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Ena-DATASET-MGH-10-02-2015-15:17:58:985-1 - samples

ABSTRACT: DNA was derived from the primary tumour, lung metastasis, and peri-aortic lymph node metastasis. DNA from the spleen was used as a normal control. For WE sequencing we user Hybrid capture (Nimblegen version 3.0) of the lymph node and lung metastases, primary tumour and spleen normal; we generated ~100-fold coverage.

PROVIDER: EGAD00001001252 | EGA |

REPOSITORIES: EGA

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Publications

Convergent loss of PTEN leads to clinical resistance to a PI(3)Kα inhibitor.

Juric Dejan D Castel Pau P Griffith Malachi M Griffith Obi L OL Won Helen H HH Ellis Haley H Ebbesen Saya H SH Ainscough Benjamin J BJ Ramu Avinash A Iyer Gopa G Shah Ronak H RH Huynh Tiffany T Mino-Kenudson Mari M Sgroi Dennis D Isakoff Steven S Thabet Ashraf A Elamine Leila L Solit David B DB Lowe Scott W SW Quadt Cornelia C Peters Malte M Derti Adnan A Schegel Robert R Huang Alan A Mardis Elaine R ER Berger Michael F MF Baselga José J Scaltriti Maurizio M

Nature 20141117 7538

Broad and deep tumour genome sequencing has shed new light on tumour heterogeneity and provided important insights into the evolution of metastases arising from different clones. There is an additional layer of complexity, in that tumour evolution may be influenced by selective pressure provided by therapy, in a similar fashion to that occurring in infectious diseases. Here we studied tumour genomic evolution in a patient (index patient) with metastatic breast cancer bearing an activating PIK3CA ...[more]

PMID: 25409150

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