Evidence map›Paper›PMID 27405474›Full record

ReviewBMC cancer2016

Insulin-like growth factor-1 signaling in renal cell carcinoma.

Adam F Tracz, Cezary Szczylik, Camillo Porta, Anna M Czarnecka

Registry-linked trialOpen access · goldAbstract readReview
In one paragraph

Review in BMC cancer, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT05119010 (A Pilot Study Evaluating a Ketogenic Diet Concomitant to Nivolumab and Ipilimumab in Patients With Metastatic Renal Cell Carcinoma), which is not on this map. Cited by 42 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed, 3 pooled it
4.2field-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.

NCT05119010 naterminatednot on this mapstarted 2023, after this paper: background citation

A Pilot Study Evaluating a Ketogenic Diet Concomitant to Nivolumab and Ipilimumab in Patients With Metastatic Renal Cell Carcinoma

TypeinterventionalSponsorGustave Roussy, Cancer Campus, Grand ParisRan2023 to 2024Enrolled3ConditionsMetastatic Renal Cell CarcinomaArmsContinuous ketogenic diet, Discontinuous ketogenic diet, beta-hydroxybutyrate (BHB) supplementation
3 · Its place in the literature

Who cites it

42 citing papers in PubMed, 3 syntheses or guidelines pooled it, 68 citations in OpenAlex.

  1. Pooled it
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  14. Review
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  17. Renal Cell Cancer and Obesity.International journal of molecular sciences · 2022
    Review
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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 2 institutions in 2 countries.

Adam F TraczDepartment of Oncology with Laboratory of Molecular Oncology, Military Institute of Medicine, Szaserow 128, 04-141, Warsaw, Poland.
Cezary SzczylikDepartment of Oncology with Laboratory of Molecular Oncology, Military Institute of Medicine, Szaserow 128, 04-141, Warsaw, Poland.
Camillo PortaDepartment of Medical Oncology, IRCCS San Matteo University Hospital Foundation, Pavia, Italy.
Anna M CzarneckaDepartment of Oncology with Laboratory of Molecular Oncology, Military Institute of Medicine, Szaserow 128, 04-141, Warsaw, Poland. cszczylik@wim.mil.pl.
Medical University of Warsaw · PLUniversity of Pavia · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Renal cell carcinoma (RCC) incidence is highest in highly developed countries and it is the seventh most common neoplasm diagnosed. RCC management include nephrectomy and targeted therapies. Type 1 insulin-like growth factor (IGF-1) pathway plays an important role in cell proliferation and apoptosis resistance. IGF-1 and insulin share overlapping downstream signaling pathways in normal and cancer cells. IGF-1 receptor (IGF1R) stimulation may promote malignant transformation promoting cell proliferation, dedifferentiation and inhibiting apoptosis. Clear cell renal cell carcinoma (ccRCC) patients with IGF1R overexpression have 70 % increased risk of death compared to patients who had tumors without IGF1R expression. IGF1R signaling deregulation may results in p53, WT, BRCA1, VHL loss of function. RCC cells with high expression of IGF1R are more resistant to chemotherapy than cells with low expression. Silencing of IGF1R increase the chemosensitivity of ccRCC cells and the effect is greater in VHL mutated cells. Understanding the role of IGF-1 signaling pathway in RCC may result in development of new targeted therapeutic interventions. First preclinical attempts with anti-IGF-1R monoclonal antibodies or fragment antigen-binding (Fab) fragments alone or in combination with an mTOR inhibitor were shown to inhibit in vitro growth and reduced the number of colonies formed by of RCC cells.

Indexed as

ApoptosisBRCA1 ProteinCarcinoma, Renal CellCell ProliferationHumansInsulin-Like Growth Factor IKidney NeoplasmsReceptor, IGF Type 1Receptors, SomatomedinSignal TransductionTOR Serine-Threonine KinasesTumor Suppressor Protein p53Von Hippel-Lindau Tumor Suppressor ProteinWT1 ProteinsBRCA1 ProteinBRCA1 protein, humanIGF1 protein, humanIGF1R protein, humanInsulin-Like Growth Factor IMTOR protein, humanReceptor, IGF Type 1Receptors, SomatomedinTOR Serine-Threonine KinasesTumor Suppressor Protein p53VHL protein, humanVon Hippel-Lindau Tumor Suppressor ProteinWT1 protein, humanWT1 ProteinsccRCC)IGF-1 receptor (IGF1R)Insulin-like growth factor-1 (IGF-1)Renal cell carcinoma (RCC

Identifiers

PMID27405474
PMCPMC4942928
OpenAlexW2474485504

What OpenQuestion holds

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Registered trials

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.