Evidence map›Paper›PMID 33304317›Full record

ReviewFrontiers in endocrinology2020

mTOR Pathway in Gastroenteropancreatic Neuroendocrine Tumor (GEP-NETs).

Sara Zanini, Serena Renzi, Francesco Giovinazzo, Giovanna Bermano

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in endocrinology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed, 1 pooled it
3.8field-weighted citation impact, top 5% 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

28 citing papers in PubMed, 1 synthesis or guideline pooled it, 44 citations in OpenAlex.

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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

4 authors at 3 institutions in 2 countries.

Sara ZaniniCentre for Obesity Research and Education (CORE), School of Pharmacy and Life Sciences, Robert Gordon University, Aberdeen, United Kingdom.
Serena RenziSchool of Biosciences and Veterinary Medicine, University of Camerino, Camerino, Italy.
Francesco GiovinazzoFondazione Policlinico Universitario A. Gemelli Istituto di ricovero e cura a carattere scientifico (IRCCS), Department of Surgery -Transplantation Service, Rome, Italy.
Giovanna BermanoCentre for Obesity Research and Education (CORE), School of Pharmacy and Life Sciences, Robert Gordon University, Aberdeen, United Kingdom.
Robert Gordon University · GBIstituti di Ricovero e Cura a Carattere Scientifico · ITUniversità di Camerino · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Gastroenteropancreatic neuroendocrine neoplasms (GEP-NENs) originate from neuroendocrine cells in the gastrointestinal tract. They are heterogeneous, and though initially considered rare tumors, the incidence of GEP-NENs has increased in the last few decades. Therapeutic approaches for the metastatic disease include surgery, radiological intervention by chemoembolisation, radiofrequency ablation, biological therapy in addition to somatostatin analogs, and PRRT therapy (177Lu-DOTATATE). The PI3K-AKT-mTOR pathway is essential in the regulation of protein translation, cell growth, and metabolism. Evidence suggests that the mTOR pathway is involved in malignant progression and resistance to treatment through over-activation of several mechanisms. PI3K, one of the main downstream of the Akt-mTOR axis, is mainly involved in the neoplastic process. This pathway is frequently deregulated in human tumors, making it a central target in the development of new anti-cancer treatments. Recent molecular studies identify potential targets within the PI3K/Akt/mTOR pathway in GEP-NENs. However, the use of target therapy has been known to lead to resistance due to several mechanisms such as feedback activation of alternative pathways, inactivation of protein kinases, and deregulation of the downstream mTOR components. Therefore, the specific role of targeted drugs for the management of GEP-NENs is yet to be well-defined. The variable clinical presentation of advanced neuroendocrine tumors is a significant challenge for designing studies. This review aims to highlight the role of the PI3K/Akt/mTOR pathway in the development of neuroendocrine tumors and further specify its potential as a therapeutic target in advanced stages.

Indexed as

AnimalsAntineoplastic AgentsCell ProliferationHumansIntestinal NeoplasmsNeuroendocrine TumorsPancreatic NeoplasmsPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktRandomized Controlled Trials as TopicSignal TransductionStomach NeoplasmsTOR Serine-Threonine KinasesAntineoplastic AgentsMTOR protein, humanPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktTOR Serine-Threonine Kinasescancer treatmentGEP-NENsGEP-NETsmTORneuroendocrine tumortarget therapy

Identifiers

PMID33304317
PMCPMC7701056
OpenAlexW3098953574

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.