Evidence map›Paper›PMID 31175376›Full record

ReviewDer Urologe. Ausg. A2019

[Molecular tumor board-renal cell carcinoma].

V Grünwald, C Doehn, P J Goebell

Abstract readReview
PubMed Publisher
In one paragraph

Review in Der Urologe. Ausg. A, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

3 authors.

V GrünwaldWestdeutsches Tumorzentrum, Innere Klinik (Tumorforschung) und Klinik für Urologie, Universitätsklinikum Essen (AöR), Essen, Deutschland.
C DoehnUrologikum Lübeck, Lübeck, Deutschland.
P J GoebellUrologische und Kinderurologische Universitätsklinik, Friedrich-Alexander Universität, Erlangen-Nürnberg, Krankenhausstrasse 12, 91054, Erlangen, Deutschland. peter.goebell@uk-erlangen.de.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The introduction of molecular targeted agents has fundamentally changed the treatment of metastatic renal cell carcinoma. A first wave of development was based on the improved understanding of tumor biology since the discovery of the importance of the von Hippel-Lindau gene as the key driver of the disease and paved the way for antiangiogenic agents. Of relevance is the overexpression of proangiogenic and proliferation-promoting factors (VEGF, vascular endothelial growth factor; PDGF, platelet-derived growth factor) as well as an overactivation of the PI3K-Akt signaling pathway: the target structure is the "mammalian target of rapamycin" (mTOR) molecule, which is involved in the regulation of cell proliferative processes. VEGF-, PDGF-, and mTOR-signals and signaling pathways are central targets of current targeted substances. A second wave is certainly to be seen in the development of therapeutic approaches with the targeted activation and modulation of the immune system, which has brought "immunotherapy" back into the focus of interest. Central development is the application of immune-checkpoint inhibitors, with the help of which (re-)activation of the cellular defense, especially of T cells, takes place, which per se holds the potential of a cytoreductive therapy by killing the tumor cells. Even though the prognosis has improved significantly due to the rapid development of recent years, treatment remains challenging as most patients experience progress, and long-term survival is only achieved in about 20% of cases because some patients are primarily refractory or do not respond. The more intensive interlocking of molecular biology, pathology, clinical research, and interdisciplinary uro-oncology, as is the claim of molecular tumor boards, can contribute to the individual selection of a suitable therapy strategy and, thus, establish the latest findings and developments for the benefit of patients in the clinic.

Indexed as

Molecular Targeted TherapyVascular Endothelial Growth Factor AAngiogenesis InhibitorsCarcinoma, Renal CellHumansKidney NeoplasmsNeoplasmsPhosphatidylinositol 3-KinasesPlatelet-Derived Growth FactorPrognosisProtein Kinase InhibitorsSignal TransductionTOR Serine-Threonine KinasesAngiogenesis InhibitorsMTOR protein, humanPhosphatidylinositol 3-KinasesPlatelet-Derived Growth FactorProtein Kinase InhibitorsTOR Serine-Threonine KinasesVascular Endothelial Growth Factor AMarkerMutational analysisPlatelet derived growth factorSignaling pathwaysVascular endothelial growth factor

Identifiers

What OpenQuestion holds

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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.