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Small-Molecule Inhibitors Targeting Receptor Tyrosine Kinases in Cancer
Published in Peter Grunwald, Pharmaceutical Biocatalysis, 2020
Mohammad Hojjat-Farsangi, Gholamreza Khamisipour
Currently, three ALK inhibitors, brigatinib, crizotinib, and ceritinib have been developed and approved by the FDA and Europe for the treatment of NSCLC patients that are ALK positive. These inhibitors are type I and bind to the ATP-binding pocket within the TK domain of ALK kinase (Hallberg and Palmer, 2016).
Core genes in lung adenocarcinoma identified by integrated bioinformatic analysis
Published in International Journal of Environmental Health Research, 2023
Liu Yang, Qi Yu, Yonghang Zhu, Manthar Ali Mallah, Wei Wang, Feifei Feng, Qiao Zhang
Lung adenocarcinoma (LUAD) is the most prevalent type of lung cancer (Simon and Turrisi 2007). A large number of clinical studies have been carried out currently, and significant progress has been made in the treatment of LUAD. However, the incidence and death rates of LUAD remain high in the world (Calvayrac et al. 2017). With the rapid advancement of cancer molecular biology, molecular targeted drugs, such as targeting the epidermal growth factor receptor (EGFR) and anaplastic lymphoma kinase (ALK) have achieved satisfactory efficacy in LUAD patients, suggesting a complex characteristic genetic background of LUAD (El-Telbany and Ma 2012) and opening up a new therapeutic strategy (Denisenko et al. 2018). Hence, it is vital to find the exact and potential targeted therapies for LUAD.
The emergence of nanoporous materials in lung cancer therapy
Published in Science and Technology of Advanced Materials, 2022
Deepika Radhakrishnan, Shan Mohanan, Goeun Choi, Jin-Ho Choy, Steffi Tiburcius, Hoang Trung Trinh, Shankar Bolan, Nikki Verrills, Pradeep Tanwar, Ajay Karakoti, Ajayan Vinu
Understanding the mechanism of targeted therapies to target specific oncogenic drivers in lung cancer is another crucial area of treatment. About 2/3rd of lung cancer patients are reported to have a mutated gene, and among them, about half of the patients have targetable lesions [52]. Usually, most of the targeted therapies are given as an add-on treatment to baseline therapies. Several genes are identified as positive and negative markers for lung cancer. Major studies were conducted for genes like epidermal growth factor receptor (EGFR; also known as ERBB1), anaplastic lymphoma kinase (ALK), ROS1 proto-oncogene receptor tyrosine kinase (ROS1) and serine/threonine-protein kinase b-raf (BRAF) for targeted therapy in lung cancers [53–55]. However, adaptive, intrinsic, or acquired resistance is reported as a challenge for targeted therapies. As these usual therapies become redundant over time with fast mutation rates, combining two or more therapies with targeting therapy is required to achieve rapid and desired results within a short period [56,57]. Several new molecular determinants of lung cancer subtypes and their mutations are being explored, and new variants are being discovered.
Mutation patterns of epidermal growth factor receptor gene in non-small cell lung cancer among Egyptian patients
Published in Egyptian Journal of Basic and Applied Sciences, 2022
Wafaa H. Elmetnawy, Mona Qenawi, Salwa Sabet, Heba Bassiony
Smoking, air pollution, exposure to carcinogenic chemicals, alcohol intake and a family history of lung cancer are all considered risk factors [11]. However, smoking seems to be a less potent oncogenic factor for adenocarcinoma than squamous cell carcinoma and SCLC [12,13]. In addition, genetic factors contribute in the development of sporadic lung cancer and may vary by ethnicity [14]. Previous studies reported that somatic mutations in the epidermal growth factor receptor (EGFR), tumor protein 53 (TP53), Kirsten rat sarcoma viral oncogene (KRAS), proto-oncogene B-Raf (BRAF), c-ROS oncogene 1 (ROS1), anaplastic lymphoma kinase (ALK), and human epidermal growth factor receptor (HER2) are common in lung cancers. These genes are involved in the regulation of gene expression, cell proliferation, differentiation and apoptosis [12,13,15].