Evidence map›Paper›PMID 22334367›Full record

ArticleGenes, chromosomes & cancer2012

A new whole genome amplification method for studying clonal evolution patterns in malignant colorectal polyps.

Daniela Hirsch, Jordi Camps, Sudhir Varma, Ralf Kemmerling, Mark Stapleton, Thomas Ried, Timo Gaiser

Open access · greenAbstract read
In one paragraph

Article in Genes, chromosomes & cancer, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
2.0field-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

19 citing papers in PubMed, 27 citations in OpenAlex.

  1. Article
  2. Molecular characterization of ulcerative colitis-associated colorectal carcinomas.Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc · 2021
    Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. Dynamics of Genome Alterations in Crohn's Disease-Associated Colorectal Carcinogenesis.Clinical cancer research : an official journal of the American Association for Cancer Research · 2018
    Article
  11. Article
  12. Evolutionary dynamics in pre-invasive neoplasia.Current opinion in systems biology · 2017
    Article
  13. Review
  14. Genomic Landscape of Colorectal Mucosa and Adenomas.Cancer prevention research (Philadelphia, Pa.) · 2016
    Article
  15. Patterns of Chromosomal Aberrations in Solid Tumors.Recent results in cancer research. Fortschritte der Krebsforschung. Progres dans les recherches sur le cancer · 2015
    Review
  16. Article
  17. Article
  18. Review
  19. Article
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

7 authors at 3 institutions in 3 countries.

Daniela HirschSection of Cancer Genomics, Genetics Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA.
Jordi Camps
Sudhir Varma
Ralf Kemmerling
Mark Stapleton
Thomas Ried
Timo Gaiser
Center for Cancer Research · USNational Institutes of Health · USParacelsus Medical University · AT

Funding

Consequences of Genomic Instability and Aneuploidy on the Colorectal Cancer TranZIABC010835 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI RIED, THOMAS · 2009 to 2016
$6.8M
Intramural NIH HHS Z99 CA999999NCI NIH HHS Y99 CA999999
6 · The paper itself

Abstract

To identify the genetic drivers of colorectal tumorigenesis, we applied array comparative genomic hybridization (aCGH) to 13 formalin-fixed paraffin-embedded (FFPE) samples of early, localized human colon adenocarcinomas arising in high-grade adenomas (so-called "malignant polyps"). These lesions are small and hence the amount of DNA is limited. Additionally, the quality of DNA is compromised due to the fragmentation as a consequence of formalin fixation. To overcome these problems, we optimized a newly developed isothermal whole genome amplification system (NuGEN Ovation® WGA FFPE System). Starting with 100 ng of FFPE DNA, the amplification system produced 4.01 ± 0.29 μg (mean ± standard deviation) of DNA. The excellent quality of amplified DNA was further indicated by a high signal-to-noise ratio and a low derivative log(2) ratio spread. Both, the amount of amplified DNA and aCGH performance were independent of the age of the FFPE blocks and the associated degradation of the extracted DNA. We observed losses of chromosome arms 5q and 18q in the adenoma components of the malignant polyp samples, while the embedded early carcinomas revealed losses of 8p, 17p, and 18, and gains of 7, 13, and 20. Aberrations detected in the adenoma components were invariably maintained in the embedded carcinomas. This approach demonstrates that using isothermally whole genome amplified FFPE DNA is technically suitable for aCGH. In addition to demonstrating the clonal origin of the adenoma and carcinoma part within a malignant polyp, the gain of chromosome arm 20q was an indicator for progression from adenoma to carcinoma.

Indexed as

Comparative Genomic HybridizationAdenomaCarcinomaChromosome AberrationsChromosomes, Human, Pair 20Clonal EvolutionColonic PolypsColorectal NeoplasmsDNA Copy Number VariationsDNA, NeoplasmHumansDNA, Neoplasm

Identifiers

PMID22334367
PMCPMC3535186
OpenAlexW2123360838

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.