ReviewCancer research2014
The structural basis of PI3K cancer mutations: from mechanism to therapy.
Review in Cancer research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
33 citing papers in PubMed, 68 citations in OpenAlex.
- Context-dependent selection sculpts mutational landscapes in the normal lung.Research square · 2026Article
- Family with sequence similarity 114 member A1 orchestrates immune evasion in triple-negative breast cancer.Signal transduction and targeted therapy · 2025Article
- Targeting the PI3K Pathway: Advancements and Achievements in Breast Cancer Therapy.Current pharmaceutical design · 2025Review
- Molecular Basis of Oncogenic PI3K Proteins.Cancers · 2024Review
- Targeting PI3K family with small-molecule inhibitors in cancer therapy: current clinical status and future directions.Molecular cancer · 2024Review
- A p85 isoform switch enhances PI3K activation on endosomes by a MAP4- and PI3P-dependent mechanism.Cell reports · 2024Article
- Structural and Dynamic Analyses of Pathogenic Variants inLife (Basel, Switzerland) · 2024Article
- Emerging role of extracellular vesicles and exogenous stimuli in molecular mechanisms of peripheral nerve regeneration.Frontiers in cellular neuroscience · 2024Review
- Mutant PIK3CA as a negative predictive biomarker for treatment with a highly selective PIM1 inhibitor in human colon cancer.Cancer biology & therapy · 2023Article
- The quest for the optimal biomarker: is extending the spectrum of targetedAnnals of translational medicine · 2023Article
- Unleashing Intrinsic Growth Pathways in Regenerating Peripheral Neurons.International journal of molecular sciences · 2022Review
- The ClinGen Brain Malformation Variant Curation Expert Panel: Rules for somatic variants in AKT3, MTOR, PIK3CA, and PIK3R2.Genetics in medicine : official journal of the American College of Medical Genetics · 2022Article
- Aspirin sensitivity of PIK3CA-mutated Colorectal Cancer: potential mechanisms revisited.Cellular and molecular life sciences : CMLS · 2022Review
- The Small-Molecule Inhibitor MRIA9 Reveals Novel Insights into the Cell Cycle Roles of SIK2 in Ovarian Cancer Cells.Cancers · 2021Article
- Targeting the PI3K/AKT/mTOR Signaling Pathway in Lung Cancer: An Update Regarding Potential Drugs and Natural Products.Molecules (Basel, Switzerland) · 2021Review
- Targeting effector pathways in RAC1Small GTPases · 2021Article
- PIK3CA mutations in lipomatosis of nerve with or without nerve territory overgrowth.Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc · 2020Article
- Visceral adipose tissue alteration ofAdipocyte · 2019Observational
- Article
- Conditional Knockdown of Osteopontin Inhibits Breast Cancer Skeletal Metastasis.International journal of molecular sciences · 2019Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 3 institutions in 2 countries.
Funding
Abstract
While genetic alteration in the p85α-p110α (PI3K) complex represents one of the most frequent driver mutations in cancer, the wild-type complex is also required for driving cancer progression through mutations in related pathways. Understanding the mechanistic basis of the function of the phosphoinositide 3-kinase (PI3K) is essential for designing optimal therapeutic targeting strategies. Recent structural data of the p85α/p110α complex unraveled key insights into the molecular mechanisms of the activation of the complex and provided plausible explanations for the well-established biochemical data on p85/p110 dimer regulation. A wealth of biochemical and biologic information supported by recent genetic findings provides a strong basis for additional p110-independent function of p85α in the regulation of cell survival. In this article, we review the structural, biochemical, and biologic mechanisms through which p85α regulates the cancer cell life cycle with an emphasis on the recently discovered genetic alterations in cancer. As cancer progression is dependent on multiple biologic processes, targeting key drivers such as the PI3K may be required for efficacious therapy of heterogeneous tumors typically present in patients with late-stage disease.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.