Molecular Biology and Precision Medicine of Lung Cancer

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

Deadline for manuscript submissions: closed (15 December 2022) | Viewed by 4822

Special Issue Editors


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Guest Editor
1. Division of Pulmonary and Critical Care Medicine, Kaohsiung Medical University Hospital, Kaohsiung Medical University, Kaohsiung, Taiwan
2. Chair, School of Post-Baccalaureate Medicine, College of Medicine, Kaohsiung Medical University, Kaohsiung, Taiwan
3. Chair, Lung Cancer Team, Cancer Center, Kaohsiung Medical University Hospital, Kaohsiung, Taiwan

Interests: lung cancer; target therapy; immunotherapy; antiangiogenic agent; chemotherapy; NGS
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Co-Guest Editor
Division of Pulmonary and Critical Care Medicine, Department of Internal Medicine, Kaohsiung Medical University Hospital, Kaohsiung Medical University, Kaohsiung 80708, Taiwan
Interests: molecular biology and precision medicine of lung cancer

Special Issue Information

Dear Colleagues,

Lung cancer is a leading cause of cancer-related mortality worldwide. In 2020, lung cancer accounted for 1.8 million deaths globally, ranking first among all the causes of cancer death. Upon diagnosis, 50% of patients have distant metastases with a 5-year survival rate that is lower than 5%. Most lung cancer patients are diagnosed at an advanced stage, meaning salvage therapy is recommended. Platinum-based chemotherapy is a standard therapy for advanced stage lung cancer but has only been proven to have modest clinical efficacy. Many new target therapies have been developed that have been proven to have better clinical efficacy compared with standard platinum-based chemotherapy. For example, several large-scale phase three clinical trials have shown that a tyrosine kinase inhibitor (TKI) received by lung cancer patients harboring susceptible epidermal growth factor receptor (EGFR) mutations had better clinical efficacy than platinum-based chemotherapy, as determined by the overall response rate, progression free survival (PFS) and quality of life.

In this Special Issue on “The Biology and Management of Lung Cancer”, we would like to gather high-quality original research or review articles on basic biology, pathology, advanced targeted therapy, immunotherapy, chemotherapy, radiotherapy, and combination therapy in lung cancer, especially precision medicine and prospective clinical trials.

Prof. Dr. Chih-Jen Yang
Dr. Hsiang-Hao Chuang
Guest Editors

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Keywords

  • tyrosine kinase inhibitor
  • anti-angiogenesis
  • immunotherapy
  • chemotherapy
  • precision medicine in lung cancer

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Published Papers (2 papers)

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Research

10 pages, 2357 KiB  
Article
FAK Executes Anti-Senescence via Regulating EZH2 Signaling in Non-Small Cell Lung Cancer Cells
by Hsiang-Hao Chuang, Ming-Shyan Huang, Yen-Yi Zhen, Cheng-Hao Chuang, Ying-Ray Lee, Michael Hsiao and Chih-Jen Yang
Biomedicines 2022, 10(8), 1937; https://doi.org/10.3390/biomedicines10081937 - 10 Aug 2022
Cited by 5 | Viewed by 1887
Abstract
Focal adhesion kinase (FAK) is a non-receptor tyrosine kinase overexpressed in various cancer types that plays a critical role in tumor progression. Accumulating evidence suggests that targeting FAK, either alone or in combination with other agents, may serve as an effective therapeutic strategy [...] Read more.
Focal adhesion kinase (FAK) is a non-receptor tyrosine kinase overexpressed in various cancer types that plays a critical role in tumor progression. Accumulating evidence suggests that targeting FAK, either alone or in combination with other agents, may serve as an effective therapeutic strategy for numerous cancers. In addition to retarding proliferation, metastasis, and angiogenesis, FAK inhibition triggers cellular senescence in lung cancer cells. However, the detailed mechanism remains enigmatic. In the present study, we found that FAK inhibition not only elicits DNA-damage signaling but also downregulates enhancer of zeste homolog 2 (EZH2) expression. The manipulation of FAK expression influences EZH2 expression and corresponding signaling in vitro. Immunohistochemistry shows that active FAK signaling corresponds with the activation of the EZH2-mediated signaling cascade in lung-cancer-cells-derived tumor tissues. We also found that ectopic EZH2 expression attenuates FAK-inhibition-induced cellular senescence in lung cancer cells. Our results identify EZH2 as a critical downstream effector of the FAK-mediated anti-senescence pathway. Targeting FAK-EZH2 axis-induced cellular senescence may represent a promising therapeutic strategy for restraining tumor growth. Full article
(This article belongs to the Special Issue Molecular Biology and Precision Medicine of Lung Cancer)
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12 pages, 894 KiB  
Article
C-Reactive Protein to Albumin Ratio as Prognostic Marker in Locally Advanced Non-Small Cell Lung Cancer Treated with Chemoradiotherapy
by Alina Frey, Daniel Martin, Louisa D’Cruz, Emmanouil Fokas, Claus Rödel and Maximilian Fleischmann
Biomedicines 2022, 10(3), 598; https://doi.org/10.3390/biomedicines10030598 - 3 Mar 2022
Cited by 12 | Viewed by 2401
Abstract
Despite the implementation of consolidative immune checkpoint inhibition after definitive chemoradiotherapy (CRT), the prognosis for locally advanced non-small-cell lung cancer (NSCLC) remains poor. We assessed the impact of the C-reactive protein (CRP) to albumin ratio (CAR) as an inflammation-based prognostic score in patients [...] Read more.
Despite the implementation of consolidative immune checkpoint inhibition after definitive chemoradiotherapy (CRT), the prognosis for locally advanced non-small-cell lung cancer (NSCLC) remains poor. We assessed the impact of the C-reactive protein (CRP) to albumin ratio (CAR) as an inflammation-based prognostic score in patients with locally advanced NSCLC treated with CRT. We retrospectively identified and analyzed 52 patients with primary unresectable NSCLC (UICC Stage III) treated with definitive/neoadjuvant CRT between 2014 and 2019. CAR was calculated by dividing baseline CRP by baseline albumin levels and correlated with clinicopathologic parameters to evaluate prognostic impact. After dichotomizing patients by the median, univariate and multivariate Cox regression analyses were performed. An increased CAR was associated with advanced T-stage (p = 0.018) and poor performance status (p = 0.004). Patients with pre-therapeutic elevated CAR had significantly lower hemoglobin and higher leukocyte levels (hemoglobin p = 0.001, leukocytes p = 0.018). High baseline CAR was shown to be associated with worse local control (LPFS, p = 0.006), shorter progression-free survival (PFS, p = 0.038) and overall survival (OS, p = 0.022), but not distant metastasis-free survival (DMFS). Multivariate analysis confirmed an impaired outcome in patients with high CAR (LPFS: HR 3.562, 95% CI 1.294–9.802, p = 0.011). CAR is an easily available and independent prognostic marker after CRT in locally advanced NSCLC. CAR may be a useful biomarker for patient stratification to individualize treatment concepts. Full article
(This article belongs to the Special Issue Molecular Biology and Precision Medicine of Lung Cancer)
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