Evidence map›Paper›PMID 33980865›Full record

ArticleNPJ genomic medicine2021

Genes and pathways monotonically dysregulated during progression from normal through leukoplakia to gingivo-buccal oral cancer.

Debodipta Das, Arindam Maitra, Chinmay K Panda, Sandip Ghose, Bidyut Roy, Rajiv Sarin, Partha P Majumder

Open access · goldAbstract read
In one paragraph

Article in NPJ genomic medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed, 2 pooled it
2.2field-weighted citation impact, top 12% 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

24 citing papers in PubMed, 2 syntheses or guidelines pooled it, 32 citations in OpenAlex.

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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

7 authors at 6 institutions in 2 countries.

Debodipta DasNational Institute of Biomedical Genomics, Kalyani, India. debodipta@gmail.com.ORCID http://orcid.org/0000-0001-7698-0736
Arindam MaitraNational Institute of Biomedical Genomics, Kalyani, India.
Chinmay K PandaChittaranjan National Cancer Institute, Kolkata, India.
Sandip GhoseDepartment of Oral Pathology, Dr. R Ahmed Dental College and Hospital, Kolkata, India.
Bidyut RoyIndian Statistical Institute, Kolkata, India.
Rajiv SarinAdvanced Centre for Treatment Research and Education in Cancer, Mumbai, India.
Partha P MajumderNational Institute of Biomedical Genomics, Kalyani, India. ppm1@nibmg.ac.in.ORCID http://orcid.org/0000-0001-7009-7360
National Institute of Biomedical Genomics · INAdvanced Centre for Treatment, Research and Education in Cancer · INChittaranjan National Cancer Institute · INDr. R. Ahmed Dental College and Hospital · INIndian Statistical Institute · INThe University of Texas Health Science Center at San Antonio · US

Funding

Department of Biotechnology, Ministry of Science and Technology (DBT) ICGC-IndiaDepartment of Biotechnology, Ministry of Science and Technology (DBT) SyMeC 2017
6 · The paper itself

Abstract

Oral squamous cell carcinoma of the gingivo-buccal region (OSCC-GB) accounts for the highest cancer morbidity and mortality among men in India. It has been observed that about one-third of individuals with oral leukoplakia, a dysplastic precancerous lesion in the oral cavity, progress to oral cancer. We aimed to identify systematic transcriptomic changes as a normal tissue in the oral cavity progresses to frank OSCC-GB. Seventy-two OSCC-GB patients, from multiple hospitals, were recruited, and transcriptome analysis of tumor and adjacent normal tissue (of all patients) and adjacent leukoplakia tissue (of a subset of 25 unselected patients with concomitant leukoplakia) was performed. We have identified many differences in the transcriptomic profiles between OSCC-GB and squamous cell carcinoma of the head and neck regions. Compared to the normal/precancerous tissue, significant enrichment of ECM-receptor interaction, PI3K-Akt signaling, cytokine-cytokine receptor interaction, focal adhesion, and cell cycle pathways were observed in OSCC-GB. Using gene set enrichment analysis, we identified a profound role of interferon receptor signaling in tumor growth by activating immune evasion mechanisms. The role of tumor-infiltrating immune cells further supported the growth and immunosuppressive mechanism of tumor tissues. Some immune evasion genes-CD274, CD80, and IDO1-were found to be activated even in the precancerous tissue. Taken together, our findings provide a clear insight into the sequential genetic dysregulation associated with progression to oral cancer. This insight provides a window to the development of predictive biomarkers and therapeutic targets for gingivo-buccal oral cancer.

Identifiers

PMID33980865
PMCPMC8115176
OpenAlexW3162445566

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Registered trials

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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.