Recent progress in targeted therapy for non-small cell lung cancer

Xiao, Yanxia; Liu, Pu; Wei, Jie; Zhang, Xin; Guo, Jun; Lin, Yajun

doi:10.3389/fphar.2023.1125547

Cited by 38 publications

(30 citation statements)

References 104 publications

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“…58,59 It occurs exclusively to other driver mutations, 60 but is frequently comutated with the tumor suppressor genes STK11 , KEAP1 , TP53 , and CDKN2A / CDKN2B . 61 KRAS G12C -mutated NSCLC is typically associated with a history of smoking, elevated tumor mutational burden, 62 and elevated markers of immune evasion. 63…”

Section: Kras G12c Mutationmentioning

confidence: 99%

Path Less Traveled: Targeting Rare Driver Oncogenes in Non–Small-Cell Lung Cancer

Lim,

Lee,

Oya

et al. 2024

JCO Oncol Pract

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Over the past decade, tremendous efforts have been made in the development of targeted agents in non–small-cell lung cancer (NSCLC) with nonsquamous histology. Pivotal studies have used next-generation sequencing to select the patient population harboring oncogenic driver alterations that are targetable with targeted therapies. As treatment paradigm rapidly evolves for patients with rare oncogene-driven NSCLC, updated comprehensive overview of diagnostic approach and treatment options is paramount in clinical settings. In this review article, we discuss the epidemiology, molecular testing, and landmark clinical trials addressing the targeted agents for ROS1 rearrangement, METex14 skipping mutation, EGFR exon 20 insertion, KRAS G12C mutation, HER2 mutation, RET fusion, NTRK fusion, and BRAF mutations.

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Section: Kras G12c Mutationmentioning

confidence: 99%

Path Less Traveled: Targeting Rare Driver Oncogenes in Non–Small-Cell Lung Cancer

Lim,

Lee,

Oya

et al. 2024

JCO Oncol Pract

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“…Recently, several FDA-approved therapies have been developed that specifically target genomic alterations in tyrosine kinase-related genes, including EGFR, ALK, ROS1, MET, RET, KRAS, BRAF, and NTRK1-3 [73]. These therapies, accompanied by their respective companion diagnostics, are now utilized in the treatment of NSCLC.…”

Section: Tissue-based Molecular Biomarkersmentioning

confidence: 99%

Exploring the Molecular Tumor Microenvironment and Translational Biomarkers in Brain Metastases of Non-Small-Cell Lung Cancer

Wen,

Yu,

Liu

et al. 2024

IJMS

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Brain metastases represent a significant clinical challenge in the treatment of non-small-cell lung cancer (NSCLC), often leading to a severe decline in patient prognosis and survival. Recent advances in imaging and systemic treatments have increased the detection rates of brain metastases, yet clinical outcomes remain dismal due to the complexity of the metastatic tumor microenvironment (TME) and the lack of specific biomarkers for early detection and targeted therapy. The intricate interplay between NSCLC tumor cells and the surrounding TME in brain metastases is pivotal, influencing tumor progression, immune evasion, and response to therapy. This underscores the necessity for a deeper understanding of the molecular underpinnings of brain metastases, tumor microenvironment, and the identification of actionable biomarkers that can inform multimodal treatment approaches. The goal of this review is to synthesize current insights into the TME and elucidate molecular mechanisms in NSCLC brain metastases. Furthermore, we will explore the promising horizon of emerging biomarkers, both tissue- and liquid-based, that hold the potential to radically transform the treatment strategies and the enhancement of patient outcomes.

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“…The impacts of the second-generation mTOR inhibitors on gastrointestinal cancers showed better treatment efficacy than monotherapies in in vitro cell experiments and preclinical studies. However, no special inhibitors of Rictor/mTORC2 have been identified ( 138 ).…”

Section: Conclusion and Future Perspectivesmentioning

confidence: 99%

Roles of Rictor alterations in gastrointestinal tumors (Review)

Cao,

Guo,

Min

et al. 2024

Oncol Rep

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Gastrointestinal tumors account for five of the top 10 causes of mortality from all cancers (colorectal, liver, stomach, esophageal and pancreatic cancer). Mammalian target of rapamycin (mTOR) signaling is commonly dysregulated in various human cancers. As a core component of the mTOR complex 2 (mTORC2), Rictor is a key effector molecule of the PI3K/Akt pathway. A high alteration rate of Rictor has been observed in gastrointestinal tumors, and such Rictor alterations are often associated with resistance to chemotherapy and related adverse clinical outcomes. However, the exact roles of Rictor in gastrointestinal tumors remain elusive. The aim of the present study was to critically discuss the following: i) Mutation and biological characteristics of Rictor in tumors with a detailed overview of Rictor in cell proliferation, angiogenesis, apoptosis, autophagy and drug resistance; ii) the role of Rictor in tumors of the digestive system, particularly colorectal, hepatobiliary, gastric, esophageal and pancreatic cancer and cholangiocarcinoma; and iii) the current status and prospects of targeted therapy for Rictor by inhibiting Akt activation. Despite the growing realization of the importance of Rictor/mTORC2 in cancer, the underlying mechanistic details remain poorly understood; this needs to change in order for the development of efficient targeted therapies and re-sensitization of therapy-resistant cancers to be made possible.

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Recent progress in targeted therapy for non-small cell lung cancer

Cited by 38 publications

References 104 publications

Path Less Traveled: Targeting Rare Driver Oncogenes in Non–Small-Cell Lung Cancer

Path Less Traveled: Targeting Rare Driver Oncogenes in Non–Small-Cell Lung Cancer

Exploring the Molecular Tumor Microenvironment and Translational Biomarkers in Brain Metastases of Non-Small-Cell Lung Cancer

Roles of Rictor alterations in gastrointestinal tumors (Review)

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