ArticleOncotarget2017
PIK3CA amplification and PTEN loss in diffused large B-cell lymphoma.
Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 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.
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Who cites it
6 citing papers in PubMed, 9 citations in OpenAlex.
- NPC2 deficiency as a potential target drives malignancy and chemo-resistance in DLBCL.Biology direct · 2026Article
- Potential Pathogenic Impact of Cow's Milk Consumption and Bovine Milk-Derived Exosomal MicroRNAs in Diffuse Large B-Cell Lymphoma.International journal of molecular sciences · 2023Review
- T-cell lymphoblastic lymphoma with extensive thrombi and cardiac thrombosis: A case report and review of literature.World journal of clinical cases · 2021Article
- Role of PI3K/AKT pathway in cancer: the framework of malignant behavior.Molecular biology reports · 2020Review
- Clinical Significance of PTEN Deletion, Mutation, and Loss of PTEN Expression in De Novo Diffuse Large B-Cell Lymphoma.Neoplasia (New York, N.Y.) · 2018Article
- Metabolic Reprogramming of Non-Hodgkin's B-Cell Lymphomas and Potential Therapeutic Strategies.Frontiers in oncology · 2018Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Although it has been known that PIK3CA was amplified and PTEN was deficient on protein level in DLBCL, the clinicopathological significance of PIK3CA and PTEN genetic change on DNA level hasn't been established. Here, in our present study, to understand the clinical significance of genetic status of PIK3CA and PTEN in DLBCL, fluorescent in-situ hybridization (FISH) was employed to evaluate the genetic change of PIK3CA and PTEN in clinical sample tissues consist of 205 cases. Incidentally, to understand the clinicopathological significance of genetic change of PIK3CA and PTEN, Cross-table analysis was used to analyze the association between genetic change of PIK3CA and PTEN versus clinicopathological variables available to us, including age, gender, size, location, international prognosis index, performance state, B-symptom, clinical stage, Extra nodal site, concentration of lactate dehydrogenase, therapeutic effects, treatment and overall prognosis. It was found that PIK3CA was amplified and PTEN was deficient on DNA level, the percentage of amplification and loss was 12.7% (26/205) and 12.2% (25/205), respectively. Additionally, no significant association was observed between genetic change of PIK3CA and PTEN versus clinicopathological variables available. Nor was the significant correlation found between loss of PTEN versus PIK3CA amplification. Our results suggest that PTEN deficiency and amplification of PIK3CA on DNA level was an event in the pathogenesis of DLBCL.
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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.