ETV1 Is a Novel Androgen Receptor-Regulated Gene that Mediates Prostate Cancer Cell Invasion

Cai, Changmeng; Hsieh, Chen-Lin; Omwancha, Josephat; Zheng, Zhe; Chen, Shaoyong; Baert, Jean-Luc; Shemshedini, Lirim

doi:10.1210/me.2006-0480

Cited by 94 publications

(89 citation statements)

References 38 publications

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“…The result prior to chemotherapy was 46,XX,t(9;22) [18]/46,XX [2] and following therapy it was 46,XX,t(2;7),t (9;22)[20] in GTG-banding (Fig. 1).…”

Section: Resultsmentioning

confidence: 99%

“…The ETS genes (including FLI, ERG, ETV4 and ETV1) encode a family of eukaryotic transcription factors that includes more than 30 members that are found in organisms from sponges to humans (17). The ETS genes are involved in multiple processes, including cell proliferation and cancer cell invasion (18). Some of these genes become oncogenic by retroviral insertional mutagenesis (17) [as in gastric cancer (18), prostate cancer (19) and breast cancer metastasis (18)] or by chromosomal translocations [as in myeloid leukemia and Ewing's sarcomas (17)].…”

Section: Discussionmentioning

confidence: 99%

“…The ETS genes are involved in multiple processes, including cell proliferation and cancer cell invasion (18). Some of these genes become oncogenic by retroviral insertional mutagenesis (17) [as in gastric cancer (18), prostate cancer (19) and breast cancer metastasis (18)] or by chromosomal translocations [as in myeloid leukemia and Ewing's sarcomas (17)]. For example, ETV1 has been mapped at position 7p21.3 and has been found to be subject to a translocation between chromosomes 7 and 22 in a human Ewing's sarcoma (17).…”

Section: Discussionmentioning

confidence: 99%

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A unique cytogenetic abnormality, t(2;7)(p13.1;p21.3), in a Philadelphia-positive chronic myeloid leukemia

Al‐Achkar¹,

Wafa²,

Moassass³

et al. 2012

Oncology Letters

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Abstract. The Philadelphia (Ph) chromosome is present in more than 90% of patients suffering from chronic myeloid leukemia (CML). It is the product of a reciprocal translocation between the long arms of chromosomes 9 and 22, resulting in the transfer of the 3' portion of the proto-oncogene ABL from 9q34 to the 5' portion of the breakpoint cluster region (BCR) on 22q11. Currently, most CML cases are treated with Imatinib and variant rearrangements are thought to have no specific prognostic significance, although the events of therapy resistance have not yet been studied. In this study we report a novel case of CML exhibiting an uncommon t(2;7)(p13.1;p21.3) besides t(9;22)(q34;q11). This unusual translocation has been characterized by fluorescence in situ hybridization (FISH) and array-proven multicolor banding (aMCB), the latter being extremely significant in characterizing breakpoint regions in detail. The underlying mechanisms and prognostic implications of this cytogenetic abnormality are discussed in this study. IntroductionChronic myeloid leukemia (CML) is a clonal malignant disorder of pluripotent hematopoietic stem cells, characterized by the presence of the Philadelphia (Ph) chromosome in more than 90% of patients. The Ph chromosome results from a reciprocal translocation of chromosomes 9 and 22, which leads to the transfer of the 3' portion of the proto-oncogene ABL from 9q34 to the 5' portion of the breakpoint cluster region (BCR) on 22q11. This results in a fused BCR/ABL gene and the production of an abnormal tyrosine kinase protein that causes the altered and disease-causing myelopoiesis found in CML. Since tyrosine kinase activity is required for the transforming function of the BCR/ABL fusion protein, the specific inhibitor of the kinase Imatinib is an effective treatment for CML patients. In a previous study, the 5-year estimated overall survival rate of 89% for patients who received Imatinib as an initial therapy was higher than that reported in any previously published prospective study of the treatment of CML and only 7% of all patients progressed to the accelerated phase or blast crisis (1).In this study, we present a previously unreported translocation of chromosomes 2 and 7 being present with the Ph chromosome in a CML patient successfully treated with Imatinib. The additional rearrangement was characterized in detail by fluorescence in situ hybridization (FISH) and high resolution array-proven multicolor banding (aMCB) as t(2;7) (p13.1;p21.3). Materials and methodsCase report. A 45-year-old female was diagnosed as suffering from CML in chronic phase (CP). In December 2008, the white blood cell count (WBC) was 15.3x10 9 /l with 58.3% neutrophils, 34.8% lymphocytes, 5.2% monocytes, 0.8% eosinophiles and 0.9% basophiles. The platelet count was 978x10 9 /l and the hemoglobin level was 11.5g/dl. The previous physical examination revealed hepatosplenomegaly. The patient was treated with imatinib mesylate at 400 mg/day for eight months and the relevant symptoms disappeared. In July 2009, she passed...

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“…The result prior to chemotherapy was 46,XX,t(9;22) [18]/46,XX [2] and following therapy it was 46,XX,t(2;7),t (9;22)[20] in GTG-banding (Fig. 1).…”

Section: Resultsmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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A unique cytogenetic abnormality, t(2;7)(p13.1;p21.3), in a Philadelphia-positive chronic myeloid leukemia

Al‐Achkar¹,

Wafa²,

Moassass³

et al. 2012

Oncology Letters

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“…Alterations of the ETV1 gene are rare in prostate cancer, but its promoter region has been shown to be regulated by androgens and the androgen receptor. 17 More interestingly, this region contains the ETV1 oncogene, a gene recently shown in several studies to be overexpressed in prostate cancer cells when fused with the TMPSSR2 gene. 18 The two Despite our positive findings, we did not find any associations with prostate cancer at the 8q24 locus.…”

Section: Sporadic Prostate Cancer Rk Nam Et Almentioning

confidence: 99%

A genome-wide association screen identifies regions on chromosomes 1q25 and 7p21 as risk loci for sporadic prostate cancer

Nam

Zhang

Loblaw

et al. 2007

Prostate Cancer Prostatic Dis

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We conducted a genome-wide association study of 3090 sporadic prostate cancer patients and controls using the Affymetrix 10 000 SNP GeneChip. Initial screening of 40 prostate cancer cases and 40 non-cancer controls revealed 237 SNPs to be associated with prostate cancer (Po0.05). Among these SNPs, 33 were selected for further association analysis of 2069 men who had undergone a cancer-screening prostate biopsy. Results identified five loci as being significantly associated with increased prostate cancer risk in this larger sample (rs1930293, OR ¼ 1.To validate these association data, 61 additional HapMap tagSNPs spanning the latter five loci were genotyped in this subject cohort and an additional 1021 men (total subject number ¼ 3090). This analysis revealed tagSNP rs4568789 (chromosome 1q25) and tagSNP rs13225697 (chromosome 7p21) to be significantly associated with prostate cancer (P-values 0.009 and 0.008, respectively). Haplotype analysis revealed significant associations of prostate cancer with two allele risk haplotypes on both chromosome 1q25 (adjusted OR of 2.7 for prostate cancer, P ¼ 0.0003) and chromosome 7p21 (adjusted OR of 1.3, P ¼ 0.0004). As linkage data have identified a putative prostate cancer gene on chromosome 1q25 (HPC1), and microarray data have revealed the ETV1 oncogene to be overexpressed in prostate cancer tissue, it appears that chromosome 1q25 and 7p21 may be sites of gene variants conferring risk for sporadic and inherited forms of prostate cancer.

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“…TMPRSS2-ERg fusions 50-80% of occurrences, TMPRSS2-ETV-1 20% of occurrences) (17,18) is suggested to be essential for the regulation of the immune system, and the regulation of immunity-related genes (19). The ETS family of transcription factors has 27 members in humans and is characterized by an evolutionary highly conserved DNA-binding domain, the ETS domain, which consists of 80 amino acids with 4 tryptophan repeats (20,21).…”

Section: Identification Of Immunity-related Genes In Prostate Cancer mentioning

confidence: 99%

Identification of immunity-related genes in prostate cancer and potential role of the ETS family of transcription factors in their regulation

Shaikhibrahim

Lindstrot²,

Ellinger³

et al. 2011

Int J Mol Med

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Abstract. The role of the immune response in tumor progression, and disease outcome is still debated, and a lack of knowledge of the immune defenses in prostate cancer still exists. In addition, the ETS family of transcription factors which is involved in translocations frequently found in prostate cancer is reported to be essential for the regulation of immunity-related genes. In order to identify immunity-related genes in prostate cancer, we performed two microarrays using RNA extracted from laser microdissected glands of the normal prostate proper (or the peripheral zone) and moderately and poorly differentiated prostate carcinomas from patients who had undergone radical prostatectomy. Many differentially expressed genes were found, however, only immunity-related genes (B cell, innate, and T cell immunity) with an expression of more than 10-fold increase or decrease and a P<0.01 between the moderately differentiated tumors and the normal glands, and the poorly differentiated tumors and the normal glands were considered significant. Based on these two microarrays, we identified a set of 37 genes that were up-or down-regulated in tumors (moderately and poorly differentiated) compared to the normal glands. Analysis of these genes revealed, strikingly, that 31/37 of these genes have potential binding sites within their promoter regions for members of the ETS family of transcription factors, and some are reported to be targets of ETS members. These findings identified immunity-related genes in prostate cancer, and provided insights into their potential regulation, which may lead to a better early detection, immunotherapy, and therapeutic drug treatment of this disease. Unraveling the dynamics of the ETS-immunity-related genes will provide an invaluable insight into understanding prostate cancer immunology.

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ETV1 Is a Novel Androgen Receptor-Regulated Gene that Mediates Prostate Cancer Cell Invasion

Cited by 94 publications

References 38 publications

A unique cytogenetic abnormality, t(2;7)(p13.1;p21.3), in a Philadelphia-positive chronic myeloid leukemia

A unique cytogenetic abnormality, t(2;7)(p13.1;p21.3), in a Philadelphia-positive chronic myeloid leukemia

A genome-wide association screen identifies regions on chromosomes 1q25 and 7p21 as risk loci for sporadic prostate cancer

Identification of immunity-related genes in prostate cancer and potential role of the ETS family of transcription factors in their regulation

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