Evidence map›Paper›PMID 25821562›Full record

ArticleGenes & cancer2015

Microarray profile of human kidney from diabetes, renal cell carcinoma and renal cell carcinoma with diabetes.

Adam Kosti, Hung-I Harry Chen, Sumathy Mohan, Sitai Liang, Yidong Chen, Samy L Habib

Open access · diamondAbstract read
In one paragraph

Article in Genes & cancer, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.5field-weighted citation impact, top 26% 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

5 citing papers in PubMed, 7 citations in OpenAlex.

  1. Article
  2. Article
  3. The Role of Metabolic Factors in Renal Cancers.International journal of molecular sciences · 2020
    Review
  4. Article
  5. 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

6 authors at 2 institutions in 1 country.

Adam KostiDepartment of Cellular & Structural Biology, University of Texas Health Science Center, San Antonio, Texas.
Hung-I Harry ChenDepartment of Greehey Children's Cancer Research Institute, University of Texas Health Science Center, San Antonio, Texas.
Sumathy MohanDepartment of Pathology, University of Texas Health Science Center, San Antonio, Texas.
Sitai LiangDepartment of Cellular & Structural Biology, University of Texas Health Science Center, San Antonio, Texas.
Yidong ChenDepartment of Greehey Children's Cancer Research Institute, University of Texas Health Science Center, San Antonio, Texas ; Department of Epidemiology and Biostatistics, University of Texas Health Science Center, San Antonio, Texas.
Samy L HabibGeriatric Research, Education and Clinical Center, South Texas Veterans Healthcare System, University of Texas Health Science Center, San Antonio, Texas ; Department of Cellular & Structural Biology, University of Texas Health Science Center, San Antonio, Texas.
The University of Texas Health Science Center at San Antonio · USGeriatric Research Education and Clinical Center · US

Funding

INSTITUTE FOR INTEGRATION OF MEDICINE & SCIENCE: A PARTNERSHIP TO IMPROVE HEALTHUL1RR025767 · NCRR · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI CLARK, ROBERT A · 2008 to 2011
$23.8M
Role of Diabetes in Development of Renal Cell CarcinomaI01BX000924 · VA · SOUTH TEXAS VETERANS HEALTH CARE SYSTEM · PI HABIB, SAMY LEWIZ · 2011 to 2017
–
BLRD VA I01 BX000924NCRR NIH HHS UL1 RR025767
6 · The paper itself

Abstract

Recent study from our laboratory showed that patients with diabetes are at a higher risk of developing kidney cancer. In the current study, we have screened whole human DNA genome from healthy control, patients with diabetes or renal cell carcinoma (RCC) or RCC+diabetes. We found that 883 genes gain/163 genes loss of copy number in RCC+diabetes group, 669 genes gain/307 genes loss in RCC group and 458 genes gain/38 genes loss of copy number in diabetes group, after removing gain/loss genes obtained from healthy control group. Data analyzed for functional annotation enrichment pathways showed that control group had the highest number (280) of enriched pathways, 191 in diabetes+RCC group, 148 in RCC group, and 81 in diabetes group. The overlap GO pathways between RCC+diabetes and RCC groups showed that nine were enriched, between RCC+diabetes and diabetes groups was four and between diabetes and RCC groups was eight GO pathways. Overall, we observed majority of DNA alterations in patients from RCC+diabetes group. Interestingly, insulin receptor (INSR) is highly expressed and had gains in copy number in RCC+diabetes and diabetes groups. The changes in INSR copy number may use as a biomarker for predicting RCC development in diabetic patients.

Indexed as

diabetesmicroarrayRCCrenal

Identifiers

PMID25821562
PMCPMC4362485
OpenAlexW2159546907

What OpenQuestion holds

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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.