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  • Open Access

Analysis of the copy number profiles of several tumor samples from the same patient reveals the successive steps in tumorigenesis

  • 1, 2, 3,
  • 4, 5,
  • 6,
  • 2, 3 and
  • 1
Genome Biology201011 (Suppl 1) :P25

https://doi.org/10.1186/gb-2010-11-s1-p25

  • Published:

Keywords

  • Cancer Research
  • Simulated Data
  • Tumor Sample
  • Research Community
  • Cancer Progression

Cancers arise from an accumulation of genetic and epigenetic alterations, through which cells acquire the properties required for malignancy. Unraveling the sequence of alterations driving tumorigenesis is crucial to understand the biological mechanisms underlying tumor initiation, invasive progression and metastasis. The idea of analyzing several tumor samples, such as recurrences or metastases, from a single patient has recently gained popularity in the cancer research community [1, 2].

Here, we present a computational method, TuMult, for reconstructing the sequence of copy number changes driving carcinogenesis, based on the analysis of several tumor samples from the same patient. We demonstrate the reliability of the method with simulated data, and describe applications to three different cancers, showing that TuMult is a valuable tool for the establishment of clonal relationships between tumor samples and the identification of chromosome aberrations occurring at crucial steps in cancer progression. This work was recently published in Genome Biology [3].

Authors’ Affiliations

(1)
INSERM, UMR-S 973, MTi, Université Paris Diderot - Paris 7, 35 rue Hélène Brion, 75205 Paris Cedex 13, France
(2)
Institut Curie, Centre de Recherche, Paris, F-75248, France
(3)
CNRS, UMR 144, 26 rue d'Ulm, 75248 Paris Cedex 05, France
(4)
INSERM, Unité 955, Créteil, F-94000, France
(5)
AP-HP, Groupe Hospitalier Albert Chenevier - Henri Mondor, Département de Pathologie, Créteil, F-94000, France
(6)
Département d'Oncologie Radiothérapie, Institut Curie, 26 rue d'Ulm, 75248 Paris Cedex 05, France

References

  1. Mullighan CG, Phillips LA, Su X, Ma J, Miller CB, Shurtleff SA, Downing JR: Genomic analysis of the clonal origins of relapsed acute lymphoblastic leukemia. Science. 2008, 322: 1377-1380. 10.1126/science.1164266.PubMedPubMed CentralView ArticleGoogle Scholar
  2. Jones SJ, Laskin J, Li YY, Griffith OL, An J, Bilenky M, Butterfield YS, Cezard T, Chuah E, Corbett R, Fejes A, Griffith M, Yee J, Martin M, Mayo M, Melnyk N, Morin RD, Pugh TJ, Severson T, Shah SP, Sutcliffe M, Tam A, Terry J, Thiessen N, Thomson T, Varhol R, Zeng T, Zhao Y, Moore RA, Huntsman DG, et al: Evolution of an adenocarcinoma in response to selection by targeted kinase inhibitors. Genome. Biol. 2010, 11: R82-10.1186/gb-2010-11-8-r82.PubMedPubMed CentralView ArticleGoogle Scholar
  3. Letouzé E, Allory Y, Bollet MA, Radvanyi F, Guyon F: Analysis of the copy number profiles of several tumor samples from the same patient reveals the successive steps in tumorigenesis. Genome Biol. 2010, 11: R76-10.1186/gb-2010-11-7-r76.PubMedPubMed CentralView ArticleGoogle Scholar

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