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Cancers
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Lung Cancer—Molecular Insights and Targeted Therapies (Volume II)
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Lung Cancer—Molecular Insights and Targeted Therapies (Volume II)

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

Deadline for manuscript submissions: 30 November 2024 | Viewed by 3719

Special Issue Editor

Dr. Sonia Molina-Pinelo

E-Mail Website
Guest Editor
Institute of Biomedicine of Seville (IBIS), HUVR, CSIC, Universidad de Sevilla, 41013 Sevilla, Spain
Interests: lung cancer; biomarkers; genetics; diagnosis; prognosis; targeted therapies; immunotherapy
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

This Special Issue is the second edition of the Special Issue Lung Cancer—Molecular Insights and Targeted Therapies https://www.mdpi.com/journal/cancers/special_issues/LCMITT.

Lung cancer is the leading cause of cancer-related death worldwide, with a 5-year survival rate of approximately 18%. Each year, more than 2 million people are diagnosed with lung cancer around the world, and most of them are diagnosed with locally advanced or metastatic disease. Therefore, early diagnosis is one of the key steps to improve and promote precision medicine for this disease. 

Lung cancer management has changed in the last decade. State-of-the-art molecular pathology has allowed the development of more effective therapeutic strategies for this disease. However, there is still a long way to go before precision medicine is available for all, which will require further research into the molecular mechanisms underlying lung cancer and potential new druggable targets based on the molecular background of tumors. The current issue aims to increase our knowledge in order to achieve these goals.

We are pleased to invite both original research and review articles that highlight recent advances in this exciting field of research. We are looking for articles on the discovery of molecular insights and targeted therapies for use in preclinical in vitro and in vivo models and/or articles investigating their role in translation to clinical practice. We also welcome articles that cover other topics with the aim of improving or providing an alternative paradigm of precision medicine in lung cancer.

I look forward to receiving your contributions.

Dr. Sonia Molina-Pinelo
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

  • lung cancer
  • non-small-cell lung cancer
  • small-cell lung cancer
  • biomarkers
  • oncogene-drive tumors
  • molecular mechanisms
  • targeted therapies
  • immunotherapy
  • precision medicine
  • preclinical models

Published Papers (4 papers)

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Research

13 pages, 7082 KiB  
Article
XPC Protects against Carcinogen-Induced Histologic Progression to Lung Squamous Cell Carcinoma by Reduced Basal Epithelial Cell Proliferation
by Catherine R. Sears, Huaxin Zhou, Emily Hulsey, Bea A. Aidoo, George E. Sandusky and Nawar Al Nasrallah
Cancers 2024, 16(8), 1495; https://doi.org/10.3390/cancers16081495 - 13 Apr 2024
Viewed by 382
Abstract
Lung squamous cell carcinoma (LUSC) is the second leading cause of lung cancer. Although characterized by high DNA mutational burdens and genomic complexity, the role of DNA repair in LUSC development is poorly understood. We sought to better understand the role of the [...] Read more.
Lung squamous cell carcinoma (LUSC) is the second leading cause of lung cancer. Although characterized by high DNA mutational burdens and genomic complexity, the role of DNA repair in LUSC development is poorly understood. We sought to better understand the role of the DNA repair protein Xeroderma Pigmentosum Group C (XPC) in LUSC development. XPC knock-out (KO), heterozygous, and wild-type (WT) mice were exposed topically to N-nitroso-tris-chloroethylurea (NTCU), and lungs were evaluated for histology and pre-malignant progression in a blinded fashion at various time-points from 8–24 weeks. High-grade dysplasia and LUSC were increased in XPC KO compared with XPC WT NTCU mice (56% vs. 34%), associated with a higher mean LUSC lung involvement (p < 0.05). N-acetylcysteine pre-treatment decreased bronchoalveolar inflammation but did not prevent LUSC development. Proliferation, measured as %Ki67+ cells, increased with NTCU treatment, in high-grade dysplasia and LUSC, and in XPC deficiency (p < 0.01, ANOVA). Finally, pre-LUSC dysplasia developed earlier and progressed to higher histologic classification sooner in XPC KO compared with WT mice. Overall, this supports the protective role of XPC in squamous dysplasia progression to LUSC. Mouse models of early LUSC development are limited; this may provide a valuable model to study mechanisms of LUSC development and progression. Full article
(This article belongs to the Special Issue Lung Cancer—Molecular Insights and Targeted Therapies (Volume II))
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24 pages, 9592 KiB  
Article
Induction of Multiple Alternative Mitogenic Signaling Pathways Accompanies the Emergence of Drug-Tolerant Cancer Cells
by Frank V. Celeste and Scott Powers
Cancers 2024, 16(5), 1001; https://doi.org/10.3390/cancers16051001 - 29 Feb 2024
Viewed by 787
Abstract
Drug resistance can evolve from a subpopulation of cancer cells that initially survive drug treatment and then gradually form a pool of drug-tolerant cells. Several studies have pinpointed the activation of a specific bypass pathway that appears to provide the critical therapeutic target [...] Read more.
Drug resistance can evolve from a subpopulation of cancer cells that initially survive drug treatment and then gradually form a pool of drug-tolerant cells. Several studies have pinpointed the activation of a specific bypass pathway that appears to provide the critical therapeutic target for preventing drug tolerance. Here, we take a systems-biology approach, using proteomics and genomics to examine the development of drug tolerance to EGFR inhibitors in EGFR-mutant lung adenocarcinoma cells and BRAF inhibitors in BRAF-mutant melanoma cells. We found that there are numerous alternative mitogenic pathways that become activated in both cases, including YAP, STAT3, IGFR1, and phospholipase C (PLC)/protein kinase C (PKC) pathways. Our results suggest that an effective therapeutic strategy to prevent drug tolerance will need to take multiple alternative mitogenic pathways into account rather than focusing on one specific pathway. Full article
(This article belongs to the Special Issue Lung Cancer—Molecular Insights and Targeted Therapies (Volume II))
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14 pages, 4735 KiB  
Article
Combinational Pulsing of TAAs Enforces Dendritic Cell-Based Immunotherapy through T-Cell Proliferation and Interferon-γ Secretion in LLC1 Mouse Model
by Jae-Ung Lee, Sang-Heon Kim, Sung-Hoon Lee, Min-Jae Ji, Jeong-Ah Jin, Hyung-Joon So, Myoung-Lim Song, Hong-Ki Lee and Tae-Wook Kang
Cancers 2024, 16(2), 409; https://doi.org/10.3390/cancers16020409 - 18 Jan 2024
Viewed by 807
Abstract
NSCLC, the most common type of lung cancer, is often diagnosed late due to minimal early symptoms. Its high risk of recurrence or metastasis post-chemotherapy makes DC-based immunotherapy a promising strategy, offering targeted cancer destruction, low side effects, memory formation, and overcoming the [...] Read more.
NSCLC, the most common type of lung cancer, is often diagnosed late due to minimal early symptoms. Its high risk of recurrence or metastasis post-chemotherapy makes DC-based immunotherapy a promising strategy, offering targeted cancer destruction, low side effects, memory formation, and overcoming the immune evasive ability of cancers. However, the limited response to DCs pulsed with single antigens remains a significant challenge. To overcome this, we enhanced DC antigen presentation by pulsing with TAAs. Our study focused on enhancing DC-mediated immune response specificity and intensity by combinatorial pulsing of TAAs, selected for their prevalence in NSCLC. We selected four types of TAAs expressed in NSCLC and pulsed DCs with the optimal combination. Next, we administered TAAs-pulsed DCs into the LLC1 mouse model to evaluate their anti-tumor efficacy. Our results showed that TAAs-pulsed DCs significantly reduced tumor size and promoted apoptosis in tumor tissue. Moreover, TAAs-pulsed DCs significantly increased total T cells in the spleen compared to the unpulsed DCs. Additionally, in vitro stimulation of splenocytes from the TAAs-pulsed DCs showed notable T-cell proliferation and increased IFN-γ secretion. Our findings demonstrate the potential of multiple TAA pulsing to enhance the antigen-presenting capacity of DCs, thereby strengthening the immune response against tumors. Full article
(This article belongs to the Special Issue Lung Cancer—Molecular Insights and Targeted Therapies (Volume II))
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11 pages, 1097 KiB  
Article
Fluorometric Quantification of Total Cell-Free DNA as a Prognostic Biomarker in Non-Small-Cell Lung Cancer Patients Treated with Immune Checkpoint Blockade
by Javier Oliver, Juan Luis Onieva, María Garrido-Barros, Manuel Cobo-Dols, Beatriz Martínez-Gálvez, Ana Isabel García-Pelícano, Jaime Dubbelman, José Carlos Benítez, Juan Zafra Martín, Alejandra Cantero, Elisabeth Pérez-Ruiz, Antonio Rueda-Domínguez and Isabel Barragán
Cancers 2023, 15(13), 3357; https://doi.org/10.3390/cancers15133357 - 26 Jun 2023
Cited by 2 | Viewed by 1271
Abstract
The present study aimed to investigate the potential of basal cell-free fluorometric DNA (cfDNA) quantification as a prognostic biomarker in advanced non-small cell lung cancer (NSCLC) patients treated with an Immune Checkpoint Blockade (ICB). A discovery and validation cohort of 61 and 31 [...] Read more.
The present study aimed to investigate the potential of basal cell-free fluorometric DNA (cfDNA) quantification as a prognostic biomarker in advanced non-small cell lung cancer (NSCLC) patients treated with an Immune Checkpoint Blockade (ICB). A discovery and validation cohort of 61 and 31 advanced lung cancer patients treated with ICB were included in this study. Quantification of cfDNA concentration was performed before the start of the treatment and patients were followed up for a median of 34 (30–40) months. The prognostic predicted value of cfDNA was evaluated based on ROC, and Cox regression was conducted via univariate and multivariate analyses to estimate the hazard ratio. We observed that a cfDNA cut-off of 0.55 ng/µL before the ICB determines the overall survival of patients with a log rank p-value of 3.3 × 10−4. That represents median survivals of 3.8 vs. 17.5 months. Similar results were obtained in the validation cohort being the log rank p-value 3.8 × 10−2 with median survivals of 5.9 vs. 24.3. The univariate and multivariate analysis revealed that the cut-off of 0.55 ng/µL before ICB treatment was an independent predictive factor and was significantly associated with a better survival outcome. High cfDNA concentrations identify patients with advanced NSCLC who do not benefit from the ICB. The determination of cfDNA is a simple test that could select a group of patients in whom new therapeutic strategies are needed. Full article
(This article belongs to the Special Issue Lung Cancer—Molecular Insights and Targeted Therapies (Volume II))
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