Related Experiment Video
Updated: May 21, 2026

06:51
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
PI3K Pathway in NSCLC
Alex Martinez-Martí1, Enriqueta Felip
1Oncology Department, Vall d'Hebron University Hospital Barcelona, Spain.
Frontiers in Oncology
|June 2, 2012
Summary
Phosphatidylinositol 3-kinases (PI3K) regulate cancer cell growth. This review examines PI3K mutations and amplification in non-small cell lung cancer.
Area of Science:
- Biochemistry
- Molecular Biology
- Oncology
Background:
- Phosphatidylinositol 3-kinases (PI3Ks) are lipid kinases crucial for cellular signaling.
- PI3K pathways regulate key cancer processes like proliferation, survival, and motility.
- Aberrant PI3K signaling, through mutations or amplification, drives oncogenesis.
Purpose of the Study:
- To review the literature on PI3K mutation status and gene amplification.
- To focus on the role of PI3K alterations in non-small cell lung cancer (NSCLC).
Main Methods:
- Literature review of studies on PI3K pathway alterations.
- Analysis of PI3K mutation and amplification data in cancer, particularly NSCLC.
Main Results:
- PI3K pathway activation via mutation and amplification is a common mechanism in various cancers.
- Specific PI3K alterations are frequently observed in non-small cell lung cancer.
- Different PI3K classes exhibit distinct roles in cancer development.
Conclusions:
- Understanding PI3K alterations is critical for targeted cancer therapies.
- PI3K mutation status and gene amplification are important biomarkers in NSCLC.
- Further research into PI3K signaling in NSCLC may reveal novel therapeutic strategies.
Related Concept Videos
PI3K/mTOR/AKT Signaling Pathway
The mammalian target of rapamycin (mTOR) is a serine/threonine kinase that regulates growth, proliferation, and cell survival in response to hormones, growth factors, or nutrient availability. This kinase exists in two structurally and functionally distinct forms: mTOR complex 1 (mTORC1) and mTOR complex 2 (mTORC2). The first form (mTORC1) is composed of a rapamycin-sensitive Raptor and proline-rich Akt substrate, PRAS40. In contrast, mTORC2 consists of a rapamycin-insensitive companion...
mTOR Signaling and Cancer Progression
The mammalian target of rapamycin or mTOR protein was discovered in 1994 due to its direct interaction with rapamycin. The protein gets its name from a yeast homolog called TOR. The mTOR protein complex in mammalian cells plays a major role in balancing anabolic processes such as the synthesis of proteins, lipids, and nucleotides and catabolic processes, such as autophagy in response to environmental cues, such as availability of nutrients and growth factors.
The mTOR pathway or the...
The mTOR pathway or the...
Interactions Between Signaling Pathways
Signaling cascades usually lack linearity. Multiple pathways interact and regulate one another, allowing cells to integrate and respond to diverse environmental stimuli.
Convergence and divergence, and cross-talk between signaling pathways
Two distinct signaling pathways can converge on a single functional unit, which may either be a single protein or a complex of proteins. The response is either functionally distinct or synergistic between the two pathways but different from the response...
Convergence and divergence, and cross-talk between signaling pathways
Two distinct signaling pathways can converge on a single functional unit, which may either be a single protein or a complex of proteins. The response is either functionally distinct or synergistic between the two pathways but different from the response...
The JAK-STAT Signaling Pathway
Several cytokine receptors have tightly bound Janus kinase or JAK proteins attached at their cytosolic tail. Small signaling molecules such as cytokines, growth hormones, or prolactins bind to the cytokine receptors and initiate their dimerization. The dimerization brings the cytosolic JAKs together that trans-phosphorylate and activates each other. The activated JAKs now phosphorylate cytosolic tails of the cytokine receptors, which serve as binding sites for adaptor proteins such as SH2...
The Intrinsic Apoptotic Pathway
Internal cellular stress, such as cellular injury or hypoxia, triggers intrinsic apoptosis. The B-cell lymphoma 2 (Bcl-2) family of proteins are the primary regulators of the intrinsic apoptotic pathway. For example, during DNA damage, checkpoint proteins, such as Ataxia Telangiectasia Mutated (ATM protein) and Checkpoints Factor-2 (Chk2) proteins, are activated. These proteins phosphorylate p53 which further activates pro-apoptotic proteins, such as Bax, Bak, PUMA, and Noxa, and inhibits...
Abnormal Proliferation
Under normal conditions, most adult cells remain in a non-proliferative state unless stimulated by internal or external factors to replace lost cells. Abnormal cell proliferation is a condition in which the cell's growth exceeds and is uncoordinated with normal cells. In such situations, cell division persists in the same excessive manner even after cessation of the stimuli, leading to persistent tumors. The tumor arises from the damaged cells that replicate to pass the damage to the daughter...
