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Special Issue "Lung Cancer: Tumor Progression and Target Therapy"

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

Deadline for manuscript submissions: closed (30 April 2023) | Viewed by 10919

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Special Issue Editors

Prof. Dr. Alberto Ricci

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Guest Editor

Department of Clinical and Molecular Medicine, Sapienza University of Rome, Rome, Italy
Interests: lung diseases; lung cancer; interstitial lung diseases

Prof. Dr. Rita Mancini

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Guest Editor

Dipartimento di Medicina Clinica e Molecolare, II Facoltà di Medicina e Chirurgia, Policlinico S. Andrea, Università "La Sapienza", 00189 Roma, Italy
Interests: biochemistry; genetics and molecular biology; cancer therapeutics; lung cancer stem cells

Special Issue Information

Lung cancer is one of the leading causes of cancer death worldwide. Among all lung cancer histotypes, about 85% of cases are represented by non-small cell lung carcinomas (NSCLC). Although great progress has been made in recent decades in the knowledge of its biology and the mechanisms of tumor progression, particularly for the adenocarcinoma histotype, lung tumors still represent a challenge. The demonstration of mutations in genes involved in the growth of the tumor cell has allowed the development of target therapy (as small molecule tyrosine kinase inhibitors). In particular, mutations have been identified in v-Ki-ras2 Kristen rat sarcoma viral oncogene homolog (KRAS), epidermal growth factor receptor (EGFR) BRAF, and the parallel PI3K pathway oncogene. More recently, interest has focused on MEK and HER2 and the rearrangements of ALK and ROS1. Amplifications of oncogenes such as MET in adenocarcinomas and of FGFR and discoidin domain receptor 2 (DDR2) in squamous carcinomas are under investigation for therapeutic intervention. In addition, immunotherapy has allowed new and unexpected benefits on the survival of selected patients.

As a consequence, such knowledge has resulted in a revolution in the diagnosis and treatment of pulmonary adenocarcinomas based on the genotype or an individual’s tumor.

The aim of the present Special Issue will be focused on well-designed studies and research able to improve our knowledge of lung cancer, our understanding of the mechanisms underlying tumor initiation, propagation, and progression, and ameliorate the influence or change direction in lung cancer diagnosis and therapy. As a consequence, these works may give the basis for novel therapeutic approaches, early or more specific diagnostic procedures. Not only clinical but also basic science research is encouraged. In addition, works aiming to translate basic knowledge into the clinic, such as treatment and prevention, diagnosis, and novel therapeutic modalities, will be also considered. Articles in this Special Issue may include reviews and researcher papers. The issue comprehensively covers many areas of interest and could be of interest to a broad range of readers, including physicians, scientists, students, and pharmaceutical companies.

Prof. Dr. Alberto Ricci
Prof. Dr. Rita Mancini
Guest Editors

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Keywords

lung cancer
NSCLC
target mutation
target therapy
EGFr
ALK
ROS1
surgery
receptors
metastasis
medical imaging

Published Papers (6 papers)

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Research

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Open AccessArticle

Genetic Polymorphisms of ACE1 Rs4646994 Associated with Lung Cancer in Patients with Pulmonary Nodules: A Case–Control Study

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Biomedicines 2023, 11(6), 1549; https://doi.org/10.3390/biomedicines11061549 - 26 May 2023

Viewed by 262

Abstract

Background: Currently, many detection methods have high sensitivity to the diagnosis of lung cancer. However, some postoperative patients with pulmonary nodules are eventually diagnosed as having benign nodules. The ideal evaluation of an individual with a pulmonary nodule would expedite therapy for a malignant nodule and minimize testing for those with a benign nodule. Methods: This case–control study is designed to explore the relationship between ACE1 rs4646994 polymorphism and the risk of lung cancer in patients with pulmonary nodules, for which 400 individuals with lung cancer and benign pulmonary nodules were included. A DNA extraction kit was used to extract DNA from peripheral blood. The relationship between ACE1 rs4646994 and the risk of lung cancer in patients with pulmonary nodules was determined by the chi-square test, logistic regression analysis and cross analysis. Results: The results showed that after adjusting for age and gender confounding factors, the risk of lung cancer in patients with pulmonary nodules carrying the DD genotype was more than three times that of the I carriers (II + ID) genotype (OR = 3.035, 95% CI, 1.252–7.356, p = 0.014). There was no significant difference between lung squamous cell carcinoma and lung adenocarcinoma in the polymorphism of ACE1 rs4646994 (p > 0.05). We also found that the ACE1 rs4646994 DD genotype frequency was inversely correlated with the risk of EGFR mutation in lung adenocarcinoma patients. Conclusions: Our study indicated that ACE1 rs4646994 polymorphism increases the risk of lung cancer in patients with pulmonary nodules from China. Full article

(This article belongs to the Special Issue Lung Cancer: Tumor Progression and Target Therapy)

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Open AccessArticle

Low-Dose Metformin Treatment Reduces In Vitro Growth of the LL/2 Non-small Cell Lung Cancer Cell Line

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Biomedicines 2023, 11(1), 65; https://doi.org/10.3390/biomedicines11010065 - 27 Dec 2022

Viewed by 895

Abstract

Lung cancer maintains a relatively small survival rate (~19%) over a 5-year period and up to 80–85% of all lung cancer diagnoses are Non-Small Cell Lung Cancer (NSCLC). To determine whether metformin reduces non-small cell lung cancer (NSCLC) LL/2 cell growth, cells were grown in vitro and treated with metformin for 48 h. qPCR was used to assess genes related to cell cycle regulation and pro-apoptotic markers, namely Cyclin D, CDK4, p27, p21, and HES1. Treatment with 10 mM metformin significantly reduced HES1 expression (p = 0.011). Furthermore, 10 mM metformin treatment significantly decreased REDD1 (p = 0.0082) and increased p-mTOR Ser2448 (p = 0.003) protein expression. Control cells showed significant reductions in phosphorylated p53 protein expression (p = 0.0367), whereas metformin treated cells exhibited reduced total p53 protein expression (p = 0.0078). There were no significant reductions in AMPK, PKB/AKT, or STAT3. In addition, NSCLC cells were treated for 48 h. with 10 mM metformin, 4 µM gamma-secretase inhibitor (GSI), or the combination of metformin (10 mM) and GSI (4 µM) to determine the contribution of respective signaling pathways. Metformin treatment significantly reduced total nucleus expression of the proliferation maker Ki-67 with an above 65% reduction in Ki-67 expression between control and metformin-treated cells (p = 0.0021). GSI (4 µM) treatment significantly reduced Ki-67 expression by ~20% over 48 h (p = 0.0028). Combination treatment (10 mM metformin and 4 µM GSI) significantly reduced Ki-67 expression by more than 50% over 48 h (p = 0.0245). As such, direct administration of metformin (10 mM for 48 h) proved to be an effective pharmaceutical agent in reducing the proliferation of cultured non-small cell cancer cells. These intriguing in vitro results, therefore, support the further study of metformin in appropriate in vivo models as an anti-oncogenic agent and/or an adjunctive therapy. Full article

(This article belongs to the Special Issue Lung Cancer: Tumor Progression and Target Therapy)

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Open AccessArticle

The “Polonium In Vivo” Study: Polonium-210 in Bronchial Lavages of Patients with Suspected Lung Cancer

Vincenzo Zagà

Maria Sofia Cattaruzza

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Biomedicines 2021, 9(1), 4; https://doi.org/10.3390/biomedicines9010004 - 23 Dec 2020

Cited by 1 | Viewed by 2340

Abstract

Few studies have reported on polonium-210, a decay breakdown product of radon-222 and lead-210, in human lungs and there has been no study in patients with suspected lung cancer. The main aim of this “Polonium in vivo” study was to evaluate polonium-210 radioactivity in bronchopulmonary systems of smoker, ex-smoker and never smoker patients with suspected lung cancer. Alpha-spectrometric analyses were performed on bronchial lavage (BL) fluids from two Italian hospitals in 2013–2016. Socio-demographic, smoking, occupational and spirometric characteristics, lung cancer confirmation and histologic type and radon-222 concentration in patients’ homes were collected. Seventy BL samples from never (n = 13), former (n = 35) and current smokers (n = 22) were analyzed; polonium-210 was detected in all samples from current and former smokers and in 54% of samples from never smokers (p < 0.001; median values: 1.20, 1.43 and 0.40 mBq, respectively). Polonium-210 levels were significantly higher in COPD versus no COPD patients (median value: 3.60 vs. 0.97 mBq; p = 0.007); former and current smokers, without and with COPD, had significantly increased polonium-210 levels (p = 0.012); 96% of confirmed versus 69% of non-confirmed lung cancer patients recorded detectable polonium-210 levels (p = 0.018). A polonium-210 detectable activity was measured in BL samples from all current and former smokers. Polonium-210 in the lungs could be the result of lead-210 entrapment, which, with its half-life of 22 years, could provide a continuous emission of alpha radioactivity, even many years after quitting, thus proposing a possible explanation for the onset of lung cancer, particularly in former smokers. Full article

(This article belongs to the Special Issue Lung Cancer: Tumor Progression and Target Therapy)

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Open AccessReview

Nano-Enabled Strategies for the Treatment of Lung Cancer: Potential Bottlenecks and Future Perspectives

Mohammed Kanan Alshammari

Eman Yaser Almomen

Kholoud Falah Alshahrani

Shroog Farhan Altwalah

Mehnaz Kamal

May Faiz Al-Twallah

Suheir Hassan Alsanad

Mariam Hassan Al-Batti

Faisal Jarallah Al-Rasheed

Abdulaziz Yousef Alsalamah

Mohammed Bader Alhazza

Faisal Abdu Alasmari

Abida

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Mohd Imran

Biomedicines 2023, 11(2), 473; https://doi.org/10.3390/biomedicines11020473 - 06 Feb 2023

Viewed by 1013

Abstract

On a global scale, lung cancer is acknowledged to be the major driver of cancer death attributable to treatment challenges and poor prognosis. Classical cancer treatment regimens, such as chemotherapy or radiotherapy, can be used to treat lung cancer, but the appended adverse effects limit them. Because of the numerous side effects associated with these treatment modalities, it is crucial to strive to develop novel and better strategies for managing lung cancer. Attributes such as enhanced bioavailability, better in vivo stability, intestinal absorption pattern, solubility, prolonged and targeted distribution, and the superior therapeutic effectiveness of numerous anticancer drugs have all been boosted with the emergence of nano-based therapeutic systems. Lipid-based polymeric and inorganic nano-formulations are now being explored for the targeted delivery of chemotherapeutics for lung cancer treatment. Nano-based approaches are pioneering the route for primary and metastatic lung cancer diagnosis and treatment. The implementation and development of innovative nanocarriers for drug administration, particularly for developing cancer therapies, is an intriguing and challenging task in the scientific domain. The current article provides an overview of the delivery methods, such as passive and active targeting for chemotherapeutics to treat lung cancer. Combinatorial drug therapy and techniques to overcome drug resistance in lung cancer cells, as potential ways to increase treatment effectiveness, are also discussed. In addition, the clinical studies of the potential therapies at different stages and the associated challenges are also presented. A summary of patent literature has also been included to keep readers aware of the new and innovative nanotechnology-based ways to treat lung cancer. Full article

(This article belongs to the Special Issue Lung Cancer: Tumor Progression and Target Therapy)

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Promising Biomarkers of Radiation-Induced Lung Injury: A Review

Xinglong Liu

Chunlin Shao

and

Jiamei Fu

Biomedicines 2021, 9(9), 1181; https://doi.org/10.3390/biomedicines9091181 - 08 Sep 2021

Cited by 11 | Viewed by 2549

Abstract

Radiation-induced lung injury (RILI) is one of the main dose-limiting side effects in patients with thoracic cancer during radiotherapy. No reliable predictors or accurate risk models are currently available in clinical practice. Severe radiation pneumonitis (RP) or pulmonary fibrosis (PF) will reduce the quality of life, even when the anti-tumor treatment is effective for patients. Thus, precise prediction and early diagnosis of lung toxicity are critical to overcome this longstanding problem. This review summarizes the primary mechanisms and preclinical animal models of RILI reported in recent decades, and analyzes the most promising biomarkers for the early detection of lung complications. In general, ideal integrated models considering individual genetic susceptibility, clinical background parameters, and biological variations are encouraged to be built up, and more prospective investigations are still required to disclose the molecular mechanisms of RILI as well as to discover valuable intervention strategies. Full article

(This article belongs to the Special Issue Lung Cancer: Tumor Progression and Target Therapy)

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Open AccessReview

Treatment of Rare Mutations in Patients with Lung Cancer

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Biomedicines 2021, 9(5), 534; https://doi.org/10.3390/biomedicines9050534 - 11 May 2021

Cited by 4 | Viewed by 2638

Abstract

Lung cancer is a worldwide prevalent malignancy. This disease has a low survival rate due to diagnosis at a late stage challenged by the involvement of metastatic sites. Non-small-cell lung cancer (NSCLC) is presented in 85% of cases. The last decade has experienced substantial advancements in scientific research, leading to a novel targeted therapeutic approach. The newly developed pharmaceutical agents are aimed towards specific mutations, detected in individual patients inflicted by lung cancer. These drugs have longer and improved response rates compared to traditional chemotherapy. Recent studies were able to identify rare mutations found in pulmonary tumors. Among the gene alterations detected were mesenchymal epithelial transition factor (MET), human epidermal growth factor 2 (HER2), B-type Raf kinase (BRAF), c-ROS proto-oncogene (ROS1), rearranged during transfection (RET) and neurotrophic tyrosine kinase (NTRK). Ongoing clinical trials are gaining insight onto possible first and second lines of medical treatment options intended to enable progression-free survival to lung cancer patients. Full article

(This article belongs to the Special Issue Lung Cancer: Tumor Progression and Target Therapy)

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