Evidence map›Paper›PMID 33552053›Full record

ReviewFrontiers in immunology2020

Phosphoinositide 3-Kinase Signaling in the Tumor Microenvironment: What Do We Need to Consider When Treating Chronic Lymphocytic Leukemia With PI3K Inhibitors?

Ebru Aydin, Sebastian Faehling, Mariam Saleh, Laura Llaó Cid, Martina Seiffert, Philipp M Roessner

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in immunology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed, 1 pooled it
2.5field-weighted citation impact, top 10% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

13 citing papers in PubMed, 1 synthesis or guideline pooled it, 25 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Biochemistry and biophysics reports · 2026
    Article
  4. Review
  5. Article
  6. Review
  7. Oncogenic activation ofGenes & diseases · 2025
    Review
  8. Review
  9. Article
  10. Article
  11. Review
  12. Review
  13. PI3K inhibitors are finally coming of age.Nature reviews. Drug discovery · 2021
    Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors at 2 institutions in 2 countries.

Ebru AydinMolecular Genetics, German Cancer Research Center (DKFZ), Heidelberg, Germany.
Sebastian FaehlingMolecular Genetics, German Cancer Research Center (DKFZ), Heidelberg, Germany.
Mariam SalehMolecular Genetics, German Cancer Research Center (DKFZ), Heidelberg, Germany.
Laura Llaó CidMolecular Genetics, German Cancer Research Center (DKFZ), Heidelberg, Germany.
Martina SeiffertMolecular Genetics, German Cancer Research Center (DKFZ), Heidelberg, Germany.
Philipp M RoessnerMolecular Genetics, German Cancer Research Center (DKFZ), Heidelberg, Germany.
German Cancer Research Center · DEHeidelberg University · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Phosphoinositide 3-kinases (PI3Ks) and their downstream proteins constitute a signaling pathway that is involved in both normal cell growth and malignant transformation of cells. Under physiological conditions, PI3K signaling regulates various cellular functions such as apoptosis, survival, proliferation, and growth, depending on the extracellular signals. A deterioration of these extracellular signals caused by mutational damage in oncogenes or growth factor receptors may result in hyperactivation of this signaling cascade, which is recognized as a hallmark of cancer. Although higher activation of PI3K pathway is common in many types of cancer, it has been therapeutically targeted for the first time in chronic lymphocytic leukemia (CLL), demonstrating its significance in B-cell receptor (BCR) signaling and malignant B-cell expansion. The biological activity of the PI3K pathway is not only limited to cancer cells but is also crucial for many components of the tumor microenvironment, as PI3K signaling regulates cytokine responses, and ensures the development and function of immune cells. Therefore, the success or failure of the PI3K inhibition is strongly related to microenvironmental stimuli. In this review, we outline the impacts of PI3K inhibition on the tumor microenvironment with a specific focus on CLL. Acknowledging the effects of PI3K inhibitor-based therapies on the tumor microenvironment in CLL can serve as a rationale for improved drug development, explain treatment-associated adverse events, and suggest novel combinatory treatment strategies in CLL.

Indexed as

AnimalsAntineoplastic AgentsHumansLeukemia, Lymphocytic, Chronic, B-CellPhosphatidylinositol 3-KinasesPhosphoinositide-3 Kinase InhibitorsSignal TransductionTumor MicroenvironmentAntineoplastic AgentsPhosphatidylinositol 3-KinasesPhosphoinositide-3 Kinase Inhibitorschronic lymphocytic leukemiaidelalisibphosphoinositide 3-kinase (PI3K)phosphoinositide 3-kinase (PI3K) inhibitiontumor microenvironment

Identifiers

PMID33552053
PMCPMC7857022
OpenAlexW3124701680

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.