Evidence map›Paper›PMID 28378747›Full record

ArticleScientific reports2017

HPV positive neuroendocrine cervical cancer cells are dependent on Myc but not E6/E7 viral oncogenes.

Hang Yuan, Ewa Krawczyk, Jan Blancato, Christopher Albanese, Dan Zhou, Naidong Wang, Siddartha Paul, Faris Alkhilaiwi, Nancy Palechor-Ceron, Aleksandra Dakic and 14 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
3.6field-weighted citation impact, top 7% 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

34 citing papers in PubMed, 49 citations in OpenAlex.

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  16. Reviewing cancer's biology: an eclectic approach.Journal of the Egyptian National Cancer Institute · 2021
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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

24 authors at 5 institutions in 2 countries.

Hang YuanDepartment of Pathology, Georgetown University Medical School, Washington DC, 20057, USA.
Ewa KrawczykDepartment of Pathology, Georgetown University Medical School, Washington DC, 20057, USA.
Jan BlancatoDepartment of Pathology, Georgetown University Medical School, Washington DC, 20057, USA.
Christopher AlbaneseDepartment of Pathology, Georgetown University Medical School, Washington DC, 20057, USA.
Dan ZhouDepartment of Pathology, Georgetown University Medical School, Washington DC, 20057, USA.
Naidong WangDepartment of Pathology, Georgetown University Medical School, Washington DC, 20057, USA.
Siddartha PaulDepartment of Pathology, Georgetown University Medical School, Washington DC, 20057, USA.
Faris AlkhilaiwiDepartment of Pathology, Georgetown University Medical School, Washington DC, 20057, USA.
Nancy Palechor-CeronDepartment of Pathology, Georgetown University Medical School, Washington DC, 20057, USA.
Aleksandra DakicDepartment of Pathology, Georgetown University Medical School, Washington DC, 20057, USA.
Shuang FangDepartment of Pathology, Georgetown University Medical School, Washington DC, 20057, USA.
Sujata ChoudharyDepartment of Pathology, Georgetown University Medical School, Washington DC, 20057, USA.
Tung-Wei HouDepartment of Pathology, Georgetown University Medical School, Washington DC, 20057, USA.
Yun-Ling ZhengDepartment of Oncology, Georgetown University Medical School, Washington DC, 20057, USA.
Bassem R HaddadDepartment of Oncology, Georgetown University Medical School, Washington DC, 20057, USA.
Yukari UsudaDepartment of Pathology, Georgetown University Medical School, Washington DC, 20057, USA.
Dan HartmannDepartment of Pathology, Georgetown University Medical School, Washington DC, 20057, USA.
David SymerHuman Cancer Genetics Program and Dept. of Molecular Virology, Immunology and Medical Genetics, Ohio State University Comprehensive Cancer Center, USA.
Maura GillisonDept. of Internal Medicine, Ohio State University Comprehensive Cancer Center, Columbus, OH 43210, USA.
Seema AgarwalDepartment of Pathology, Georgetown University Medical School, Washington DC, 20057, USA.
Danny WangsaCancer Genomics Section, Center for Cancer Research, National Cancer Institute, Bethesda, MD 20892, USA.
Thomas RiedCancer Genomics Section, Center for Cancer Research, National Cancer Institute, Bethesda, MD 20892, USA.
Xuefeng LiuDepartment of Pathology, Georgetown University Medical School, Washington DC, 20057, USA.
Richard SchlegelDepartment of Pathology, Georgetown University Medical School, Washington DC, 20057, USA.
Georgetown University · USCancer Genetics (United States) · USCenter for Cancer Research · USNational Cancer Institute · USThe Ohio State University · US

Funding

Tissue Culture Shared ResourceP30CA051008 · NCI · GEORGETOWN UNIVERSITY · PI STEPHEN W BYERS · 1990 to 2026
$71.5M
Identification and functional characterization of colorectal cancer genesZIABC010833 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI RIED, THOMAS · 2009 to 2022
$12.1M
Conditionally reprogrammed cells as a novel tool for biobankingR33CA177466 · NCI · GEORGETOWN UNIVERSITY · PI SCHLEGEL, RICHARD, WELLSTEIN, ANTON · 2013 to 2015
$1.2M
Emerging Papillomaviruses in Immunosuppressed DogsR01RR032315 · NCRR · GEORGETOWN UNIVERSITY · PI SCHLEGEL, RICHARD · 2011 to 2011
$399k
NON-CANONICAL FUNCTIONS OF HTERT IN CELL IMMORTALIZATION BY HPVR21CA180524 · NCI · GEORGETOWN UNIVERSITY · PI LIU, XUEFENG · 2013 to 2014
$366k
NCI NIH HHS P30 CA051008NCI NIH HHS R21 CA180524NCI NIH HHS R33 CA177466NCRR NIH HHS R01 RR032315
6 · The paper itself

Abstract

Using conditional cell reprogramming, we generated a stable cell culture of an extremely rare and aggressive neuroendocrine cervical cancer. The cultured cells contained HPV-16, formed colonies in soft agar and rapidly produced tumors in immunodeficient mice. The HPV-16 genome was integrated adjacent to the Myc gene, both of which were amplified 40-fold. Analysis of RNA transcripts detected fusion of the HPV/Myc genes, arising from apparent microhomologous recombination. Spectral karyotyping (SKY) and fluorescent-in-situ hybridization (FISH) demonstrated coordinate localization and translocation of the amplified Myc and HPV genes on chromosomes 8 and 21. Similar to the primary tumor, tumor cell cultures expressed very high levels of the Myc protein and, in contrast to all other HPV-positive cervical cancer cell lines, they harbored a gain-of-function mutation in p53 (R273C). Unexpectedly, viral oncogene knockdown had no effect on the growth of the cells, but it did inhibit the proliferation of a conventional HPV-16 positive cervical cancer cell line. Knockdown of Myc, but not the mutant p53, significantly inhibited tumor cell proliferation. On the basis of these data, we propose that the primary driver of transformation in this aggressive cervical cancer is not HPV oncogene expression but rather the overexpression of Myc.

Indexed as

Cell ProliferationCell Transformation, NeoplasticAnimalsFemaleGene FusionHuman papillomavirus 16In Situ Hybridization, FluorescenceKaryotypingMiceModels, BiologicalOncogene Proteins, ViralPapillomavirus E7 ProteinsProto-Oncogene Proteins c-mycRecombination, GeneticRepressor ProteinsTumor Cells, CulturedE6 protein, Human papillomavirus type 16Myc protein, mouseoncogene protein E7, Human papillomavirus type 16Oncogene Proteins, ViralPapillomavirus E7 ProteinsProto-Oncogene Proteins c-mycRepressor Proteins

Identifiers

PMID28378747
PMCPMC5381214
OpenAlexW2604927512

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.