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Cancers
Special Issues
Lung Adenocarcinoma: Issues and Challenges
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Lung Adenocarcinoma: Issues and Challenges

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

Deadline for manuscript submissions: closed (31 October 2021) | Viewed by 6488

Special Issue Editor

Dr. Giuseppe Palmieri

E-Mail Website
Guest Editor
Institute of Genetic and Biomedical Research (IRGB), Cancer Genetics Unit, CNR, 07100 Sassari, Italy
Interests: cancer genetics; melanoma; NSCLC; molecular profiling; biomarkers

Special Issue Information

Dear Colleagues,

In the current era of personalized medicine, the rapid increase in the number of biomarkers identified in lung adenocarcinoma is continuously changing the paradigms for patients’ classification and treatment decision-making. In the advanced lung adenocarcinoma setting, next-generation sequencing (NGS)-based approaches and circulating tumour DNA (ctDNA) assays may be helpful in this sense and further contribute to changing the clinical practice. This Special Issue is aimed at better defining the most actual scenario of clinical and translational researches for the diagnosis, treatment, and management of patients with lung adenocarcinoma, according to the following tentative (but not exhaustive) list of topics:

  • Integrated treatments in lung adenocarcinoma
  • KRAS, BRAF, and other targetable gene mutations in lung adenocarcinoma: changes into treatment paradigms
  • Advances in immunological therapies for lung adenocarcinoma
  • Multiple pathways in the diagnosis and treatment of lung adenocarcinoma
  • Microsatellite instability in lung adenocarcinoma
  • Prognostic biomarkers in lung adenocarcinoma
  • Clinical and molecular aspects of lung cancer in patients with chronic pulmonary diseases
  • The relevance of molecular tumour boards in managing lung adenocarcinoma
  • Microbiome and immunotherapy in lung adenocarcinoma

Dr. Giuseppe Palmieri
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 adenocarcinoma
  • gene mutations
  • factors in response to immunotherapy

Published Papers (2 papers)

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Research

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16 pages, 3351 KiB  
Article
PD-L1 Dependent Immunogenic Landscape in Hot Lung Adenocarcinomas Identified by Transcriptome Analysis
by Jutta Kirfel, Christiane Charlotte Kümpers, Anke Fähnrich, Carsten Heidel, Mladen Jokic, Ignacija Vlasic, Sebastian Marwitz, Torsten Goldmann, Helen Pasternack, Sabine Bohnet, Danny Jonigk, Mark P. Kühnel, Anne Offermann, Hauke Busch and Sven Perner
Cancers 2021, 13(18), 4562; https://doi.org/10.3390/cancers13184562 - 11 Sep 2021
Cited by 2 | Viewed by 2530
Abstract
Background: Lung cancer is the most frequent cause of cancer-related deaths worldwide. The clinical development of immune checkpoint blockade has dramatically changed the treatment paradigm for patients with lung cancer. Yet, an improved understanding of PD-1/PD-L1 checkpoint blockade-responsive biology is warranted. Methods: We [...] Read more.
Background: Lung cancer is the most frequent cause of cancer-related deaths worldwide. The clinical development of immune checkpoint blockade has dramatically changed the treatment paradigm for patients with lung cancer. Yet, an improved understanding of PD-1/PD-L1 checkpoint blockade-responsive biology is warranted. Methods: We aimed to identify the landscape of immune cell infiltration in primary lung adenocarcinoma (LUAD) in the context of tumoral PD-L1 expression and the extent of immune infiltration (“hot” vs. “cold” phenotype). The study comprises LUAD cases (n = 138) with “hot” (≥150 lymphocytes/HPF) and “cold” (<150 lymphocytes/HPF) tumor immune phenotype and positive (>50%) and negative (<1%) tumor PD-L1 expression, respectively. Tumor samples were immunohistochemically analyzed for expression of PD-L1, CD4, and CD8, and further investigated by transcriptome analysis. Results: Gene set enrichment analysis defined complement, IL-JAK-STAT signaling, KRAS signaling, inflammatory response, TNF-alpha signaling, interferon-gamma response, interferon-alpha response, and allograft rejection as significantly upregulated pathways in the PD-L1-positive hot subgroup. Additionally, we demonstrated that STAT1 is upregulated in the PD-L1-positive hot subgroup and KIT in the PD-L1-negative hot subgroup. Conclusion: The presented study illustrates novel aspects of PD-L1 regulation, with potential biological relevance, as well as relevance for immunotherapy response stratification. Full article
(This article belongs to the Special Issue Lung Adenocarcinoma: Issues and Challenges)
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Review

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12 pages, 975 KiB  
Review
New Insights into the Clinical Implications of Yes-Associated Protein in Lung Cancer: Roles in Drug Resistance, Tumor Immunity, Autophagy, and Organoid Development
by Geon Yoo, Dongil Park, Yoonjoo Kim and Chaeuk Chung
Cancers 2021, 13(12), 3069; https://doi.org/10.3390/cancers13123069 - 20 Jun 2021
Cited by 10 | Viewed by 3454
Abstract
Despite significant innovations in lung cancer treatment, such as targeted therapy and immunotherapy, lung cancer is still the principal cause of cancer-associated death. Novel strategies to overcome drug resistance and inhibit metastasis in cancer are urgently needed. The Hippo pathway and its effector, [...] Read more.
Despite significant innovations in lung cancer treatment, such as targeted therapy and immunotherapy, lung cancer is still the principal cause of cancer-associated death. Novel strategies to overcome drug resistance and inhibit metastasis in cancer are urgently needed. The Hippo pathway and its effector, Yes-associated protein (YAP), play crucial roles in lung development and alveolar differentiation. YAP is known to mediate mechanotransduction, an important process in lung homeostasis and fibrosis. In lung cancer, YAP promotes metastasis and confers resistance against chemotherapeutic drugs and targeted agents. Recent studies revealed that YAP directly controls the expression of programmed death-ligand 1 (PD-L1) and modulates the tumor microenvironment (TME). YAP not only has a profound relationship with autophagy in lung cancer but also controls alveolar differentiation, and is responsible for tubular structure formation in lung organoids. In this review, we discuss the various roles and clinical implications of YAP in lung cancer and propose that targeting YAP can be a promising strategy for treating lung cancer. Full article
(This article belongs to the Special Issue Lung Adenocarcinoma: Issues and Challenges)
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