🏆 Finalist — NIH Data Sharing Index (“S-Index”) Challenge
Demo corpus. Scores are computed on a select set of biomedical paper/datasets and may be inaccurate for papers outside this corpus — DataRank relies on network effects that improve with scale. We aim to expand this into a fully open resource pending additional funding.

Multiscale protein networks systematically identify aberrant protein interactions and oncogenic regulators in seven cancer types

Journal of Hematology & Oncology(2023)10.1186/s13045-023-01517-2Source: DataRank Database

Multiscale protein networks systematically identify aberrant protein interactions and oncogenic regulators in seven cancer types is a dataset published in Journal of Hematology & Oncology (2023). On theSindex it has a DataRank of 0.416, placing it in the top 50% of the data-sharing corpus. It has been cited 14 times, with 10 citing works in its 1-hop citation network. Its calibrated FAIR score is 44/100.

Top 50%percentile
0.416DataRank
0.416Top 50%
Dataset Open Access14 citations · base score 2.4
Cite:
datarank_citation_only_1hop_v6· scope data_onlyMethodology

Abstract

Global proteomic data generated by advanced mass spectrometry (MS) technologies can help bridge the gap between genome/transcriptome and functions and hold great potential in elucidating unbiased functional models of pro-tumorigenic pathways. To this end, we collected the high-throughput, whole-genome MS data and conducted integrative proteomic network analyses of 687 cases across 7 cancer types including breast carcinoma (115 tumor samples; 10,438 genes), clear cell renal carcinoma (100 tumor samples; 9,910 genes), colorectal cancer (91 tumor samples; 7,362 genes), hepatocellular carcinoma (101 tumor samples; 6,478 genes), lung adenocarcinoma (104 tumor samples; 10,967 genes), stomach adenocarcinoma (80 tumor samples; 9,268 genes), and uterine corpus endometrial carcinoma UCEC (96 tumor samples; 10,768 genes). Through the protein co-expression network analysis, we identified co-expressed protein modules enriched for differentially expressed proteins in tumor as disease-associated pathways. Comparison with the respective transcriptome network models revealed proteome-specific cancer subnetworks associated with heme metabolism, DNA repair, spliceosome, oxidative phosphorylation and several oncogenic signaling pathways. Cross-cancer comparison identified highly preserved protein modules showing robust pan-cancer interactions and identified endoplasmic reticulum-associated degradation (ERAD) and N-acetyltransferase activity as the central functional axes. We further utilized these network models to predict pan-cancer protein regulators of disease-associated pathways. The top predicted pan-cancer regulators including RSL1D1, DDX21 and SMC2, were experimentally validated in lung, colon, breast cancer and fetal kidney cells. In summary, this study has developed interpretable network models of cancer proteomes, showcasing their potential in unveiling novel oncogenic regulators, elucidating underlying mechanisms, and identifying new therapeutic targets.

Data sources & pipeline
Pipeline:MetadataData-paper checkEnrichmentCitation networkScoring
Enrichment:Pending

FAIR Checklist

Context only (not used in score)
Findable (1/2)
  • Has DOI
Accessible (1/2)
  • Open Access
Interoperable (0/2)
    Reusable (1/3)
    • Dataset classification

    FAIR checklist signals are shown for context only and do not affect DataRank scoring.

    44FAIR score
    F Findable
    53
    A Accessible
    68
    I Interoperable
    13
    R Reusable
    42
    Top 57% by FAIRLLM-assessed✓ full text read

    Calibrated FAIR score — a parallel quality metric, independent of the DataRank citation score. See the full evaluation →

    DataRank Breakdown

    Base Score 86%Citation Network 14%

    Base Score Contribution

    0.360

    From this paper's citation signal

    Citation Network Contribution

    0.0563

    From 3 citing papers with measurable signal

    Learn more about DataRank methodology →

    Top 2 citers driving the network score

    Ranked by citation count — the same ordering the engine uses when summing log1p(Cq) over citers.

    Why this DataRank?

    DataRank blends this paper's own citation count with the influence of the papers that cite it. Here, roughly 86% comes from its base citations and 14% from the citation network (3 citing papers contributed measurable signal).

    Base score B(p)
    log1p(citation_count) — grows sub-linearly, so a paper with 1,000 citations is not 10× a paper with 100.
    Network N(p)
    Σ over citers of log1p(Cq) ÷ max(outdegreeq, 1). Being cited by a highly-cited paper with few references counts most.
    Damping factor d = 0.85
    DataRank = (1−d)·B(p) + d·N(p) — the two cards above are each already multiplied by their share.
    Self-citations excluded
    Citers sharing any OpenAlex author ID with this paper are filtered out before the network sum.

    Citers are pulled from OpenAlex sorted by cited_by_count:descand capped per paper, so when the cap binds we keep the highest-signal references and the score is reproducible across reruns.

    Read the full methodology →

    Click a node to highlight its connections. Use scroll to zoom. Drag to pan.

    Node colors:CenterData PaperData + Open AccessNon-dataSelected & links| Node size = percentile rank

    Authors (9)

    Richard Farias,Peng XuORCID,Xianxiao ZhouORCID,Benjamin Hopkins,Kuan-lin HuangORCID