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Sequence analysis of mutations and translocations across breast cancer subtypes | Nature
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This paper reports one of the largest breast cancer whole-exome and whole-genome sequencing efforts so far, identifying previously unknown recurrent mutations in CBFB, deletions of RUNX1 and recurrent MAGI1–AKT3 fusion; the fusion suggests that the use of ATP-competitive AKT inhibitors should be evaluated in clinical trials. This paper reports one of the largest whole-exome sequencing efforts in human breast cancers so far, complemented by whole-genome sequences of 22 breast cancer/normal pairs. The authors analysed diverse subtypes from patients in Mexico and Vietnam and identified recurrent mutations in the CBFB transcription factor gene and deletions of its partner RUNX1, as well as a recurrent MAGI3–AKT3 fusion enriched in triple-negative breast cancers (those lacking oestrogen and progesterone receptors and ERBB2 expression). The fusion leads to constitutive activation of AKT kinase, which can be counteracted by treatment with a small-molecule inhibitor. Breast carcinoma is the leading cause of cancer-related mortality in women worldwide, with an estimated 1.38 million new cases and 458,000 deaths in 2008 alone1. This malignancy represents a heterogeneous group of tumours with characteristic molecular features, prognosis and responses to available therapy2,3,4. Recurrent somatic alterations in breast cancer have been described, including mutations and copy number alterations, notably ERBB2 amplifications, the first successful therapy target defined by a genomic aberration5. Previous DNA sequencing studies of breast cancer genomes have revealed additional candidate mutations and gene rearrangements6,7,8,9,10. Here we report the whole-exome sequences of DNA from 103 human breast cancers of diverse subtypes from patients in Mexico and Vietnam compared to matched-normal DNA, together with whole-genome sequences of 22 breast cancer/normal pairs. Beyond confirming recurrent somatic mutations in PIK3CA11, TP536, AKT112, GATA313 and MAP3K110, we discovered recurrent mutations in the CBFB transcription factor gene and deletions of its partner RUNX1. Furthermore, we have identified a recurrent MAGI3–AKT3 fusion enriched in triple-negative breast cancer lacking oestrogen and progesterone receptors and ERBB2 expression. The MAGI3–AKT3 fusion leads to constitutive activation of AKT kinase, which is abolished by treatment with an ATP-competitive AKT small-molecule inhibitor.
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nature portfolio privacy policy core-binding-factor beta subunit hormone-receptor-negative breast cancers29 advertising gerardo jimenez-sanchez oestrogen-receptor-positive breast cancers10 chimeric gene cbfb/pebp2b-mhy11 library construction uk/genetics/cgp/cosmic/ low-serum media reprints atp-competitive akt inhibitors triple-negative breast cancers v-erbb-related gene small-cell lung cancer dana-farber/harvard spore dana-farber cancer institute oestrogen-receptor-positive disease notch family-gene fusions25 antonio maffuz-aziz disrupts zinc-finger domains alfredo hidalgo-miranda target protein-coding regions predicted 5′-magi3–akt3-3′ fusion org/display/cgatools/mutect org/display/cgatools/indelocator org/display/cgatools/home social media nature biotechnol nature med shin nature magi3–akt3 fusion protein oestrogen-receptor-positive subtypes van de sluis mass-spectrometry-based genotyping commercial-share alike licence inferred segmental copy-ratios accession number phs000369 tumour/normal dna pairs higher copy-ratio allele magi3–akt3 overexpressing cells magi3–akt3 fusion gene oestrogen-receptor-positive samples allele-specific copy number small-molecule inhibitor protein-altering point mutations org/display/cgatools/mutsig received fellowship support 5′-magi3–akt3-3′ fusion event
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headline:Sequence analysis of mutations and translocations across breast cancer subtypes
description:This paper reports one of the largest breast cancer whole-exome and whole-genome sequencing efforts so far, identifying previously unknown recurrent mutations in CBFB, deletions of RUNX1 and recurrent MAGI1âAKT3 fusion; the fusion suggests that the use of ATP-competitive AKT inhibitors should be evaluated in clinical trials. This paper reports one of the largest whole-exome sequencing efforts in human breast cancers so far, complemented by whole-genome sequences of 22 breast cancer/normal pairs. The authors analysed diverse subtypes from patients in Mexico and Vietnam and identified recurrent mutations in the CBFB transcription factor gene and deletions of its partner RUNX1, as well as a recurrent MAGI3âAKT3 fusion enriched in triple-negative breast cancers (those lacking oestrogen and progesterone receptors and ERBB2 expression). The fusion leads to constitutive activation of AKT kinase, which can be counteracted by treatment with a small-molecule inhibitor. Breast carcinoma is the leading cause of cancer-related mortality in women worldwide, with an estimated 1.38 million new cases and 458,000 deaths in 2008 alone1. This malignancy represents a heterogeneous group of tumours with characteristic molecular features, prognosis and responses to available therapy2,3,4. Recurrent somatic alterations in breast cancer have been described, including mutations and copy number alterations, notably ERBB2 amplifications, the first successful therapy target defined by a genomic aberration5. Previous DNA sequencing studies of breast cancer genomes have revealed additional candidate mutations and gene rearrangements6,7,8,9,10. Here we report the whole-exome sequences of DNA from 103 human breast cancers of diverse subtypes from patients in Mexico and Vietnam compared to matched-normal DNA, together with whole-genome sequences of 22 breast cancer/normal pairs. Beyond confirming recurrent somatic mutations in PIK3CA11, TP536, AKT112, GATA313 and MAP3K110, we discovered recurrent mutations in the CBFB transcription factor gene and deletions of its partner RUNX1. Furthermore, we have identified a recurrent MAGI3âAKT3 fusion enriched in triple-negative breast cancer lacking oestrogen and progesterone receptors and ERBB2 expression. The MAGI3âAKT3 fusion leads to constitutive activation of AKT kinase, which is abolished by treatment with an ATP-competitive AKT small-molecule inhibitor.
datePublished:2012-06-20T00:00:00Z
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headline:Sequence analysis of mutations and translocations across breast cancer subtypes
description:This paper reports one of the largest breast cancer whole-exome and whole-genome sequencing efforts so far, identifying previously unknown recurrent mutations in CBFB, deletions of RUNX1 and recurrent MAGI1âAKT3 fusion; the fusion suggests that the use of ATP-competitive AKT inhibitors should be evaluated in clinical trials. This paper reports one of the largest whole-exome sequencing efforts in human breast cancers so far, complemented by whole-genome sequences of 22 breast cancer/normal pairs. The authors analysed diverse subtypes from patients in Mexico and Vietnam and identified recurrent mutations in the CBFB transcription factor gene and deletions of its partner RUNX1, as well as a recurrent MAGI3âAKT3 fusion enriched in triple-negative breast cancers (those lacking oestrogen and progesterone receptors and ERBB2 expression). The fusion leads to constitutive activation of AKT kinase, which can be counteracted by treatment with a small-molecule inhibitor. Breast carcinoma is the leading cause of cancer-related mortality in women worldwide, with an estimated 1.38 million new cases and 458,000 deaths in 2008 alone1. This malignancy represents a heterogeneous group of tumours with characteristic molecular features, prognosis and responses to available therapy2,3,4. Recurrent somatic alterations in breast cancer have been described, including mutations and copy number alterations, notably ERBB2 amplifications, the first successful therapy target defined by a genomic aberration5. Previous DNA sequencing studies of breast cancer genomes have revealed additional candidate mutations and gene rearrangements6,7,8,9,10. Here we report the whole-exome sequences of DNA from 103 human breast cancers of diverse subtypes from patients in Mexico and Vietnam compared to matched-normal DNA, together with whole-genome sequences of 22 breast cancer/normal pairs. Beyond confirming recurrent somatic mutations in PIK3CA11, TP536, AKT112, GATA313 and MAP3K110, we discovered recurrent mutations in the CBFB transcription factor gene and deletions of its partner RUNX1. Furthermore, we have identified a recurrent MAGI3âAKT3 fusion enriched in triple-negative breast cancer lacking oestrogen and progesterone receptors and ERBB2 expression. The MAGI3âAKT3 fusion leads to constitutive activation of AKT kinase, which is abolished by treatment with an ATP-competitive AKT small-molecule inhibitor.
datePublished:2012-06-20T00:00:00Z
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Cancer genetics
DNA sequencing
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name:The Broad Institute of MIT and Harvard, Cambridge, USA
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name:The Broad Institute of MIT and Harvard, Cambridge, USA
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address:
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affiliation:
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address:
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affiliation:
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address:
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type:PostalAddress
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address:
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email:[email protected]
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affiliation:
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address:
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type:PostalAddress
type:Organization
email:[email protected]
name:Alfredo Hidalgo-Miranda
affiliation:
name:Instituto Nacional de Medicina Genómica
address:
name:Instituto Nacional de Medicina Genómica, Mexico City, Mexico
type:PostalAddress
type:Organization
email:[email protected]
name:Matthew Meyerson
affiliation:
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address:
name:The Broad Institute of MIT and Harvard, Cambridge, USA
type:PostalAddress
type:Organization
name:Dana-Farber Cancer Institute
address:
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address:
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name:Dana-Farber Cancer Institute
address:
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email:[email protected]
PostalAddress:
name:The Broad Institute of MIT and Harvard, Cambridge, USA
name:Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, USA
name:Harvard Medical School, Boston, USA
name:Present addresses: Department of Medical Oncology, CancerCare Manitoba, Winnipeg, Manitoba R3E 0V9, Canada (S.B.); Global Biotech Consulting Group, Mexico City 01900, Mexico (G.J.-S.).,
name:The Broad Institute of MIT and Harvard, Cambridge, USA
name:Instituto Nacional de Medicina Genómica, Mexico City, Mexico
name:Department of Pathology, Beth Israel Deaconess Medical Center, 330 Brookline Avenue, Boston, Massachusetts 02215,
name:The Broad Institute of MIT and Harvard, Cambridge, USA
name:The Broad Institute of MIT and Harvard, Cambridge, USA
name:The Broad Institute of MIT and Harvard, Cambridge, USA
name:The Broad Institute of MIT and Harvard, Cambridge, USA
name:The Broad Institute of MIT and Harvard, Cambridge, USA
name:The Broad Institute of MIT and Harvard, Cambridge, USA
name:The Broad Institute of MIT and Harvard, Cambridge, USA
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name:Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, USA
name:The Broad Institute of MIT and Harvard, Cambridge, USA
name:The Broad Institute of MIT and Harvard, Cambridge, USA
name:Instituto de Enfermedades de la Mama FUCAM, Mexico City, Mexico
name:The Broad Institute of MIT and Harvard, Cambridge, USA
name:The Broad Institute of MIT and Harvard, Cambridge, USA
name:The Broad Institute of MIT and Harvard, Cambridge, USA
name:Instituto de Enfermedades de la Mama FUCAM, Mexico City, Mexico
name:The Broad Institute of MIT and Harvard, Cambridge, USA
name:The Broad Institute of MIT and Harvard, Cambridge, USA
name:The Broad Institute of MIT and Harvard, Cambridge, USA
name:Instituto Nacional de Medicina Genómica, Mexico City, Mexico
name:The Broad Institute of MIT and Harvard, Cambridge, USA
name:Instituto Nacional de Medicina Genómica, Mexico City, Mexico
name:Instituto de Enfermedades de la Mama FUCAM, Mexico City, Mexico
name:Instituto Nacional de Medicina Genómica, Mexico City, Mexico
name:The Broad Institute of MIT and Harvard, Cambridge, USA
name:Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, USA
name:The Broad Institute of MIT and Harvard, Cambridge, USA
name:The Broad Institute of MIT and Harvard, Cambridge, USA
name:Instituto Nacional de Medicina Genómica, Mexico City, Mexico
name:Harvard Medical School, Boston, USA
name:Division of Hematology and Oncology, Massachusetts General Hospital, Boston, USA
name:The Broad Institute of MIT and Harvard, Cambridge, USA
name:Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, USA
name:Harvard Medical School, Boston, USA
name:Department of Cancer Biology, Dana-Farber Cancer Institute, Boston, USA
name:Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, USA
name:Harvard Medical School, Boston, USA
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name:Harvard Medical School, Boston, USA
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name:Harvard Medical School, Boston, USA
name:Department of Pathology, Brigham and Women's Hospital, Boston, USA
name:Instituto Nacional de Medicina Genómica, Mexico City, Mexico
name:Present addresses: Department of Medical Oncology, CancerCare Manitoba, Winnipeg, Manitoba R3E 0V9, Canada (S.B.); Global Biotech Consulting Group, Mexico City 01900, Mexico (G.J.-S.).,
name:The Broad Institute of MIT and Harvard, Cambridge, USA
name:Harvard Medical School, Boston, USA
name:Massachusetts Institute of Technology, Cambridge, USA
name:The Broad Institute of MIT and Harvard, Cambridge, USA
name:The Broad Institute of MIT and Harvard, Cambridge, USA
name:Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, USA
name:Harvard Medical School, Boston, USA
name:The Broad Institute of MIT and Harvard, Cambridge, USA
name:Harvard Medical School, Boston, USA
name:Department of Pediatric Oncology, Dana-Farber Cancer Institute, Boston, USA
name:Howard Hughes Medical Institute, Chevy Chase, USA
name:Instituto Nacional de Medicina Genómica, Mexico City, Mexico
name:Harvard Medical School, Boston, USA
name:Department of Pathology, Beth Israel Deaconess Medical Center, 330 Brookline Avenue, Boston, Massachusetts 02215,
name:The Broad Institute of MIT and Harvard, Cambridge, USA
name:Instituto Nacional de Medicina Genómica, Mexico City, Mexico
name:The Broad Institute of MIT and Harvard, Cambridge, USA
name:Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, USA
name:Harvard Medical School, Boston, USA
name:Department of Cancer Biology, Dana-Farber Cancer Institute, Boston, USA
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