<i>ZNF703</i> is a common Luminal B breast cancer oncogene that differentially regulates luminal and basal progenitors in human mammary epithelium

Holland, Daniel G.; Burleigh, Angela; Git, Anna; Goldgraben, Mae A.; Pérez–Mancera, Pedro A.; Chin, Suet-Feung; Hurtado, Antoni; Bruna, Alejandra; Ali, H. Raza; Greenwood, Wendy; Dunning, Mark J.; Samarajiwa, Shamith A.; Menon, Suraj; Rueda, Oscar M.; Lynch, Andy G.; McKinney, Steven; Ellis, Ian O.; Eaves, Connie J.; Carroll, Jason S.; Curtis, Christina; Aparicio, Samuel; Caldas, Carlos

doi:10.1002/emmm.201100122

Cited by 120 publications

(157 citation statements)

References 35 publications

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“…We also saw amplification in 69.23% of patients' plasma samples in four markers from the 10-kb interval that spans ZNF703, although amplification was also seen in 50.00% of plasmas from the healthy controls and 32.30% of patients' normal leukocytes. This gene has recently been shown to be a novel oncogene in Luminal B breast cancer (Holland et al 2011). Overall, the pattern of genomic alteration seen, with focal highlevel DNA amplification clustered at several chromosome arms, resembles the ''amplifier'' or ''firestorm'' type of DNA CN alterations, detected in previous genomic profiling of breast tumors (Kwei et al 2010).…”

Section: Cfdna Of Breast Cancer Patients Infers Dormancymentioning

confidence: 58%

Genomic analysis of circulating cell-free DNA infers breast cancer dormancy

Shaw¹,

Page²,

Blighe³

et al. 2011

Genome Res.

169

112

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Biomarkers in breast cancer to monitor minimal residual disease have remained elusive. We hypothesized that genomic analysis of circulating free DNA (cf DNA) isolated from plasma may form the basis for a means of detecting and monitoring breast cancer. We profiled 251 genomes using Affymetrix SNP 6.0 arrays to determine copy number variations (CNVs) and loss of heterozygosity (LOH), comparing 138 cf DNA samples with matched primary tumor and normal leukocyte DNA in 65 breast cancer patients and eight healthy female controls. Concordance of SNP genotype calls in paired cfDNA and leukocyte DNA samples distinguished between breast cancer patients and healthy female controls (P < 0.0001) and between preoperative patients and patients on follow-up who had surgery and treatment (P = 0.0016). Principal component analyses of cf DNA SNP/copy number results also separated presurgical breast cancer patients from the healthy controls, suggesting specific CNVs in cf DNA have clinical significance. We identified focal high-level DNA amplification in paired tumor and cf DNA clustered in a number of chromosome arms, some of which harbor genes with oncogenic potential, including USP17L2 (DUB3), BRF1, MTA1, and JAG2. Remarkably, in 50 patients on follow-up, specific CNVs were detected in cf DNA, mirroring the primary tumor, up to 12 yr after diagnosis despite no other evidence of disease. These data demonstrate the potential of SNP/CNV analysis of cf DNA to distinguish between patients with breast cancer and healthy controls during routine follow-up. The genomic profiles of cf DNA infer dormancy/minimal residual disease in the majority of patients on follow-up.

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Section: Cfdna Of Breast Cancer Patients Infers Dormancymentioning

confidence: 58%

Genomic analysis of circulating cell-free DNA infers breast cancer dormancy

Shaw¹,

Page²,

Blighe³

et al. 2011

Genome Res.

169

112

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“…A number of the changes of FLHCC have the hallmarks of some forms of breast cancer (SI Appendix, Table S13). Some of transcripts that are considered oncogenic for breast cancers are also increased in FLHCC including AURKA CYP19A1 (67), the breast cancer anti-estrogen resistance 1 (BCAR1), and ZNF 703, a luminal B breast cancer oncogene (68), as well as members of the EGF receptor pathway, including EGFR, ErbB2, and their ligands NRG2, EREG, AREG, and NGF.…”

Section: Discussionmentioning

confidence: 99%

Transcriptomic characterization of fibrolamellar hepatocellular carcinoma

Simon

Freije

Farber

et al. 2015

Proc. Natl. Acad. Sci. U.S.A.

110

174

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Fibrolamellar hepatocellular carcinoma (FLHCC) tumors all carry a deletion of ∼400 kb in chromosome 19, resulting in a fusion of the genes for the heat shock protein, DNAJ (Hsp40) homolog, subfamily B, member 1, DNAJB1, and the catalytic subunit of protein kinase A, PRKACA. The resulting chimeric transcript produces a fusion protein that retains kinase activity. No other recurrent genomic alterations have been identified. Here we characterize the molecular pathogenesis of FLHCC with transcriptome sequencing (RNA sequencing). Differential expression (tumor vs. adjacent normal tissue) was detected for more than 3,500 genes (log2 fold change ≥1, false discovery rate ≤0.01), many of which were distinct from those found in hepatocellular carcinoma. Expression of several known oncogenes, such as ErbB2 and Aurora Kinase A, was increased in tumor samples. These and other dysregulated genes may serve as potential targets for therapeutic intervention.

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“…ZNF703 is a zinc finger transcription factor belongs to NET/NLZ family and contributes to the development and progression of various cancer, including NSCLC, breast cancer, gastric cancer (GC), and colorectal cancer (CRC). [40][41][42] Moreover, ZNF703 is involved in the activation of the Akt/mammalian target of rapamycin (mTOR) signaling pathway in breast cancer cell lines. 43 Therefore, Shi et al 11 detected the potential roles of ZNF703 in breast cancer cell lines and discovered that ZNF703 is augmented in breast cancer tissues and cell lines.…”

Section: Breast Cancermentioning

confidence: 99%

SPRY4-IT1: A novel oncogenic long non-coding RNA in human cancers

Chen

et al. 2017

Tumour Biol.

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Long non-coding RNAs are classified as a kind of RNA, which are longer than 200 nucleotides in length and cannot be translated into proteins. Multiple studies have demonstrated that long non-coding RNAs are involved in various cellular processes, including proliferation, differentiation, cell death, and metastasis. Among numerous long non-coding RNAs, we focus on Sprouty4-Intron 1 (SPRY4-IT1), a well-known long non-coding RNA that is overexpressed in various kinds of tumor tissues and cell lines. Accumulating evidences show that SPRY4-IT1 was dysregulated in various cancers, including melanoma, breast cancer, esophageal squamous cell carcinoma, non-small cell lung cancer, gastric cancer, colon cancer, and hepatocellular carcinoma, and amplification of SPRY4-IT1 was associated with different clinicopathological features of cancer patients. Importantly, SPRY4-IT1 exerts important roles in tumor progression and metastasis. However, detailed molecular mechanisms of SPRY4-IT1 in cancer progression and metastasis were poorly understood. In this review, we have focused on the characteristics of SPRY4-IT1 and illustrated the biological function and mechanism of SPRY4-IT1 in cancer development.

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ZNF703 is a common Luminal B breast cancer oncogene that differentially regulates luminal and basal progenitors in human mammary epithelium

Cited by 120 publications

References 35 publications

Genomic analysis of circulating cell-free DNA infers breast cancer dormancy

Genomic analysis of circulating cell-free DNA infers breast cancer dormancy

Transcriptomic characterization of fibrolamellar hepatocellular carcinoma

SPRY4-IT1: A novel oncogenic long non-coding RNA in human cancers

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