Evidence map›Paper›PMID 29430197›Full record

ReviewBreast cancer (Dove Medical Press)2018

Profile of buparlisib and its potential in the treatment of breast cancer: evidence to date.

Carmen Criscitiello, Giulia Viale, Giuseppe Curigliano, Aron Goldhirsch

Erratum issuedOpen access · goldAbstract readReview
In one paragraph

Review in Breast cancer (Dove Medical Press), 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.0field-weighted citation impact, top 20% 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, 24 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Review
  5. Article
  6. Review
  7. Frontiers in oncology · 2021
    Review
  8. Review
  9. Review
  10. Review
  11. Article
  12. Article
  13. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

4 authors at 1 institution in 1 country.

Carmen CriscitielloEuropean Institute of Oncology, Milano, Italy.
Giulia VialeEuropean Institute of Oncology, Milano, Italy.
Giuseppe CuriglianoEuropean Institute of Oncology, Milano, Italy.
Aron GoldhirschEuropean Institute of Oncology, Milano, Italy.
European Institute of Oncology · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Alteration of the phosphatidylinositol 3-kinase (PI3K)/AKT/mammalian target of rapamycin signaling pathway is key for the growth and survival of several cancers, including breast cancer. In addition, dysregulation of PI3K signaling may contribute to resistance to several anticancer agents. PI3K inhibitors may, therefore, be effective as antineoplastic therapy. Buparlisib is a potent and highly specific oral inhibitor of the pan-class I PI3K family. Buparlisib specifically inhibits class I PIK3 in the PI3K/AKT kinase signaling pathway in an ATP-competitive manner, thus inhibiting the production of the secondary messenger phosphatidylinositol (3,4,5)-trisphosphate and activation of the PI3K signaling pathway. This may induce inhibition of tumor cell growth and survival in susceptible tumor cell populations. Buparlisib is currently under investigation in patients with a variety of solid tumors, including breast cancer. Buparlisib has been validated as a promising anticancer agent, and tremendous efforts have been taken to develop it. However, buparlisib monotherapy has resulted in humble benefit so far. Results from studies combining buparlisib with different anticancer agents - namely, endocrine therapy, anti-HER2 therapy, and chemotherapy - have showed variable efficacy with consistent substantial toxicity.

Indexed as

breast cancerbuparlisibPI3K

Identifiers

PMID29430197
PMCPMC5796458
OpenAlexW2793843180

What OpenQuestion 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 OpenQuestion graph.