Evidence map›Paper›PMID 30072823›Full record

ReviewIndian journal of clinical biochemistry : IJCB2018

Renal Cell Carcinoma: Molecular Aspects.

Aman Kumar, Niti Kumari, Vinny Gupta, Rajendra Prasad

Open access · hybridAbstract readReview
In one paragraph

Review in Indian journal of clinical biochemistry : IJCB, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
5.1field-weighted citation impact, top 4% 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

38 citing papers in PubMed, 66 citations in OpenAlex.

  1. Review
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  6. Cancers · 2025
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  11. The role of m5C, m1A and m7G modifications in tumors of urinary system.Frontiers in cell and developmental biology · 2025
    Review
  12. Review
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  17. 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 1 institution in 1 country.

Aman KumarDepartment of Biochemistry, Post Graduate Institute of Medical Education and Research (PGIMER), Sector 12, Chandigarh, India.
Niti KumariDepartment of Biochemistry, Post Graduate Institute of Medical Education and Research (PGIMER), Sector 12, Chandigarh, India.
Vinny GuptaDepartment of Biochemistry, Post Graduate Institute of Medical Education and Research (PGIMER), Sector 12, Chandigarh, India.
Rajendra PrasadDepartment of Biochemistry, Post Graduate Institute of Medical Education and Research (PGIMER), Sector 12, Chandigarh, India.ORCID 0000-0002-7104-9077
Post Graduate Institute of Medical Education and Research · IN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Renal cell carcinoma is the most common form of the kidney cancer accounting for more than 85% of the cases of which clear cell renal cell carcinoma (ccRCC) is the major histological subtype. The central molecular signature for ccRCC pathogenesis is the biallelic inactivation of VHL gene due to the presence of mutations/hyper-methylation/complete gene loss, which results in the downstream HIF activation. These events lead to increased tyrosine kinase receptor signalling pathways (RAS/MEK/ERK pathway, PI3K/AKT/mTOR pathway and NF-κB pathway), which through their downstream effector proteins causes the cell to proliferate and migrate. Recent studies have shown that VHL inactivation alone is not sufficient to induce the tumor. Mutations in numerous other genes that codes for chromatin modifiers (PBRM1, SETD2 and BAP1) and signalling proteins (PTEN and mTOR) have been identified along with activation of alternate signalling pathways like STAT and Sonic Hedgehog (SHH) pathway. It has also been shown that STAT pathway also works cooperatively with HIF to enhance the tumor progression. However, SHH pathway reactivation resulted in tumor regardless of the VHL status, indicating the complex nature of the tumor at the molecular level. Therefore, understanding the complete aetiology of ccRCC is important for future therapeutics.

Indexed as

Chromatin modifiersGenomicsHypoxia inducible factor (HIF)Renal cell carcinomaSignallingVon Hippel–Lindau (VHL)

Identifiers

PMID30072823
PMCPMC6052717
OpenAlexW2770399330

What OpenQuestion 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 OpenQuestion graph.