🏆 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.

Pan-cancer analysis of whole genomes

Nature(2020)10.1038/s41586-020-1969-6Source: DataRank Database

Pan-cancer analysis of whole genomes is a dataset published in Nature (2020). On theSindex it has a DataRank of 5.9, placing it in the top 27.1% of the data-sharing corpus. It has been cited 3,267 times, with 102 citing works in its 1-hop citation network. Its calibrated FAIR score is 84/100.

Top 27%percentile
5.9DataRank
5.9Top 27%
Dataset Open Access3267 citations · base score 8.0
Cite:
datarank_citation_only_1hop_v6· scope data_onlyMethodology

Abstract

Cancer is driven by genetic change, and the advent of massively parallel sequencing has enabled systematic documentation of this variation at the whole-genome scale1-3. Here we report the integrative analysis of 2,658 whole-cancer genomes and their matching normal tissues across 38 tumour types from the Pan-Cancer Analysis of Whole Genomes (PCAWG) Consortium of the International Cancer Genome Consortium (ICGC) and The Cancer Genome Atlas (TCGA). We describe the generation of the PCAWG resource, facilitated by international data sharing using compute clouds. On average, cancer genomes contained 4-5 driver mutations when combining coding and non-coding genomic elements; however, in around 5% of cases no drivers were identified, suggesting that cancer driver discovery is not yet complete. Chromothripsis, in which many clustered structural variants arise in a single catastrophic event, is frequently an early event in tumour evolution; in acral melanoma, for example, these events precede most somatic point mutations and affect several cancer-associated genes simultaneously. Cancers with abnormal telomere maintenance often originate from tissues with low replicative activity and show several mechanisms of preventing telomere attrition to critical levels. Common and rare germline variants affect patterns of somatic mutation, including point mutations, structural variants and somatic retrotransposition. A collection of papers from the PCAWG Consortium describes non-coding mutations that drive cancer beyond those in the TERT promoter4; identifies new signatures of mutational processes that cause base substitutions, small insertions and deletions and structural variation5,6; analyses timings and patterns of tumour evolution7; describes the diverse transcriptional consequences of somatic mutation on splicing, expression levels, fusion genes and promoter activity8,9; and evaluates a range of more-specialized features of cancer genomes8,10-18.

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

FAIR Checklist

Context only (not used in score)
Findable (2/2)
  • Has DOI
  • Indexed in repositories
Accessible (1/2)
  • Open Access
Interoperable (2/2)
  • DataCite relations
  • Linked datasets
Reusable (1/3)
  • Dataset classification

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

84FAIR score
F Findable
100
A Accessible
70
I Interoperable
100
R Reusable
67
Top 0% by FAIRdeterministic✓ full text read

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

DataRank Breakdown

Base Score 20%Citation Network 80%

Base Score Contribution

1.2

From this paper's citation signal

Citation Network Contribution

4.7

From 102 citing papers with measurable signal

Learn more about DataRank methodology →

Top 5 citers driving the network score

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

  1. Hallmarks of Cancer: The Next Generation
    Cell201165,643 citationsDataRank 1.7
  2. A global reference for human genetic variation
    Nature201519,823 citationsDataRank 11.1Top 19%
  3. An integrated map of structural variation in 2,504 human genomes
    Nature20152,648 citationsDataRank 12.2Top 17%
Why this DataRank?

DataRank blends this paper's own citation count with the influence of the papers that cite it. Here, roughly 20% comes from its base citations and 80% from the citation network (102 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 (1249)