Related Experiment Video
Updated: Dec 29, 2025
Utilizing 18F-FDG PET/CT Imaging and Quantitative Histology to Measure Dynamic Changes in the Glucose Metabolism in Mouse Models of Lung Cancer
Published on: July 21, 2018
mTOR in Lung Neoplasms
Ildiko Krencz1, Anna Sebestyen1, Andras Khoor2
11st Department of Pathology and Experimental Cancer Research, Semmelweis University, Budapest, Hungary.
Abstract:
With the discovery of rapamycin 45 years ago, studies in the mechanistic target of rapamycin (mTOR) field started 2 decades before the identification of the mTOR kinase. Over the years, studies revealed that the mTOR signaling is a master regulator of homeostasis and integrates a variety of environmental signals to regulate cell growth, proliferation, and metabolism. Deregulation of mTOR signaling, particularly hyperactivation, frequently occurs in human tumors. Recent advances in molecular profiling have identified mutations or amplification of certain genes coding proteins involved in the mTOR pathway (eg, PIK3CA, PTEN, STK11, and RICTOR) as the most common reasons contributing to mTOR hyperactivation. These genetic alterations of the mTOR pathway are frequently observed in lung neoplasms and may serve as a target for personalized therapy. mTOR inhibitor monotherapy has met limited clinical success so far; however, rational drug combinations are promising to improve efficacy and overcome acquired resistance. A better understanding of mTOR signaling may have the potential to help translation of mTOR pathway inhibitors into the clinical setting.
Insights
The mechanistic target of rapamycin (mTOR) pathway is crucial for cell growth and metabolism, but its hyperactivation drives cancer. Genetic alterations in mTOR signaling are common in lung cancer, offering therapeutic targets.
Area of Science:
- Oncology
- Molecular Biology
- Cell Signaling
Background:
- The mechanistic target of rapamycin (mTOR) pathway is a critical regulator of cellular homeostasis, integrating environmental cues to control cell growth, proliferation, and metabolism.
- Dysregulation, particularly hyperactivation, of the mTOR pathway is a common hallmark of human cancers.
- Genetic alterations in key mTOR pathway components (e.g., PIK3CA, PTEN, STK11, RICTOR) are frequently identified as drivers of mTOR hyperactivation.
Purpose of the Study:
- To review the role of mTOR signaling in cancer, focusing on its genetic alterations and therapeutic implications.
- To highlight the prevalence of mTOR pathway genetic alterations in lung neoplasms.
- To discuss the potential of mTOR pathway inhibitors in personalized cancer therapy.
Main Methods:
- Literature review of studies on mTOR signaling, its role in cancer, and therapeutic strategies.
- Analysis of genetic profiling data identifying common mutations and amplifications in mTOR pathway genes.
- Examination of clinical trial outcomes for mTOR inhibitors.
Main Results:
- mTOR hyperactivation, driven by genetic alterations in genes like PIK3CA, PTEN, STK11, and RICTOR, is prevalent in human tumors.
- These genetic alterations are frequently observed in lung neoplasms, suggesting their potential as therapeutic targets.
- mTOR inhibitor monotherapy has shown limited clinical success, but combination therapies show promise.
Conclusions:
- Targeting the mTOR pathway holds potential for personalized therapy in lung cancer.
- Rational drug combinations targeting the mTOR pathway are crucial for improving efficacy and overcoming resistance.
- Further understanding of mTOR signaling is essential for successful clinical translation of mTOR pathway inhibitors.
More Related Videos
Related Concept Videos
03:03mTOR Signaling and Cancer Progression
The mTOR pathway or the...
01:22PI3K/mTOR/AKT Signaling Pathway