Evidence map›Paper›PMID 28945111›Full record

ReviewExpert opinion on investigational drugs2017

PI3Kδ-selective and PI3Kα/δ-combinatorial inhibitors in clinical development for B-cell non-Hodgkin lymphoma.

Benjamin L Lampson, Jennifer R Brown

Abstract readReview
In one paragraph

Review in Expert opinion on investigational drugs, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed, 1 pooled it
4.9field-weighted citation impact, top 4% 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

40 citing papers in PubMed, 1 synthesis or guideline pooled it, 72 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Review
  4. Article
  5. Review
  6. Review
  7. Review
  8. Article
  9. Article
  10. Duvelisib Eliminates CLL B Cells, Impairs CLL-Supporting Cells, and Overcomes Ibrutinib Resistance in a Xenograft Model.Clinical cancer research : an official journal of the American Association for Cancer Research · 2023
    Article
  11. Article
  12. Review
  13. Review
  14. PI3k Inhibitors in NHL and CLL: An Unfulfilled Promise.Blood and lymphatic cancer : targets and therapy · 2023
    Review
  15. Article
  16. Copanlisib plus rituximab combination therapyAnnals of translational medicine · 2022
    Article
  17. Review
  18. Review
  19. PI3K inhibitors are finally coming of age.Nature reviews. Drug discovery · 2021
    Review
  20. Article
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

2 authors at 1 institution in 1 country.

Benjamin L Lampsona Department of Medical Oncology , Dana-Farber Cancer Institute , Boston , MA , USA.
Jennifer R Browna Department of Medical Oncology , Dana-Farber Cancer Institute , Boston , MA , USA.
Dana-Farber Cancer Institute · US

Funding

Physician Scientist Training in Cancer ResearchT32CA009172 · NCI · DANA-FARBER CANCER INSTITUTE · PI Jennifer R Brown, James A. DeCaprio · 1985 to 2026
$17.1M
Unlocking the Potential of PI3K Inhibition in CLLR01CA213442 · NCI · DANA-FARBER CANCER INST · PI BROWN, JENNIFER R · 2017 to 2021
$2.9M
NCI NIH HHS R01 CA213442NCI NIH HHS T32 CA009172
6 · The paper itself

Abstract

introductionThe efficacy of the prototypical phosphatidylinositol-3-kinase (PI3K) inhibitor idelalisib for the treatment of chronic lymphocytic leukemia (CLL) and indolent non-Hodgkin lymphoma (iNHL) has led to development of multiple compounds targeting this pathway. Areas Covered: We review the hypothesized therapeutic mechanisms of PI3K inhibitors, including abrogation of B cell receptor signaling, blockade of microenvironmental pro-survival signals, and enhancement of anti-tumor immunity. We examine toxicities of idelalisib, including bacterial infections (possibly secondary to drug-induced neutropenia), opportunistic infections (possibly attributable to on-target inhibition of T cell function), and organ toxicities such as transaminitis and enterocolitis (possibly autoimmune, secondary to on-target inhibition of p110δ in regulatory T cells). We evaluate PI3K inhibitors that have entered trials for the treatment of lymphoma, focusing on agents with selectivity for PI3Kα and PI3Kδ. Expert Opinion: PI3K inhibitors, particularly those that target p110δ, have robust efficacy in the treatment of CLL and iNHL. However, idelalisib has infectious and autoimmune toxicities that limit its use. Outside of trials, idelalisib should be restricted to CLL patients with progression on ibrutinib or iNHL patients with progression on two prior therapies. Whether newer PI3K inhibitors will demonstrate differentiated toxicity profiles in comparable patient populations while retaining efficacy remains to be seen.

Indexed as

AnimalsAntineoplastic AgentsClass I Phosphatidylinositol 3-KinasesDrug DesignEnzyme InhibitorsHumansLeukemia, Lymphocytic, Chronic, B-CellLymphoma, Non-HodgkinMolecular Targeted TherapyPurinesQuinazolinonesAntineoplastic AgentsClass I Phosphatidylinositol 3-KinasesEnzyme InhibitorsidelalisibPIK3CA protein, humanPIK3CD protein, humanPurinesQuinazolinoneschronic lymphocytic leukemiacopanlisibduvelisibidelalisibindolent non-Hodgkin lymphomaPI3-kinase inhibitorsumbralisib

Identifiers

PMID28945111
PMCPMC5747968
OpenAlexW2760227417

What OpenQuestion holds

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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.