ReviewCurrent topics in microbiology and immunology2010
Phosphatidylinositol 3-kinase: the oncoprotein.
Review in Current topics in microbiology and immunology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 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
62 citing papers in PubMed, 109 citations in OpenAlex.
- Safety and antitumor activity of copanlisib in Japanese patients with relapsed/refractory indolent non-Hodgkin lymphoma: a phase Ib/II study.International journal of hematology · 2023Trial
- JAK3/STAT5 signaling-triggered upregulation of PIK3CD contributes to gastric carcinoma development.Journal of cell communication and signaling · 2024Article
- Overcoming Resistance in Cancer Therapy: Computational Exploration of PIK3CA Mutations, Unveiling Novel Non-Toxic Inhibitors, and Molecular Insights Into Targeting PI3Kα.Bioinformatics and biology insights · 2024Article
- Genetic Mutations Associated with Inflammatory Response Caused by HPV Integration in Oropharyngeal Squamous Cell Carcinoma.Biomedicines · 2023Article
- Appraisal of Systemic Treatment Strategies in Early HER2-Positive Breast Cancer-A Literature Review.Cancers · 2023Review
- The Role of PIK3R1 in Metabolic Function and Insulin Sensitivity.International journal of molecular sciences · 2023Review
- Therapeutic Importance of Kaempferol in the Treatment of Cancer through the Modulation of Cell Signalling Pathways.Molecules (Basel, Switzerland) · 2022Review
- The Flavagline Compound 1-(2-(dimethylamino)acetyl)-Rocaglaol Induces Apoptosis in K562 Cells by Regulating the PI3K/Akt/mTOR, JAK2/STAT3, and MAPK Pathways.Drug design, development and therapy · 2022Article
- Current understanding of gliomagenesis: from model to mechanism.International journal of medical sciences · 2022Review
- Control of CD4Current topics in microbiology and immunology · 2022Article
- Molecular and cellular characterization of two patient-derived ductal carcinoma in situ (DCIS) cell lines, ETCC-006 and ETCC-010.BMC cancer · 2021Article
- Copanlisib for the Treatment of Malignant Lymphoma: Clinical Experience and Future Perspectives.Targeted oncology · 2021Review
- Potential Therapeutic Targets of Quercetin, a Plant Flavonol, and Its Role in the Therapy of Various Types of Cancer through the Modulation of Various Cell Signaling Pathways.Molecules (Basel, Switzerland) · 2021Review
- Molecular Mechanisms of Hepatoblastoma.Seminars in liver disease · 2021Article
- MiR-155 promotes interleukin-1β-induced chondrocyte apoptosis and catabolic activity by targeting PIK3R1-mediated PI3K/Akt pathway.Journal of cellular and molecular medicine · 2020Article
- A PI3K- and GTPase-independent Rac1-mTOR mechanism mediates MET-driven anchorage-independent cell growth but not migration.Science signaling · 2020Article
- Epithelial PI3K-δ Promotes House Dust Mite-Induced Allergic Asthma in NLRP3 Inflammasome-Dependent and -Independent Manners.Allergy, asthma & immunology research · 2020Article
- Heterozygous p53-R280T Mutation Enhances the Oncogenicity of NPC Cells Through Activating PI3K-Akt Signaling Pathway.Frontiers in oncology · 2020Article
- PI3K/mTOR Pathway Inhibition: Opportunities in Oncology and Rare Genetic Diseases.International journal of molecular sciences · 2019Review
- Systematic analysis of breast atypical hyperplasia-associated hub genes and pathways based on text mining.European journal of cancer prevention : the official journal of the European Cancer Prevention Organisation (ECP) · 2019Article
2 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 3 institutions in 1 country.
Funding
Abstract
The catalytic and regulatory subunits of class I phosphoinositide 3-kinase (PI3K) have oncogenic potential. The catalytic subunit p110α and the regulatory subunit p85 undergo cancer-specific gain-of-function mutations that lead to enhanced enzymatic activity, ability to signal constitutively, and oncogenicity. The β, γ, and δ isoforms of p110 are cell-transforming as overexpressed wild-type proteins. Class I PI3Ks have the unique ability to generate phosphoinositide 3,4,5 trisphosphate (PIP(3)). Class II and class III PI3Ks lack this ability. Genetic and cell biological evidence suggests that PIP(3) is essential for PI3K-mediated oncogenicity, explaining why class II and class III enzymes have not been linked to cancer. Mutational analysis reveals the existence of at least two distinct molecular mechanisms for the gain of function seen with cancer-specific mutations in p110α; one causing independence from upstream receptor tyrosine kinases, the other inducing independence from Ras. An essential component of the oncogenic signal that is initiated by PI3K is the TOR (target of rapamycin) kinase. TOR is an integrator of growth and of metabolic inputs. In complex with the raptor protein (TORC1), it controls cap-dependent translation, and this function is essential for PI3K-initiated oncogenesis.
Indexed as
Identifiers
What Socratic 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 Socratic graph.