Evidence map›Paper›PMID 23925245›Full record

ArticleNature2013

The haplotype-resolved genome and epigenome of the aneuploid HeLa cancer cell line.

Andrew Adey, Joshua N Burton, Jacob O Kitzman, Joseph B Hiatt, Alexandra P Lewis, Beth K Martin, Ruolan Qiu, Choli Lee, Jay Shendure

Abstract read
In one paragraph

Article in Nature, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 210 papers.

0numbers the graph read from it
0cells of the map it votes in
210citing papers in PubMed
–field-weighted citation impact
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

210 citing papers in PubMed.

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150 more citing papers are in PubMed but not listed here.

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

9 authors.

Andrew AdeyDepartment of Genome Sciences, University of Washington, Seattle, Washington 98115, USA.
Joshua N Burton
Jacob O Kitzman
Joseph B Hiatt
Alexandra P Lewis
Beth K Martin
Ruolan Qiu
Choli Lee
Jay Shendure

Funding

University of Washington Medical Scientist Training Program: MD/PhDT32GM007266 · NIGMS · UNIVERSITY OF WASHINGTON · PI HORWITZ, MARSHALL S. · 1985 to 2023
$30.4M
INTERDISCIPLINARY TRAINING IN GENOMIC SCIENCEST32HG000035 · NHGRI · UNIVERSITY OF WASHINGTON · PI Bruce Colston Trapnell · 1995 to 2026
$24.2M
Massively Parallel Contiguity MappingR01HG006283 · NHGRI · UNIVERSITY OF WASHINGTON · PI SHENDURE, JAY ASHOK · 2011 to 2016
$3.4M
Ultrasensitive identification and precise quantitation of low frequency somatic mR21CA160080 · NCI · UNIVERSITY OF WASHINGTON · PI SHENDURE, JAY ASHOK · 2011 to 2013
$588k
Massively parallel measurement of mitochondrial DNA mutation during human aging tF30AG039173 · NIA · UNIVERSITY OF WASHINGTON · PI HIATT, JOSEPH · 2010 to 2013
$151k
NCI NIH HHS CA160080NCI NIH HHS R21 CA160080NHGRI NIH HHS HG006283NHGRI NIH HHS R01 HG006283NHGRI NIH HHS T32 HG000035NHGRI NIH HHS T32HG000035NIA NIH HHS AG039173NIA NIH HHS F30 AG039173NIGMS NIH HHS T32 GM007266
6 · The paper itself

Abstract

The HeLa cell line was established in 1951 from cervical cancer cells taken from a patient, Henrietta Lacks. This was the first successful attempt to immortalize human-derived cells in vitro. The robust growth and unrestricted distribution of HeLa cells resulted in its broad adoption--both intentionally and through widespread cross-contamination--and for the past 60 years it has served a role analogous to that of a model organism. The cumulative impact of the HeLa cell line on research is demonstrated by its occurrence in more than 74,000 PubMed abstracts (approximately 0.3%). The genomic architecture of HeLa remains largely unexplored beyond its karyotype, partly because like many cancers, its extensive aneuploidy renders such analyses challenging. We carried out haplotype-resolved whole-genome sequencing of the HeLa CCL-2 strain, examined point- and indel-mutation variations, mapped copy-number variations and loss of heterozygosity regions, and phased variants across full chromosome arms. We also investigated variation and copy-number profiles for HeLa S3 and eight additional strains. We find that HeLa is relatively stable in terms of point variation, with few new mutations accumulating after early passaging. Haplotype resolution facilitated reconstruction of an amplified, highly rearranged region of chromosome 8q24.21 at which integration of the human papilloma virus type 18 (HPV-18) genome occurred and that is likely to be the event that initiated tumorigenesis. We combined these maps with RNA-seq and ENCODE Project data sets to phase the HeLa epigenome. This revealed strong, haplotype-specific activation of the proto-oncogene MYC by the integrated HPV-18 genome approximately 500 kilobases upstream, and enabled global analyses of the relationship between gene dosage and expression. These data provide an extensively phased, high-quality reference genome for past and future experiments relying on HeLa, and demonstrate the value of haplotype resolution for characterizing cancer genomes and epigenomes.

Indexed as

EpigenomicsAneuploidyDNA Copy Number VariationsFemaleGenes, mycGenome, HumanHaplotypesHeLa CellsHuman papillomavirus 18HumansMolecular Sequence DataMutationProto-Oncogene MasSequence Analysis, DNATranscriptional ActivationUterine Cervical NeoplasmsProto-Oncogene Mas

Identifiers

PMID23925245
PMCPMC3740412

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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.