 2019, 11(1), 104; https://doi.org/10.3390/cancers11010104
Received: 11 December 2018 / Revised: 11 January 2019 / Accepted: 14 January 2019 / Published: 17 January 2019
Cited by 1 | PDF Full-text (7139 KB) | HTML Full-text | XML Full-text | Supplementary Files
Abstract
Anaplastic lymphoma kinase (ALK) translocation is an actionable mutation in lung adenocarcinoma. Nonetheless tumour consists of heterogeneous cell subpopulations with diverse phenotypes and genotypes, and cancer cells can actively release extracellular vesicles (EVs) to modulate the phenotype of other cells in [...] Read more.
Anaplastic lymphoma kinase (ALK) translocation is an actionable mutation in lung adenocarcinoma. Nonetheless tumour consists of heterogeneous cell subpopulations with diverse phenotypes and genotypes, and cancer cells can actively release extracellular vesicles (EVs) to modulate the phenotype of other cells in the tumour microenvironment. We hypothesized that EVs derived from a drug-resistant subpopulation of cells could induce drug resistance in recipient cells. We have established ALK-translocated lung adenocarcinoma cell lines and subclones. The subclones have been characterized and the expression of EV-RNAs determined by quantitative polymerase chain reaction. The effects of EV transfer on drug resistance were examined in vitro. Serum EV-RNA was assayed serially in two patients prescribed ALK-tyrosine kinase inhibitor (ALK-TKI) treatment. We demonstrated that the EVs from an ALK-TKI-resistant subclone could induce drug resistance in the originally sensitive subclone. EV-RNA profiling revealed that miRNAs miR-21-5p and miR-486-3p, and lncRNAs MEG3 and XIST were differentially expressed in the EVs secreted by the resistant subclones. These circulating EV-RNA levels have been found to correlate with disease progression of EML4-ALK-translocated lung adenocarcinoma in patients prescribed ALK-TKI treatment. The results from this study suggest that EVs released by a drug-resistant subpopulation can induce drug resistance in other subpopulations and may sustain intratumoural heterogeneity. Full article
(This article belongs to the Special Issue Molecular Profiling of Lung Cancer)
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Review

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Open AccessReview Brain Metastases from Lung Cancer: Is MET an Actionable Target?
Cancers 2019, 11(3), 271; https://doi.org/10.3390/cancers11030271
Received: 15 January 2019 / Revised: 6 February 2019 / Accepted: 21 February 2019 / Published: 26 February 2019
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Abstract
The process of metastatic dissemination begins when malignant cells start to migrate and leave the primary mass. It is now known that neoplastic progression is associated with a combination of genetic and epigenetic events. Cancer is a genetic disease and this pathogenic concept [...] Read more.
The process of metastatic dissemination begins when malignant cells start to migrate and leave the primary mass. It is now known that neoplastic progression is associated with a combination of genetic and epigenetic events. Cancer is a genetic disease and this pathogenic concept is the basis for a new classification of tumours, based precisely on the presence of definite genetic lesions to which the clones are addicted. Regarding the scatter factor receptors MET and Recepteur d’Origin Nantais (RON), it is recognised that MET is an oncogene necessary for a narrow subset of tumours (MET-addicted) while it works as an adjuvant metastogene for many others. This notion highlights that the anti-MET therapy can be effective as the first line of intervention in only a few MET-addicted cases, while it is certainly more relevant to block MET in cases of advanced neoplasia that exploit the activation of the invasive growth program to promote dissemination in other body parts. Few data are instead related to the role played by RON, a receptor homologous to MET. We have already demonstrated an implication of MET and RON genes in brain metastases from lung cancer. On this basis, the aim of this work is to recapitulate and dissect the molecular basis of metastatic brain dissemination from lung cancer. The latter is among the big killers and frequently gives rise to brain metastases, most often discovered at diagnosis. Molecular mechanisms leading to tumour spread to the brain are mostly unknown and in turn these tragic cases are still lacking effective therapies. Based on previously published data from our group, we aim to summarise and analyse the pathogenic mechanisms leading to activation of the scatter factor receptor in brain metastatic lesions of lung primaries, from the point of view of replacing the currently used empirical treatment with a more targeted approach. Full article
(This article belongs to the Special Issue Molecular Profiling of Lung Cancer)
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Open AccessReview The Role of Molecular Profiling to Predict the Response to Immune Checkpoint Inhibitors in Lung Cancer
Cancers 2019, 11(2), 201; https://doi.org/10.3390/cancers11020201
Received: 18 December 2018 / Revised: 17 January 2019 / Accepted: 23 January 2019 / Published: 10 February 2019
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Abstract
Immune checkpoint inhibitors radically changed the treatment of patients with non-small cell lung cancer (NSCLC). However, only one-quarter of patients benefit from these new therapies when used as monotherapy. The assessment of Program Death Ligand-1 (PD-L1) tumor expression by immunohistochemistry is used to [...] Read more.
Immune checkpoint inhibitors radically changed the treatment of patients with non-small cell lung cancer (NSCLC). However, only one-quarter of patients benefit from these new therapies when used as monotherapy. The assessment of Program Death Ligand-1 (PD-L1) tumor expression by immunohistochemistry is used to select potential responder patients, but this not an optimal marker since it does not predict the absence of anti PD-1 efficacy. Despite this shortcoming, PD-L1 remains the gold standard biomarker in many studies and the only biomarker available for clinicians. In addition to histological markers, transcriptomic and exome analyses have revealed potential biomarkers requiring further confirmation. Recently, tumor mutational burden has emerged as a good surrogate marker of outcome. In this review we will detail current knowledge on DNA and RNA related biomarkers. Full article
(This article belongs to the Special Issue Molecular Profiling of Lung Cancer)
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