We are analyzing https://link.springer.com/article/10.1007/s10549-013-2699-3.

Title:
The molecular diversity of Luminal A breast tumors | Breast Cancer Research and Treatment
Description:
Breast cancer is a collection of diseases with distinct molecular traits, prognosis, and therapeutic options. Luminal A breast cancer is the most heterogeneous, both molecularly and clinically. Using genomic data from over 1,000 Luminal A tumors from multiple studies, we analyzed the copy number and mutational landscape of this tumor subtype. This integrated analysis revealed four major subtypes defined by distinct copy-number and mutation profiles. We identified an atypical Luminal A subtype characterized by high genomic instability, TP53 mutations, and increased Aurora kinase signaling; these genomic alterations lead to a worse clinical prognosis. Aberrations of chromosomes 1, 8, and 16, together with PIK3CA, GATA3, AKT1, and MAP3K1 mutations drive the other subtypes. Finally, an unbiased pathway analysis revealed multiple rare, but mutually exclusive, alterations linked to loss of activity of co-repressor complexes N-Cor and SMRT. These rare alterations were the most prevalent in Luminal A tumors and may predict resistance to endocrine therapy. Our work provides for a further molecular stratification of Luminal A breast tumors, with potential direct clinical implications.
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Keywords {🔍}

cancer, breast, luminal, tumors, mutations, article, number, google, scholar, pubmed, copy, cas, genes, analysis, alterations, genomic, dataset, fig, multiple, cnh, mapk, subtypes, clinical, table, samples, data, subtype, tcga, tumor, expression, clusters, gene, loss, cluster, molecular, mutation, high, shows, identified, characterized, pikca, survival, somatic, recurrent, distinct, metabric, cna, observed, amplification, size,

Topics {✒️}

tamoxifen-bound estrogen receptor-alpha org/web/packages/survival/index 8p−/8q+/16p+/16q− pattern observed article download pdf relapsed classic e-cadherin mitotic serine/threonine kinase triple-negative breast cancer open software development pre-processed acgh data european genome–phenome archive node-negative breast cancer suggesting bi-allelic inactivation regulating er-α transcription growth factor receptors ras/erk signaling cascades copy number-driven clusters dark blue frame-shift cancer genome atlas gene-expression-based predictors subtype-specific genomic events 8p−/8q+/16p+/16q− tamoxifen anti-proliferative effects lobular breast cancer research-based versions pam50 mrna-derived signatures breast cancer prognosis/prediction nonsense/light blue missense promote er-driven proliferation reduced jnk signaling human breast tumours human colorectal cancers full access breast cancer based breast cancer cells �mitotic cell cycle” highlighting multiple ways privacy choices/manage cookies splicing factor sf3b1 identifies distinct subgroups identifies micro-pathways dna homozygous deletion mutual exclusivity analysis mutual exclusivity modules advanced breast cancer defining breast cancer breast cancer pathophysiologies breast cancer detected metastatic breast cancer breast cancer chemoresistance comprehensive genomic profile

Questions {❓}

Dar AA et al (2010) Aurora kinase inhibitors—rising stars in cancer therapeutics?
Kapp AV, Tibshirani R (2007) Are clusters found in one dataset present in another dataset?

Schema {🗺️}

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         headline:The molecular diversity of Luminal A breast tumors
         description:Breast cancer is a collection of diseases with distinct molecular traits, prognosis, and therapeutic options. Luminal A breast cancer is the most heterogeneous, both molecularly and clinically. Using genomic data from over 1,000 Luminal A tumors from multiple studies, we analyzed the copy number and mutational landscape of this tumor subtype. This integrated analysis revealed four major subtypes defined by distinct copy-number and mutation profiles. We identified an atypical Luminal A subtype characterized by high genomic instability, TP53 mutations, and increased Aurora kinase signaling; these genomic alterations lead to a worse clinical prognosis. Aberrations of chromosomes 1, 8, and 16, together with PIK3CA, GATA3, AKT1, and MAP3K1 mutations drive the other subtypes. Finally, an unbiased pathway analysis revealed multiple rare, but mutually exclusive, alterations linked to loss of activity of co-repressor complexes N-Cor and SMRT. These rare alterations were the most prevalent in Luminal A tumors and may predict resistance to endocrine therapy. Our work provides for a further molecular stratification of Luminal A breast tumors, with potential direct clinical implications.
         datePublished:2013-10-06T00:00:00Z
         dateModified:2013-10-06T00:00:00Z
         pageStart:409
         pageEnd:420
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            Breast cancer genomics
            Oncology
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      headline:The molecular diversity of Luminal A breast tumors
      description:Breast cancer is a collection of diseases with distinct molecular traits, prognosis, and therapeutic options. Luminal A breast cancer is the most heterogeneous, both molecularly and clinically. Using genomic data from over 1,000 Luminal A tumors from multiple studies, we analyzed the copy number and mutational landscape of this tumor subtype. This integrated analysis revealed four major subtypes defined by distinct copy-number and mutation profiles. We identified an atypical Luminal A subtype characterized by high genomic instability, TP53 mutations, and increased Aurora kinase signaling; these genomic alterations lead to a worse clinical prognosis. Aberrations of chromosomes 1, 8, and 16, together with PIK3CA, GATA3, AKT1, and MAP3K1 mutations drive the other subtypes. Finally, an unbiased pathway analysis revealed multiple rare, but mutually exclusive, alterations linked to loss of activity of co-repressor complexes N-Cor and SMRT. These rare alterations were the most prevalent in Luminal A tumors and may predict resistance to endocrine therapy. Our work provides for a further molecular stratification of Luminal A breast tumors, with potential direct clinical implications.
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      dateModified:2013-10-06T00:00:00Z
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         Luminal A breast cancer
         Breast cancer genomics
         Oncology
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      name:Computational Biology Center, Memorial Sloan-Kettering Cancer Center, New York, USA
      name:Computational Biology Center, Memorial Sloan-Kettering Cancer Center, New York, USA
      name:Lineberger Comprehensive Cancer Center, University of North Carolina, Chapel Hill, USA
      name:Computational Biology Center, Memorial Sloan-Kettering Cancer Center, New York, USA
      name:Computational Biology Center, Memorial Sloan-Kettering Cancer Center, New York, USA

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