Evidence map›Paper›PMID 24630729›Full record

ArticleCell2014

Genetic and clonal dissection of murine small cell lung carcinoma progression by genome sequencing.

David G McFadden, Thales Papagiannakopoulos, Amaro Taylor-Weiner, Chip Stewart, Scott L Carter, Kristian Cibulskis, Arjun Bhutkar, Aaron McKenna, Alison Dooley, Amanda Vernon and 11 more

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

Article in Cell, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 196 papers.

0numbers the graph read from it
0cells of the map it votes in
196citing papers in PubMed
16.0field-weighted citation impact, top 1% 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

196 citing papers in PubMed, 295 citations in OpenAlex.

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136 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

21 authors at 3 institutions in 1 country.

David G McFaddenKoch Institute for Integrative Cancer Research and Department of Biology, Massachusetts Institute of Technology, Cambridge, MA 02142, USA.
Thales PapagiannakopoulosKoch Institute for Integrative Cancer Research and Department of Biology, Massachusetts Institute of Technology, Cambridge, MA 02142, USA.
Amaro Taylor-WeinerCancer Program, Broad Institute of MIT and Harvard, Cambridge, MA 02142, USA.
Chip StewartCancer Program, Broad Institute of MIT and Harvard, Cambridge, MA 02142, USA.
Scott L CarterCancer Program, Broad Institute of MIT and Harvard, Cambridge, MA 02142, USA.
Kristian CibulskisCancer Program, Broad Institute of MIT and Harvard, Cambridge, MA 02142, USA.
Arjun BhutkarKoch Institute for Integrative Cancer Research and Department of Biology, Massachusetts Institute of Technology, Cambridge, MA 02142, USA.
Aaron McKennaCancer Program, Broad Institute of MIT and Harvard, Cambridge, MA 02142, USA.
Alison DooleyKoch Institute for Integrative Cancer Research and Department of Biology, Massachusetts Institute of Technology, Cambridge, MA 02142, USA.
Amanda VernonKoch Institute for Integrative Cancer Research and Department of Biology, Massachusetts Institute of Technology, Cambridge, MA 02142, USA.
Carrie SougnezCancer Program, Broad Institute of MIT and Harvard, Cambridge, MA 02142, USA.
Scott MalstromKoch Institute for Integrative Cancer Research and Department of Biology, Massachusetts Institute of Technology, Cambridge, MA 02142, USA.
Megan HeimannKoch Institute for Integrative Cancer Research and Department of Biology, Massachusetts Institute of Technology, Cambridge, MA 02142, USA.
Jennifer ParkKoch Institute for Integrative Cancer Research and Department of Biology, Massachusetts Institute of Technology, Cambridge, MA 02142, USA.
Frances ChenKoch Institute for Integrative Cancer Research and Department of Biology, Massachusetts Institute of Technology, Cambridge, MA 02142, USA.
Anna F FaragoKoch Institute for Integrative Cancer Research and Department of Biology, Massachusetts Institute of Technology, Cambridge, MA 02142, USA.
Talya DaytonKoch Institute for Integrative Cancer Research and Department of Biology, Massachusetts Institute of Technology, Cambridge, MA 02142, USA.
Erica SheflerCancer Program, Broad Institute of MIT and Harvard, Cambridge, MA 02142, USA.
Stacey GabrielCancer Program, Broad Institute of MIT and Harvard, Cambridge, MA 02142, USA.
Gad GetzCancer Program, Broad Institute of MIT and Harvard, Cambridge, MA 02142, USA; Cancer Center and Department of Pathology, Massachusetts General Hospital, Boston, MA 02114, USA. Electronic address: gadgetz@broadinstitute.org.
Tyler JacksKoch Institute for Integrative Cancer Research and Department of Biology, Massachusetts Institute of Technology, Cambridge, MA 02142, USA; Howard Hughes Medical Institute, Massachusetts Institute of Technology, Cambridge, MA 02142, USA. Electronic address: tjacks@mit.edu.
Massachusetts Institute of Technology · USBroad Institute · USHoward Hughes Medical Institute · US

Funding

Large Scale Sequencing and Analysis of GenomesU54HG003067 · NHGRI · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · PI GABRIEL, STACEY, LANDER, ERIC S · 2004 to 2015
$568.6M
VIRUS PRODUCTION COREP30CA014051 · NCI · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · PI Andreea O'Connell · 1985 to 2026
$93.9M
STUDIES OF INTEGRATIVE SYSTEMST32GM007484 · NIGMS · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · PI DICARLO, JAMES J · 1985 to 2017
$8.5M
"Comparative gene resequencing in mouse cancer models"K08CA160658 · NCI · UT SOUTHWESTERN MEDICAL CENTER · PI MCFADDEN, DAVID GLENN · 2011 to 2015
$900k
Howard Hughes Medical InstituteNCI NIH HHS K08 CA160658NCI NIH HHS K08CA160658NCI NIH HHS P30 CA014051NHGRI NIH HHS U54 HG003067NIGMS NIH HHS T32 GM007484
6 · The paper itself

Abstract

Small cell lung carcinoma (SCLC) is a highly lethal, smoking-associated cancer with few known targetable genetic alterations. Using genome sequencing, we characterized the somatic evolution of a genetically engineered mouse model (GEMM) of SCLC initiated by loss of Trp53 and Rb1. We identified alterations in DNA copy number and complex genomic rearrangements and demonstrated a low somatic point mutation frequency in the absence of tobacco mutagens. Alterations targeting the tumor suppressor Pten occurred in the majority of murine SCLC studied, and engineered Pten deletion accelerated murine SCLC and abrogated loss of Chr19 in Trp53; Rb1; Pten compound mutant tumors. Finally, we found evidence for polyclonal and sequential metastatic spread of murine SCLC by comparative sequencing of families of related primary tumors and metastases. We propose a temporal model of SCLC tumorigenesis with implications for human SCLC therapeutics and the nature of cancer-genome evolution in GEMMs.

Indexed as

CarcinogenesisDisease Models, AnimalAnimalsHumansLiver NeoplasmsLung NeoplasmsLymphatic MetastasisMicePTEN PhosphohydrolaseSmall Cell Lung CarcinomaPTEN PhosphohydrolasePten protein, mouse

Identifiers

PMID24630729
PMCPMC4040459
OpenAlexW2023975001

What OpenQuestion holds

Textmetadata
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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.