Evidence map›Paper›PMID 26793003›Full record

ReviewOncoTargets and therapy2016

PI3K inhibitors as new cancer therapeutics: implications for clinical trial design.

Cristian Massacesi, Emmanuelle Di Tomaso, Patrick Urban, Caroline Germa, Cornelia Quadt, Lucia Trandafir, Paola Aimone, Nathalie Fretault, Bharani Dharan, Ranjana Tavorath and 1 more

Open access · goldAbstract readReview
In one paragraph

Review in OncoTargets and therapy, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 122 papers.

0numbers the graph read from it
0cells of the map it votes in
122citing papers in PubMed
36.9field-weighted citation impact, top 1% 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

122 citing papers in PubMed, 230 citations in OpenAlex.

  1. Trial
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  17. Antitumor effects of valdecoxib on hypopharyngeal squamous carcinoma cells.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2022
    Article
  18. Synthesis andRSC medicinal chemistry · 2022
    Article
  19. Article
  20. Article

62 more citing papers are in PubMed but not listed here.

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

11 authors at 4 institutions in 4 countries.

Cristian MassacesiNovartis Oncology, Paris, France.
Emmanuelle Di TomasoNovartis Institutes for BioMedical Research Inc, Cambridge, MA, USA.
Patrick UrbanNovartis Pharma AG, Basel, Switzerland.
Caroline GermaNovartis Pharmaceuticals Corporation, East Hanover, NJ, USA.
Cornelia QuadtNovartis Pharmaceuticals KK, Tokyo, Japan.
Lucia TrandafirNovartis Oncology, Paris, France.
Paola AimoneNovartis Pharma AG, Basel, Switzerland.
Nathalie FretaultNovartis Oncology, Paris, France.
Bharani DharanNovartis Pharmaceuticals Corporation, East Hanover, NJ, USA.
Ranjana TavorathNovartis Pharmaceuticals Corporation, East Hanover, NJ, USA.
Samit HirawatNovartis Pharmaceuticals Corporation, East Hanover, NJ, USA.
Novartis (United States) · USNovartis (France) · FRNovartis (Switzerland) · CHNovartis (Japan) · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The PI3K-AKT-mTOR pathway is frequently activated in cancer. PI3K inhibitors, including the pan-PI3K inhibitor buparlisib (BKM120) and the PI3Kα-selective inhibitor alpelisib (BYL719), currently in clinical development by Novartis Oncology, may therefore be effective as anticancer agents. Early clinical studies with PI3K inhibitors have demonstrated preliminary antitumor activity and acceptable safety profiles. However, a number of unanswered questions regarding PI3K inhibition in cancer remain, including: what is the best approach for different tumor types, and which biomarkers will accurately identify the patient populations most likely to benefit from specific PI3K inhibitors? This review summarizes the strategies being employed by Novartis Oncology to help maximize the benefits of clinical studies with buparlisib and alpelisib, including stratification according to PI3K pathway activation status, selective enrollment/target enrichment (where patients with PI3K pathway-activated tumors are specifically recruited), nonselective enrollment with mandatory tissue collection, and enrollment of patients who have progressed on previous targeted agents, such as mTOR inhibitors or endocrine therapy. An overview of Novartis-sponsored and Novartis-supported trials that are utilizing these approaches in a range of cancer types, including breast cancer, head and neck squamous cell carcinoma, non-small cell lung carcinoma, lymphoma, and glioblastoma multiforme, is also described.

Indexed as

biomarkersclinical trial designpatient selectionPI3K–AKT–mTOR pathwayPI3K inhibitors

Identifiers

PMID26793003
PMCPMC4708174
OpenAlexW2229509093

What Socratic holds

Textmetadata
LicenceCC BY-NC
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 Socratic graph.