Evidence map›Paper›PMID 9683604›Full record

ArticleAmerican journal of human genetics1998

From amplification to gene in thyroid cancer: a high-resolution mapped bacterial-artificial-chromosome resource for cancer chromosome aberrations guides gene discovery after comparative genome hybridization.

X Chen, J A Knauf, R Gonsky, M Wang, E H Lai, S Chissoe, J A Fagin, J R Korenberg

Open access · bronzeAbstract readComparative Study
In one paragraph

Article in American journal of human genetics, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed, 1 pooled it
2.2field-weighted citation impact, top 12% 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

15 citing papers in PubMed, 1 synthesis or guideline pooled it, 63 citations in OpenAlex.

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  13. Conditional rescue of protein kinase C epsilon regulates ethanol preference and hypnotic sensitivity in adult mice.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2002
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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

8 authors at 4 institutions in 1 country.

X ChenAhmanson Department of Pediatrics, Division of Genetics, Cedars-Sinai Research Institute, UCLA School of Medicine, Los Angeles, USA.
J A Knauf
R Gonsky
M Wang
E H Lai
S Chissoe
J A Fagin
J R Korenberg
University of Cincinnati · USUniversity of North Carolina at Chapel Hill · USCedars-Sinai Medical Center · USWashington University in St. Louis · US

Funding

MOLECULAR PATHOPHYSIOLOGY OF THYROID CELL GROWTHR01CA050706 · NCI · UNIVERSITY OF CINCINNATI · PI FAGIN, JAMES A · 1995 to 2023
$7.5M
ONCOGENIC EVENTS IN THYROID NEOPLASIAR01CA072597 · NCI · UNIVERSITY OF CINCINNATI · PI FAGIN, JAMES A · 1997 to 2020
$6.7M
HEART AND LUNG DEFECTS IN DOWN SYNDROMER01HL050025 · NHLBI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI KURNIT, DAVID MARTIN · 1993 to 1997
–
MOLECULAR PATHOPHYSIOLOGY OF THYROID CELL GROWTHR29CA050706 · NCI · CEDARS-SINAI MEDICAL CENTER · PI FAGIN, JAMES A · 1989 to 1993
–
NCI NIH HHS CA50706NCI NIH HHS CA72597NHLBI NIH HHS R01 HL50025
6 · The paper itself

Abstract

Chromosome rearrangements associated with neoplasms provide a rich resource for definition of the pathways of tumorigenesis. The power of comparative genome hybridization (CGH) to identify novel genes depends on the existence of suitable markers, which are lacking throughout most of the genome. We now report a general approach that translates CGH data into higher-resolution genomic-clone data that are then used to define the genes located in aneuploid regions. We used CGH to study 33 thyroid-tumor DNAs and two tumor-cell-line DNAs. The results revealed amplifications of chromosome band 2p21, with less-intense amplification on 2p13, 19q13.1, and 1p36 and with least-intense amplification on 1p34, 1q42, 5q31, 5q33-34, 9q32-34, and 14q32. To define the 2p21 region amplified, a dense array of 373 FISH-mapped chromosome 2 bacterial artificial chromosomes (BACs) was constructed, and 87 of these were hybridized to a tumor-cell line. Four BACs carried genomic DNA that was amplified in these cells. The maximum amplified region was narrowed to 3-6 Mb by multicolor FISH with the flanking BACs, and the minimum amplicon size was defined by a contig of 420 kb. Sequence analysis of the amplified BAC 1D9 revealed a fragment of the gene, encoding protein kinase C epsilon (PKCepsilon), that was then shown to be amplified and rearranged in tumor cells. In summary, CGH combined with a dense mapped resource of BACs and large-scale sequencing has led directly to the definition of PKCepsilon as a previously unmapped candidate gene involved in thyroid tumorigenesis.

Indexed as

Chromosome AberrationsChromosome MappingChromosomes, HumanAdenocarcinoma, FollicularAdenomaCarcinomaCarcinoma, PapillaryChromosomes, BacterialChromosomes, Human, Pair 1Chromosomes, Human, Pair 2DNA, NeoplasmGene AmplificationGenetic MarkersHumansIn Situ Hybridization, FluorescenceKaryotypingDNA, NeoplasmGenetic Markers

Identifiers

PMID9683604
PMCPMC1377314
OpenAlexW2019002150

What OpenQuestion holds

Textmetadata
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.