Evidence map›Paper›PMID 31602010›Full record

ReviewNature reviews. Urology2019

Drug resistance in papillary RCC: from putative mechanisms to clinical practicalities.

Anna Brodziak, Paweł Sobczuk, Ewa Bartnik, Michał Fiedorowicz, Camillo Porta, Cezary Szczylik, Anna M Czarnecka

Abstract readReview
PubMed Publisher
In one paragraph

Review in Nature reviews. Urology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
2.8field-weighted citation impact, top 9% 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

22 citing papers in PubMed, 34 citations in OpenAlex.

  1. Article
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  5. Observational
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  8. Review
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  16. Essential mJournal of oncology · 2022
    Article
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  18. Angiogenesis as a hallmark of solid tumors - clinical perspectives.Cellular oncology (Dordrecht, Netherlands) · 2021
    Review
  19. Article
  20. 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

7 authors at 5 institutions in 3 countries.

Anna BrodziakDepartment of Oncology, Military Institute of Medicine, Warsaw, Poland.ORCID http://orcid.org/0000-0002-0017-1040
Paweł SobczukDepartment of Oncology, Military Institute of Medicine, Warsaw, Poland.ORCID http://orcid.org/0000-0002-4103-1626
Ewa BartnikInstitute of Genetics and Biotechnology, Faculty of Biology, University of Warsaw, Warsaw, Poland.
Michał FiedorowiczDepartment of Experimental Pharmacology, Mossakowski Medical Research Centre, Polish Academy of Sciences, Warsaw, Poland.ORCID http://orcid.org/0000-0001-5755-3608
Camillo PortaDivision of Translational Oncology, IRCCS Istituti Clinici Scientifici Maugeri, Pavia, Italy.
Cezary SzczylikDepartment of Oncology, Military Institute of Medicine, Warsaw, Poland.
Anna M CzarneckaDepartment of Oncology, Military Institute of Medicine, Warsaw, Poland. anna.czarnecka@gmail.com.ORCID http://orcid.org/0000-0002-2107-3810
Medical University of Warsaw · PLInstitute of Biochemistry and Biophysics, Polish Academy of Sciences · PLMossakowski Medical Research Institute, Polish Academy of Sciences · PLNational Academy of Medicine · USUniversity of Pavia · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Papillary renal cell carcinoma (pRCC) is the second most common renal cell carcinoma (RCC) subtype and accounts for 10-15% of all RCCs. Despite clinical need, few pharmacogenomics studies in pRCC have been performed. Moreover, current research fails to adequately include pRCC laboratory models, such as the ACHN or Caki-2 pRCC cell lines. The molecular mechanisms involved in pRCC development and drug resistance are more diverse than in clear-cell RCC, in which inactivation of VHL occurs in the majority of tumours. Drug resistance to multiple therapies in pRCC occurs via genetic alteration (such as mutations resulting in abnormal receptor tyrosine kinase activation or RALBP1 inhibition), dysregulation of signalling pathways (such as GSK3β-EIF4EBP1, PI3K-AKT and the MAPK or interleukin signalling pathways), deregulation of cellular processes (such as resistance to apoptosis or epithelial-to-mesenchymal transition) and interactions between the cell and its environment (for example, through activation of matrix metalloproteinases). Improved understanding of resistance mechanisms will facilitate drug discovery and provide new effective therapies. Further studies on novel resistance biomarkers are needed to improve patient prognosis and stratification as well as drug development.

Indexed as

Drug Resistance, NeoplasmAnimalsBiomedical ResearchCarcinoma, Renal CellDisease Models, AnimalHumansKidney NeoplasmsSignal TransductionTumor Cells, Cultured

Identifiers

PMID31602010
OpenAlexW2980155728

What Socratic holds

Textmetadata
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.