Observations on the presence of E domain variants of estrogen receptor‐α in the breast tumors

Kumar, Vijay; Kumar, Suresh; Srivastava, Anurag

doi:10.1002/jso.20588

Cited by 6 publications

(2 citation statements)

References 35 publications

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“…We highlight the fact that expression profiles across the isoforms of the same gene vary substantially. So, particularly for key breast-cancer genes, such as ESR1 , isoform-level data are more informative than gene-level data, allowing us to determine how variants contribute to the hormone dependence and treatment response of the tumor [41, 42]. …”

Section: Discussionmentioning

confidence: 99%

Comprehensive landscape of subtype-specific coding and non-coding RNA transcripts in breast cancer

Pramana

Calza

et al. 2016

Oncotarget

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Molecular classification of breast cancer into clinically relevant subtypes helps improve prognosis and adjuvant-treatment decisions. The aim of this study is to provide a better characterization of the molecular subtypes by providing a comprehensive landscape of subtype-specific isoforms including coding, long non-coding RNA and microRNA transcripts. Isoform-level expression of all coding and non-coding RNAs is estimated from RNA-sequence data of 1168 breast samples obtained from The Cancer Genome Atlas (TCGA) project. We then search the whole transcriptome systematically for subtype-specific isoforms using a novel algorithm based on a robust quasi-Poisson model. We discover 5451 isoforms specific to single subtypes. A total of 27% of the subtype-specific isoforms have better accuracy in classifying the intrinsic subtypes than that of their corresponding genes. We find three subtype-specific miRNA and 707 subtype-specific long non-coding RNAs. The isoforms from long non-coding RNAs also show high performance for separation between Luminal A and Luminal B subtypes with an AUC of 0.97 in the discovery set and 0.90 in the validation set. In addition, we discover 1500 isoforms preferentially co-expressed in two subtypes, including 369 isoforms co-expressed in both Normal-like and Basal subtypes, which are commonly considered to have distinct ER-receptor status. Finally, analyses at protein level reveal four subtype-specific proteins and two subtype co-expression proteins that successfully validate results from the isoform level.

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Section: Discussionmentioning

confidence: 99%

Comprehensive landscape of subtype-specific coding and non-coding RNA transcripts in breast cancer

Pramana

Calza

et al. 2016

Oncotarget

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“…These variants have been identified in both breast cancer cell lines (Flouriot et al, 2000) and breast cancer tissues (Kumar et al, 2006). The novel 36 kDa variant (here termed ER-α36) which was first identified and cloned in 2005 (Wang et al, 2005), lacks both transcriptional activation function domains (AF-1 and AF-2) but retains the DNA-binding domain, partial dimerization, and ligand-binding domains campared to the full-length ER-α66 (Fig.…”

Section: Introductionmentioning

confidence: 99%

Quantitative profiles of the mRNAs of ER-α and its novel variant ER-α36 in breast cancers and matched normal tissues

Zheng

Zhang

et al. 2010

J. Zhejiang Univ. Sci. B

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Abstract:Objective: The novel estrogen receptor-α (ER-α) variant ER-α36 is reported to be functional in the estrogen signaling pathway and is related to tamoxifen resistance in breast cancer. However, ER-α36 tends to be a favorable factor for survival in patients without tamoxifen therapy. To investigate the mechanisms behind this paradox, we determined the differences between the transcriptional profiles of ER-α36 and full-length ER-α (ER-α66) in breast cancers and matched normal tissues. Methods: We analyzed ER-α36 and ER-α66 messenger RNA (mRNA) levels in 74 pairs of breast cancers and matched normal tissues using a real-time quantitative polymerase chain reaction (PCR) assay, and correlated the results with their clinicopathological characteristics. Results: Breast cancers expressed lower ER-α36 mRNA levels than matched normal tissues regardless of their ER-α66 expression status. Down-regulation of ER-α36 mRNA was correlated with local progression, lymph node metastasis, and advanced cancer stage. The level of ER-α66 mRNA was lower in ER-α negative breast cancers compared with matched normal tissues. No differences in ER-α66 mRNA levels were observed during cancer progression. Conclusion: Down-regulation of ER-α36 is associated with carcinogenesis and progression of breast cancer.

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Oestrogen receptor splice variants in the pathogenesis of disease

2010

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Observations on the presence of E domain variants of estrogen receptor‐α in the breast tumors

Abstract: Estimation of ER levels combined with composite analysis of ER variants may be a better prognostic marker for breast cancer.

Cited by 6 publications

References 35 publications

Comprehensive landscape of subtype-specific coding and non-coding RNA transcripts in breast cancer

Comprehensive landscape of subtype-specific coding and non-coding RNA transcripts in breast cancer

Quantitative profiles of the mRNAs of ER-α and its novel variant ER-α36 in breast cancers and matched normal tissues

Oestrogen receptor splice variants in the pathogenesis of disease

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