Evidence map›Paper›PMID 19383354›Full record

ArticleMolecular oncology2008

CAMK1D amplification implicated in epithelial-mesenchymal transition in basal-like breast cancer.

Anna Bergamaschi, Young H Kim, Kevin A Kwei, Yoon La Choi, Melanie Bocanegra, Anita Langerød, Wonshik Han, Dong-Young Noh, David G Huntsman, Stefanie S Jeffrey and 2 more

Open access · greenAbstract read
In one paragraph

Article in Molecular oncology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed
1.6field-weighted citation impact, top 14% 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

44 citing papers in PubMed, 60 citations in OpenAlex.

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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

12 authors at 6 institutions in 4 countries.

Anna BergamaschiDepartment of Genetics, Institute for Cancer Research, Rikshospitalet-Radiumhospitalet Medical Center, Oslo, Norway.
Young H Kim
Kevin A Kwei
Yoon La Choi
Melanie Bocanegra
Anita Langerød
Wonshik Han
Dong-Young Noh
David G Huntsman
Stefanie S Jeffrey
Anne-Lise Børresen-Dale
Jonathan R Pollack
Stanford University · USNorwegian Cancer Society · NOSeoul National University · KRBC Cancer Agency · CASamsung Medical Center · KRUniversity of Oslo · NO

Funding

Leveraging innovative technologies in basic and clinical cancer researchT32CA009302 · NCI · STANFORD UNIVERSITY · PI LAURA D ATTARDI, Aaron M Newman · 1985 to 2026
$19.1M
Role of Gene Amplification in Breast CancerR01CA097139 · NCI · STANFORD UNIVERSITY · PI POLLACK, JONATHAN R · 2003 to 2007
$1.6M
Gene Amplification and Deletion in Pancreatic CancerR01CA112016 · NCI · STANFORD UNIVERSITY · PI POLLACK, JONATHAN R · 2006 to 2010
$1.4M
NCI NIH HHS CA112016NCI NIH HHS R01 CA097139NCI NIH HHS R01 CA112016NCI NIH HHS T32 CA009302
6 · The paper itself

Abstract

Breast cancer exhibits clinical and molecular heterogeneity, where expression profiling studies have identified five major molecular subtypes. The basal-like subtype, expressing basal epithelial markers and negative for estrogen receptor (ER), progesterone receptor (PR) and HER2, is associated with higher overall levels of DNA copy number alteration (CNA), specific CNAs (like gain on chromosome 10p), and poor prognosis. Discovering the molecular genetic basis of tumor subtypes may provide new opportunities for therapy. To identify the driver oncogene on 10p associated with basal-like tumors, we analyzed genomic profiles of 172 breast carcinomas. The smallest shared region of gain spanned just seven genes at 10p13, including calcium/calmodulin-dependent protein kinase ID (CAMK1D), functioning in intracellular signaling but not previously linked to cancer. By microarray, CAMK1D was overexpressed when amplified, and by immunohistochemistry exhibited elevated expression in invasive carcinomas compared to carcinoma in situ. Engineered overexpression of CAMK1D in non-tumorigenic breast epithelial cells led to increased cell proliferation, and molecular and phenotypic alterations indicative of epithelial-mesenchymal transition (EMT), including loss of cell-cell adhesions and increased cell migration and invasion. Our findings identify CAMK1D as a novel amplified oncogene linked to EMT in breast cancer, and as a potential therapeutic target with particular relevance to clinically unfavorable basal-like tumors.

Indexed as

Gene AmplificationBreast NeoplasmsCalcium-Calmodulin-Dependent Protein Kinase Type 1Cell AdhesionCell ProliferationChromosomes, Human, Pair 10Epithelial CellsFemaleHumansImmunohistochemistryMesenchymal Stem CellsNeoplasm InvasivenessOligonucleotide Array Sequence AnalysisCalcium-Calmodulin-Dependent Protein Kinase Type 1CAMK1D protein, human

Identifiers

PMID19383354
PMCPMC2653212
OpenAlexW2152274241

What OpenQuestion holds

Textmetadata
LicenceTDM
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.