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From Bench to Bedside: Advances in Non-small Cell Lung Cancer...
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From Bench to Bedside: Advances in Non-small Cell Lung Cancer in the Era of Precision Oncology

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Cancer Biology and Oncology".

Deadline for manuscript submissions: closed (30 April 2025) | Viewed by 3942

Special Issue Editor

Dr. Iyare Izevbaye

E-Mail Website
Guest Editor
Department of Patholog & Laboratory Medicine, Emory University, Atlanta, GA, USA
Interests: non-small cell lung cancer; liquid biopsy; comprehensive genomic profiling

Special Issue Information

Dear Colleagues,

Non-small-cell lung cancer (NSCLC) is a leading cause of cancer-related mortality worldwide. Recent progress in the understanding of molecular mechanisms of NSCLC initiation and progression has led to the identification of novel biomarkers for diagnosis and therapy. A better understanding of the interplay between intrinsic cancer cell mechanisms and the extrinsic tumor microenvironment is a gateway towards innovation and biomarker development in immune checkpoint inhibition (ICI) therapy. Advances in next-generation sequencing have made comprehensive genomic profiling (CGP) a mainstay for therapy selection. Techniques such as liquid biopsy in the management of NSCLC enable the noninvasive acquisition of diagnostic and surveillance samples with reduced patient morbidity and cost to the healthcare system. The use of diagnostic predictive modeling has further advanced the goals of precision medicine.

This Special Issue on NSCLC aims to highlight recent advances from bench-to-bedside research in NSCLC in the era of genomics and precision medicine. We seek original basic and translational studies and review articles in NSCLC pathogenesis, biomarker discovery, and development and laboratory genomic medicine. The scope of this Special Issue includes the following:

  1. Advances in the molecular pathogenesis of NSCLC.
  2. Advances in molecular methods for NSCLC diagnosis, including CGP.
  3. Identification of novel biomarkers and predictive machine learning modeling of molecular biomarkers, targeted therapy, and ICI therapy for risk stratification and patient outcomes.
  4. Advances in liquid biopsy in NSCLC.

Dr. Iyare Izevbaye
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. Biomedicines 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 2600 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

  • non-small-cell lung cancer
  • precision medicine
  • liquid biopsy
  • biomarkers
  • predictive modeling
  • comprehensive genomic profiling
  • biomarkers
  • immuno-oncology
  • lung cancer biology

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Published Papers (2 papers)

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Research

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17 pages, 7844 KiB  
Article
TGM2-Mediated Autophagy Contributes to the Radio-Resistance of Non-Small Cell Lung Cancer Stem-like Cells
by Qian Wang, Qiuning Zhang, Xiaohu Wang, Hongtao Luo, Tianqi Du, Luyao Wu, Mingyu Tan, Yanliang Chen, Xun Wu, Shilong Sun, Zhiqiang Liu, Yi Xie and Wenzhen Yuan
Biomedicines 2024, 12(10), 2231; https://doi.org/10.3390/biomedicines12102231 - 30 Sep 2024
Cited by 1 | Viewed by 1388
Abstract
Objectives: Cancer cells with ‘stemness’ are generally resistant to chemoradiotherapy. This study aims to compare the differences in radiation sensitivity of A549 and CD44+A549 stem-like cells to X-rays and carbon ion radiation (C-ions), and to find a target that can [...] Read more.
Objectives: Cancer cells with ‘stemness’ are generally resistant to chemoradiotherapy. This study aims to compare the differences in radiation sensitivity of A549 and CD44+A549 stem-like cells to X-rays and carbon ion radiation (C-ions), and to find a target that can kill cancer stem-like cells (CSCs) of non-small cell lung cancer (NSCLC). Methods: The study used two cell lines (A549 and CD44+A549). The tumorigenicity of cells was tested with animal experiments. The cells were irradiated with X-rays and C-ions. Cell viability was detected using the CCK-8 and EdU assay. A liquid chromatograph-mass spectrometer (LC–MS) helped detect metabolic differences. Protein and mRNA expression were detected using a Western blot, reverse transcription-quantitative (RT-qPCR), and PCR array. The autophagic activity was monitored with a CYTO-ID® Autophagy Detection Kit 2.0. Immunofluorescence and co-immunoprecipitation helped to observe the localization and interaction relationships. Results: First, we verified the radio-resistance of CD44+A549 stem-like cells. LC-MS indicated the difference in autophagy between the two cells, followed by establishing a correlation between the radio-resistance and autophagy. Subsequently, the PCR array proved that TGM2 is significantly upregulated in CD44+A549 stem-like cells. Moreover, the TGM2 knockdown by small interfering RNA could decrease the radio-resistance of CD44+A549 cells. Bioinformatic analyses and experiments showed that TGM2 is correlated with the expression of CD44 and LC3B. Additionally, TGM2 could directly interact with LC3B. Conclusions: We established the CD44-TGM2-LC3 axis: CD44 mediates radio-resistance of CD44+A549 stem-like cells through TGM2 regulation of autophagy. Our study may provide new biomarkers and strategies to alleviate the radio-resistance of CSCs in NSCLC. Full article
(This article belongs to the Special Issue From Bench to Bedside: Advances in Non-small Cell Lung Cancer in the Era of Precision Oncology)
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Review

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30 pages, 1962 KiB  
Review
Personalizing Therapy Outcomes through Mitogen-Activated Protein Kinase Pathway Inhibition in Non-Small Cell Lung Cancer
by Hasan Alsharoh, Paul Chiroi, Ekaterina Isachesku, Radu Andrei Tanasa, Ovidiu-Laurean Pop, Radu Pirlog and Ioana Berindan-Neagoe
Biomedicines 2024, 12(7), 1489; https://doi.org/10.3390/biomedicines12071489 - 5 Jul 2024
Cited by 2 | Viewed by 1890
Abstract
Lung cancer (LC) is a highly invasive malignancy and the leading cause of cancer-related deaths, with non-small cell lung cancer (NSCLC) as its most prevalent histological subtype. Despite all breakthroughs achieved in drug development, the prognosis of NSCLC remains poor. The mitogen-activated protein [...] Read more.
Lung cancer (LC) is a highly invasive malignancy and the leading cause of cancer-related deaths, with non-small cell lung cancer (NSCLC) as its most prevalent histological subtype. Despite all breakthroughs achieved in drug development, the prognosis of NSCLC remains poor. The mitogen-activated protein kinase signaling cascade (MAPKC) is a complex network of interacting molecules that can drive oncogenesis, cancer progression, and drug resistance when dysregulated. Over the past decades, MAPKC components have been used to design MAPKC inhibitors (MAPKCIs), which have shown varying efficacy in treating NSCLC. Thus, recent studies support the potential clinical use of MAPKCIs, especially in combination with other therapeutic approaches. This article provides an overview of the MAPKC and its inhibitors in the clinical management of NSCLC. It addresses the gaps in the current literature on different combinations of selective inhibitors while suggesting two particular therapy approaches to be researched in NSCLC: parallel and aggregate targeting of the MAPKC. This work also provides suggestions that could serve as a potential guideline to aid future research in MAPKCIs to optimize clinical outcomes in NSCLC. Full article
(This article belongs to the Special Issue From Bench to Bedside: Advances in Non-small Cell Lung Cancer in the Era of Precision Oncology)
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