ArticleCancer cell2009
Evidence that inositol polyphosphate 4-phosphatase type II is a tumor suppressor that inhibits PI3K signaling.
Article in Cancer cell, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 265 papers.
What it found
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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
265 citing papers in PubMed, 457 citations in OpenAlex.
- Phase 2 study of buparlisib (BKM120), a pan-class I PI3K inhibitor, in patients with metastatic triple-negative breast cancer.Breast cancer research : BCR · 2020Trial
- BEECH: a dose-finding run-in followed by a randomised phase II study assessing the efficacy of AKT inhibitor capivasertib (AZD5363) combined with paclitaxel in patients with estrogen receptor-positive advanced or metastatic breast cancer, and in a PIK3CA mutant sub-population.Annals of oncology : official journal of the European Society for Medical Oncology · 2019Trial
- A comprehensive analysis of phosphatase and tensin homolog deleted on chromosome 10 (PTEN) loss in colorectal cancer.World journal of surgical oncology · 2015Trial
- Targeting Insulin Signaling and TRAF2/JNK Pathway: A Comprehensive In Silico Study ofInternational journal of molecular sciences · 2026Article
- Single cell transcriptomics reveals dendritic cell subsets in bovine afferent lymph and immune cell-resolved responses to BCG vaccination.Frontiers in immunology · 2026Article
- Non-redundant roles of the phosphoinositide phosphatases PTEN and PIPP in PI3K/AKT signaling in breast cancer.Communications biology · 2025Article
- Imbalance of stem-like and effector T cell states in children with early type 1 diabetes across conventional and regulatory subsets.Nature communications · 2025Article
- Androgen deprivation-mediated activation of AKT is enhanced in prostate cancer with TMPRSS2:ERG fusion.The Journal of clinical investigation · 2025Article
- SFTSV utilizes AXL/GAS6 for entry via PI3K-PLC-dependent macropinocytosis activated by AXL-kinase.Journal of virology · 2025Article
- Cardamomin Inhibits the Proliferation and Tumorigenesis of Bladder Cancer by ESR1 in PI3K/AKT Pathway.Biochemical genetics · 2025Article
- The Inositol-5-Phosphatase SHIP1: Expression, Regulation and Role in Acute Lymphoblastic Leukemia.International journal of molecular sciences · 2025Review
- Immunometabolism and oxidative stress: roles and therapeutic strategies in cancer and aging.npj aging · 2025Review
- Lysosomal PIPProceedings of the National Academy of Sciences of the United States of America · 2025Article
- Class I PI3Ks activate stretch-induced autophagy in trabecular meshwork cells.Cellular and molecular life sciences : CMLS · 2025Article
- INPP4B promotes PDAC aggressiveness via PIKfyve and TRPML-1-mediated lysosomal exocytosis.The Journal of cell biology · 2024Article
- Breast cancer immunotherapy: Realities and advances.Cancer innovation · 2024Review
- Role of INPP4B in the proliferation, migration, invasion, and survival of human endometrial cancer cells.Histology and histopathology · 2024Article
- PTEN acts as a crucial inflammatory checkpoint controlling TLR9/IL-6 axis in B cells.iScience · 2024Article
- Article
- Molecular pathways and therapeutic targets linked to triple-negative breast cancer (TNBC).Molecular and cellular biochemistry · 2024Review
205 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
12 authors at 6 institutions in 2 countries.
Funding
Abstract
We report that knocking down the expression of inositol polyphosphate 4-phosphatase type II (INPP4B) in human epithelial cells, like knockdown of PTEN, resulted in enhanced Akt activation and anchorage-independent growth and enhanced overall motility. In xenograft experiments, overexpression of INPP4B resulted in reduced tumor growth. INPP4B preferentially hydrolyzes phosphatidylinositol-3,4-bisphosphate (PI(3,4)P(2)) with no effect on phosphatidylinositol-3.4.5-triphosphate (PI(3,4,5)P(3)), suggesting that PI(3,4)P(2) and PI(3,4,5)P(3) may cooperate in Akt activation and cell transformation. Dual knockdown of INPP4B and PTEN resulted in cellular senescence. Finally, we found loss of heterozygosity (LOH) at the INPP4B locus in a majority of basal-like breast cancers, as well as in a significant fraction of ovarian cancers, which correlated with lower overall patient survival, suggesting that INPP4B is a tumor suppressor.
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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.