Evidence map›Paper›PMID 32351542›Full record

ReviewFrontiers in genetics2020

Sequential or Concomitant Inhibition of Cyclin-Dependent Kinase 4/6 Before mTOR Pathway in Hormone-Positive HER2 Negative Breast Cancer: Biological Insights and Clinical Implications.

Giulia Occhipinti, Emanuela Romagnoli, Matteo Santoni, Alessia Cimadamore, Giulia Sorgentoni, Monia Cecati, Matteo Giulietti, Nicola Battelli, Alessandro Maccioni, Nadia Storti and 4 more

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in genetics, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
1.3field-weighted citation impact, top 17% 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

8 citing papers in PubMed, 10 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. mTOR Activity and Autophagy in Senescent Cells, a Complex Partnership.International journal of molecular sciences · 2021
    Review
  6. Review
  7. Review
  8. 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

14 authors at 5 institutions in 2 countries.

Giulia OcchipintiDepartment of Specialistic Clinical and Odontostomatological Sciences, Polytechnic University of Marche, Ancona, Italy.
Emanuela RomagnoliOncology Unit, Macerata Hospital, Macerata, Italy.
Matteo SantoniOncology Unit, Macerata Hospital, Macerata, Italy.
Alessia CimadamoreSection of Pathological Anatomy, School of Medicine, United Hospitals, Polytechnic University of the Marche Region, Ancona, Italy.
Giulia SorgentoniOncology Unit, Macerata Hospital, Macerata, Italy.
Monia CecatiDepartment of Specialistic Clinical and Odontostomatological Sciences, Polytechnic University of Marche, Ancona, Italy.
Matteo GiuliettiDepartment of Specialistic Clinical and Odontostomatological Sciences, Polytechnic University of Marche, Ancona, Italy.
Nicola BattelliOncology Unit, Macerata Hospital, Macerata, Italy.
Alessandro MaccioniDirezione Area Vasta 3, Macerata, Italy.
Nadia StortiDirezione Sanitaria Azienda Sanitaria Unica Regionale, Ancona, Italy.
Liang ChengDepartment of Pathology and Laboratory Medicine, Indiana University School of Medicine, Indianapolis, IN, United States.
Giovanni PrincipatoDepartment of Specialistic Clinical and Odontostomatological Sciences, Polytechnic University of Marche, Ancona, Italy.
Rodolfo MontironiSection of Pathological Anatomy, School of Medicine, United Hospitals, Polytechnic University of the Marche Region, Ancona, Italy.
Francesco PivaDepartment of Specialistic Clinical and Odontostomatological Sciences, Polytechnic University of Marche, Ancona, Italy.
Ospedale di MacerataMarche Polytechnic University · ITAgenzia Regionale Sanitaria della Puglia · ITIndiana University School of MedicineUniversity of Macerata · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

About 75% of all breast cancers are hormone receptor-positive (HR+). However, the efficacy of endocrine therapy is limited due to the high rate of either pre-existing or acquired resistance. In this work we reconstructed the pathways around estrogen receptor (ER), mTOR, and cyclin D in order to compare the effects of CDK4/6 and PI3K/AKT/mTOR inhibitors. A positive feedback loop links mTOR and ER that support each other. We subsequently considered whether a combined or sequential inhibition of CDK4/6 and PI3K/AKT/mTOR could ensure better results. Studies indicate that inhibition of CDK4/6 activates mTOR as an escape mechanism to ensure cell proliferation. In literature, the little evidence dealing with this topic suggests that pre-treatment with mTOR pathway inhibitors could prevent or delay the onset of CDK4/6 inhibitor resistance. Additional studies are needed in order to find biomarkers that can identify patients who will develop this resistance and in whom the sensitivity to CDK4/6 inhibitors can be restored.

Indexed as

breast cancerCDK inhibitorscyclin-dependent kinases (CDKs)estrogen receptormechanisms of resistance

Identifiers

PMID32351542
PMCPMC7174681
OpenAlexW3016495342

What Socratic 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 Socratic graph.