The molecular profile of luminal B breast cancer

Chad J CreightonDepartment of Medicine and Dan L Duncan Cancer Center Division of Biostatistics. Baylor College of Medicine, Houston, TX, USAAbstract: Molecular profiling studies have found that estrogen receptor-positive (ER+) human breast cancers are comprised of at least two distinct diseases wit...

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Autor principal:	Creighton CJ
Formato:	article
Lenguaje:	EN
Publicado:	Dove Medical Press 2012
Materias:	Medicine (General) R5-920
Acceso en línea:	https://doaj.org/article/bd5bf0ea2a234ec5ad9c19ddc12dd19d
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spelling	oai:doaj.org-article:bd5bf0ea2a234ec5ad9c19ddc12dd19d2021-12-02T03:34:57ZThe molecular profile of luminal B breast cancer1177-54751177-5491https://doaj.org/article/bd5bf0ea2a234ec5ad9c19ddc12dd19d2012-08-01T00:00:00Zhttp://www.dovepress.com/the-molecular-profile-of-luminal-b-breast-cancer-a10804https://doaj.org/toc/1177-5475https://doaj.org/toc/1177-5491Chad J CreightonDepartment of Medicine and Dan L Duncan Cancer Center Division of Biostatistics. Baylor College of Medicine, Houston, TX, USAAbstract: Molecular profiling studies have found that estrogen receptor-positive (ER+) human breast cancers are comprised of at least two distinct diseases with differing biologies. With the advent of DNA microarrays, global gene expression patterns were used to define the luminal A and luminal B subtypes of ER+ breast cancer, with luminal B cancers showing a more aggressive phenotype including substantially worse outcomes in patients. The luminal B subtype designation could be considered a surrogate for those ER+ tumors having low progesterone receptors, high proliferation, high grade, and predicted poor response to hormone therapy. While they express estrogen receptors, luminal B cancers do not show a corresponding expression of estrogen-regulated genes, and may therefore rely upon alternative pathways for growth. At the molecular level, luminal B cancers appear dramatically distinct from luminal A cancers, at the levels of gene expression, gene copy, somatic mutation, and DNA methylation; luminal B cancers are also genetically and genomically altered to a greater extent than luminal A cancers. While, in the clinical setting, luminal B is typically regarded as an ER+, hormone-sensitive disease, more research is needed into how to better treat it. Comprehensive profiling initiatives, such as The Cancer Genome Atlas, have recently provided us a catalog of mutated or copy altered genes, from which new therapeutic targets could potentially be mined. Candidate pathways that might be targeted in luminal B include those involving growth factor receptors, including HER2 and EGFR, as well as PI3K/Akt/mTor.Keywords: luminal B, molecular profiling, integrative analysis, breast cancer, TCGACreighton CJDove Medical PressarticleMedicine (General)R5-920ENBiologics: Targets & Therapy, Vol 2012, Iss default, Pp 289-297 (2012)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine (General) R5-920
spellingShingle	Medicine (General) R5-920 Creighton CJ The molecular profile of luminal B breast cancer
description	Chad J CreightonDepartment of Medicine and Dan L Duncan Cancer Center Division of Biostatistics. Baylor College of Medicine, Houston, TX, USAAbstract: Molecular profiling studies have found that estrogen receptor-positive (ER+) human breast cancers are comprised of at least two distinct diseases with differing biologies. With the advent of DNA microarrays, global gene expression patterns were used to define the luminal A and luminal B subtypes of ER+ breast cancer, with luminal B cancers showing a more aggressive phenotype including substantially worse outcomes in patients. The luminal B subtype designation could be considered a surrogate for those ER+ tumors having low progesterone receptors, high proliferation, high grade, and predicted poor response to hormone therapy. While they express estrogen receptors, luminal B cancers do not show a corresponding expression of estrogen-regulated genes, and may therefore rely upon alternative pathways for growth. At the molecular level, luminal B cancers appear dramatically distinct from luminal A cancers, at the levels of gene expression, gene copy, somatic mutation, and DNA methylation; luminal B cancers are also genetically and genomically altered to a greater extent than luminal A cancers. While, in the clinical setting, luminal B is typically regarded as an ER+, hormone-sensitive disease, more research is needed into how to better treat it. Comprehensive profiling initiatives, such as The Cancer Genome Atlas, have recently provided us a catalog of mutated or copy altered genes, from which new therapeutic targets could potentially be mined. Candidate pathways that might be targeted in luminal B include those involving growth factor receptors, including HER2 and EGFR, as well as PI3K/Akt/mTor.Keywords: luminal B, molecular profiling, integrative analysis, breast cancer, TCGA
format	article
author	Creighton CJ
author_facet	Creighton CJ
author_sort	Creighton CJ
title	The molecular profile of luminal B breast cancer
title_short	The molecular profile of luminal B breast cancer
title_full	The molecular profile of luminal B breast cancer
title_fullStr	The molecular profile of luminal B breast cancer
title_full_unstemmed	The molecular profile of luminal B breast cancer
title_sort	molecular profile of luminal b breast cancer
publisher	Dove Medical Press
publishDate	2012
url	https://doaj.org/article/bd5bf0ea2a234ec5ad9c19ddc12dd19d
work_keys_str_mv	AT creightoncj themolecularprofileofluminalbbreastcancer AT creightoncj molecularprofileofluminalbbreastcancer
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The molecular profile of luminal B breast cancer

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