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Packagehl7.fhir.uv.ebm
Resource TypeCitation
IdCitation-179559.json
FHIR VersionR6

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Narrative

Note: links and images are rebased to the (stated) source

Generated Narrative: Citation 179559

version: 9; Last updated: 2025-10-12 18:47:15+0000

Profile: DatasetCitation

ArtifactPublicationStatus: Active

url: Citation DatasetCitation: Extrachromosomal DNA Amplification Contributes to Small Cell Lung Cancer Heterogeneity and is Associated with Worse Outcomes

identifier: FEvIR Object Identifier/179559, Uniform Resource Identifier (URI)/urn:oid:2.16.840.1.113883.4.642.40.44.15.24

version: 1.0.0-ballot3

title: DatasetCitation: Extrachromosomal DNA Amplification Contributes to Small Cell Lung Cancer Heterogeneity and is Associated with Worse Outcomes

status: Active

date: 2026-02-10 14:00:26+0000

author: Brian S. Alper:

publisher: HL7 International / Clinical Decision Support

contact: HL7 International / Clinical Decision Support: http://www.hl7.org/Special/committees/dss

description:

This Citation Resource is referenced in an example for the EBMonFHIR Implementation Guide.

jurisdiction: World

copyright:

https://creativecommons.org/licenses/by-nc-sa/4.0/

Summaries

-StyleText
*Computable Publishing

Extrachromosomal DNA Amplification Contributes to Small Cell Lung Cancer Heterogeneity and is Associated with Worse Outcomes [Dataset]. Contributors: Anish Thomas, Lorinc S. Pongor, Rajesh Kumar, Parth Desai [Authors]. In: database of Genotypes and Phenotypes, Accession Number phs003190.v1.p1. Published October 16, 2023. Available at: https://www.ncbi.nlm.nih.gov/projects/gap/cgi-bin/study.cgi?study_id=phs003190.v1.p1.

citedArtifact

identifier: dbGaP Study Accession/phs003190.v1.p1

Titles

-TypeText
*Primary title

Extrachromosomal DNA Amplification Contributes to Small Cell Lung Cancer Heterogeneity and is Associated with Worse Outcomes

Abstracts

-TypeText
*Study Description

Small-cell lung cancer (SCLC) is a very aggressive neuroendocrine lung cancer often associated with oncogenic MYC amplifications, which are known to drive SCLC heterogeneity marked by neuroendocrine (NE) and non-neuroendocrine (non-NE) cell states. The genetic mechanisms of MYC amplification and phenotypic plasticity between cell states is not known. Using data from cell-lines and a few patient-derived samples along with integrated whole-genome sequencing, long-range optical mapping, single-cell DNA sequencing, and fluorescence in situ hybridization, we have attempted to successfully characterize extrachromosomal DNA (ecDNA) as the primary source of MYC amplifications and driver fusions in SCLC.

Study Design: Cross-Sectional Study Type: Observational Total number of consented subjects: 5

publicationForm

PublishedIns

-TypeIdentifierTitlePublisherPublisherLocation
*DatabaseAbbreviation/dbGaPdatabase of Genotypes and PhenotypesNLMBethesda, MD, USA

citedMedium: Internet

articleDate: 2023-10-16

accessionNumber: phs003190.v1.p1

pageCount: Total number of consented subjects: 5

copyright:

Data access provided by: dbGaP Authorized Access. For publicly available data (public ftp), Connect to the public download site. The site contains release notes and manifests. The site also contains data dictionaries, variable summaries, documents, and truncated analyses, whenever available.

webLocation

classifier: Webpage

url: https://www.ncbi.nlm.nih.gov/projects/gap/cgi-bin/study.cgi?study_id=phs003190.v1.p1

webLocation

classifier: public download site

url: https://ftp.ncbi.nlm.nih.gov/dbgap/studies/phs003190/phs003190.v1.p1

classification

type: Knowledge Artifact Type

classifier: Dataset

classification

type: Study Design

classifier: Cross-Sectional, Observational Research

classification

type: Primary Phenotype

classifier: Small Cell Lung Carcinoma

contributorship

complete: true

entry

contributor: Practitioner Anish Thomas

affiliation: Developmental Therapeutics Branch, Center for Cancer Research, National Cancer Institute, Bethesda, MD, USA

contributionType: Principal Investigator

role: Author/Creator

entry

contributor: Practitioner Lorinc S. Pongor

affiliation: Developmental Therapeutics Branch, Center for Cancer Research, National Cancer Institute, Bethesda, MD, USA

contributionType: Co-Investigator

role: Author/Creator

entry

contributor: Practitioner Rajesh Kumar

affiliation: Developmental Therapeutics Branch, Center for Cancer Research, National Cancer Institute, Bethesda, MD, USA

contributionType: Co-Investigator

role: Author/Creator

entry

contributor: Practitioner Parth Desai

affiliation: Developmental Therapeutics Branch, Center for Cancer Research, National Cancer Institute, Bethesda, MD, USA

contributionType: Co-Investigator

role: Author/Creator


Generated Narrative: Practitioner #contributor0

name: Anish Thomas


Generated Narrative: Practitioner #contributor1

name: Lorinc S. Pongor


Generated Narrative: Practitioner #contributor2

name: Rajesh Kumar


Generated Narrative: Practitioner #contributor3

name: Parth Desai


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