Publications (26)290.59 Total impact
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Article: Modulation of MicroRNA-194 and Cell Migration by HER2-Targeting Trastuzumab in Breast Cancer
PLoS ONE 07/2012; 7(7-10.1371/journal.pone.0041170). · 4.09 Impact Factor -
Article: Strand-specific miR-28-5p and miR-28-3p have distinct effects in colorectal cancer cells.
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ABSTRACT: MicroRNAs (miRNAs) can promote or inhibit tumor growth and are therefore being developed as targets for cancer therapies. They are diverse not only in the messenger RNAs (mRNA) they target, but in their production; the same hairpin RNA structure can generate mature products from each strand, termed 5p and 3p, that can bind different mRNAs. We analyzed the expression, functions, and mechanisms of miR-28-5p and miR-28-3p in colorectal cancer (CRC) cells. We measured levels of miR-28-5p and miR-28-3p expression in 108 CRC and 49 normal colorectal samples (47 paired) by reverse transcription, quantitative real-time polymerase chain reaction. The roles of miR-28 in CRC development were studied using cultured HCT116, RKO, and SW480 cells and tumor xenograft analyses in immunodeficient mice; their mRNA targets were also investigated. miR-28-5p and miR-28-3p were down-regulated in CRC samples compared with normal colon samples. Overexpression of miRNAs in CRC cells had different effects and the miRNAs interacted with different mRNAs: miR-28-5p altered expression of CCND1 and HOXB3, whereas miR-28-3p bound NM23-H1. Overexpression of miR-28-5p reduced CRC cell proliferation, migration, and invasion in vitro, whereas miR-28-3p increased CRC cell migration and invasion in vitro. CRC cells overexpressing miR-28 developed tumors more slowly in mice compared with control cells, but miR-28 promoted tumor metastasis in mice. miR-28-5p and miR-28-3p are transcribed from the same RNA hairpin and are down-regulated in CRC cells. Overexpression of each has different effects on CRC cell proliferation and migration. Such information has a direct application for the design of miRNA gene therapy trials.Gastroenterology 01/2012; 142(4):886-896.e9. · 11.68 Impact Factor -
Article: Modulation of MicroRNA-194 and cell migration by HER2-targeting trastuzumab in breast cancer.
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ABSTRACT: Trastuzumab, a humanized monoclonal antibody directed against the extracellular domain of the HER2 oncoprotein, can effectively target HER2-positive breast cancer through several mechanisms. Although the effects of trastuzumab on cancer cell proliferation, angiogenesis and apoptosis have been investigated in depth, the effect of trastuzumab on microRNA (miRNA) has not been extensively studied. We have performed miRNA microarray profiling before and after trastuzumab treatment in SKBr3 and BT474 human breast cancer cells that overexpress HER2. We found that trastuzumab treatment of SKBr3 cells significantly decreased five miRNAs and increased three others, whereas treatment of BT474 cells significantly decreased two miRNAs and increased nine. The only change in miRNA expression observed in both cell lines following trastuzumab treatment was upregulation of miRNA-194 (miR-194) that was further validated in vitro and in vivo. Forced expression of miR-194 in breast cancer cells that overexpress HER2 produced no effect on apoptosis, modest inhibition of proliferation, significant inhibition of cell migration/invasion in vitro and significant inhibition of xenograft growth in vivo. Conversely, knockdown of miR-194 promoted cell migration. Increased miR-194 expression markedly reduced levels of the cytoskeletal protein talin2 and specifically inhibited luciferase reporter activity of a talin2 wild-type 3'-untranslated region, but not that of a mutant reporter, indicating that talin2 is a direct downstream target of miR-194. Trastuzumab treatment inhibited breast cancer cell migration and reduced talin2 expression in vitro and in vivo. Knockdown of talin2 inhibited cell migration/invasion. Knockdown of trastuzumab-induced miR-194 expression with a miR-194 inhibitor compromised trastuzumab-inhibited cell migration in HER2-overexpressing breast cancer cells. Consequently, trastuzumab treatment upregulates miR-194 expression and may exert its cell migration-inhibitory effect through miR-194-mediated downregulation of cytoskeleton protein talin2 in HER2-overexpressing human breast cancer cells.PLoS ONE 01/2012; 7(7):e41170. · 4.09 Impact Factor -
Article: Association of a microRNA/TP53 feedback circuitry with pathogenesis and outcome of B-cell chronic lymphocytic leukemia.
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ABSTRACT: Chromosomal abnormalities (namely 13q, 17p, and 11q deletions) have prognostic implications and are recurrent in chronic lymphocytic leukemia (CLL), suggesting that they are involved in a common pathogenetic pathway; however, the molecular mechanism through which chromosomal abnormalities affect the pathogenesis and outcome of CLL is unknown. To determine whether the microRNA miR-15a/miR-16-1 cluster (located at 13q), tumor protein p53 (TP53, located at 17p), and miR-34b/miR-34c cluster (located at 11q) are linked in a molecular pathway that explains the pathogenetic and prognostic implications (indolent vs aggressive form) of recurrent 13q, 17p, and 11q deletions in CLL. CLL Research Consortium institutions provided blood samples from untreated patients (n = 206) diagnosed with B-cell CLL between January 2000 and April 2008. All samples were evaluated for the occurrence of cytogenetic abnormalities as well as the expression levels of the miR-15a/miR-16-1 cluster, miR-34b/miR-34c cluster, TP53, and zeta-chain (TCR)-associated protein kinase 70 kDa (ZAP70), a surrogate prognostic marker of CLL. The functional relationship between these genes was studied using in vitro gain- and loss-of-function experiments in cell lines and primary samples and was validated in a separate cohort of primary CLL samples. Cytogenetic abnormalities; expression levels of the miR-15a/miR-16-1 cluster, miR-34 family, TP53 gene, downstream effectors cyclin-dependent kinase inhibitor 1A (p21, Cip1) (CDKN1A) and B-cell CLL/lymphoma 2 binding component 3 (BBC3), and ZAP70 gene; genetic interactions detected by chromatin immunoprecipitation. In CLLs with 13q deletions the miR-15a/miR-16-1 cluster directly targeted TP53 (mean luciferase activity for miR-15a vs scrambled control, 0.68 relative light units (RLU) [95% confidence interval {CI}, 0.63-0.73]; P = .02; mean for miR-16 vs scrambled control, 0.62 RLU [95% CI, 0.59-0.65]; P = .02) and its downstream effectors. In leukemic cell lines and primary CLL cells, TP53 stimulated the transcription of miR-15/miR-16-1 as well as miR-34b/miR-34c clusters, and the miR-34b/miR-34c cluster directly targeted the ZAP70 kinase (mean luciferase activity for miR-34a vs scrambled control, 0.33 RLU [95% CI, 0.30-0.36]; P = .02; mean for miR-34b vs scrambled control, 0.31 RLU [95% CI, 0.30-0.32]; P = .01; and mean for miR-34c vs scrambled control, 0.35 RLU [95% CI, 0.33-0.37]; P = .02). A microRNA/TP53 feedback circuitry is associated with CLL pathogenesis and outcome. This mechanism provides a novel pathogenetic model for the association of 13q deletions with the indolent form of CLL that involves microRNAs, TP53, and ZAP70.JAMA The Journal of the American Medical Association 01/2011; 305(1):59-67. · 30.03 Impact Factor -
Article: microRNA fingerprinting of CLL patients with chromosome 17p deletion identify a miR-21 score that stratifies early survival.
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ABSTRACT: Aberrant expression of microRNAs (miRNAs) has been associated with clinical outcome in patients with chronic lymphocytic leukemia (CLL). To identify a powerful and easily assessable miRNA bio-marker of prognosis and survival, we performed quantitative reverse-transcription polymerase chain reaction (qRT-PCR) profiling in 104 CLL patients with a well-defined chromosome 17p status, and we validated our findings with miRNA microarray data from an independent cohort of 80 patients. We found that miR-15a, miR-21, miR-34a, miR-155, and miR-181b were differentially expressed between CLLs with chromosome 17p deletion and CLLs with normal 17p and normal karyotype, and that miR-181b was down-regulated in therapy-refractory cases. miR-21 expression levels were significantly higher in patients with poor prognosis and predicted overall survival (OS), and miR-181b expression levels significantly predicted treatment-free survival. We developed a 21FK score (miR-21 qRT-PCR, fluorescence in situ hybridization, Karyotype) to stratify patients according to OS and found that patients with a low score had a significantly longer OS time. When we evaluated the relative power of the 21FK score with the most used prognostic factors, the score was the most significant in both CLL cohorts. We conclude that the 21FK score represents a useful tool for distinguishing between good-prognosis and poor-prognosis CLL patients.Blood 08/2010; 116(6):945-52. · 9.90 Impact Factor -
Article: Single-nucleotide polymorphisms inside microRNA target sites influence tumor susceptibility.
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ABSTRACT: Single-nucleotide polymorphisms (SNP) associated with polygenetic disorders, such as breast cancer (BC), can create, destroy, or modify microRNA (miRNA) binding sites; however, the extent to which SNPs interfere with miRNA gene regulation and affect cancer susceptibility remains largely unknown. We hypothesize that disruption of miRNA target binding by SNPs is a widespread mechanism relevant to cancer susceptibility. To test this, we analyzed SNPs known to be associated with BC risk, in silico and in vitro, for their ability to modify miRNA binding sites and miRNA gene regulation and referred to these as target SNPs. We identified rs1982073-TGFB1 and rs1799782-XRCC1 as target SNPs, whose alleles could modulate gene expression by differential interaction with miR-187 and miR-138, respectively. Genome-wide bioinformatics analysis predicted approximately 64% of transcribed SNPs as target SNPs that can modify (increase/decrease) the binding energy of putative miRNA::mRNA duplexes by >90%. To assess whether target SNPs are implicated in BC susceptibility, we conducted a case-control population study and observed that germline occurrence of rs799917-BRCA1 and rs334348-TGFR1 significantly varies among populations with different risks of developing BC. Luciferase activity of target SNPs, allelic variants, and protein levels in cancer cell lines with different genotypes showed differential regulation of target genes following overexpression of the two interacting miRNAs (miR-638 and miR-628-5p). Therefore, we propose that transcribed target SNPs alter miRNA gene regulation and, consequently, protein expression, contributing to the likelihood of cancer susceptibility, by a novel mechanism of subtle gene regulation.Cancer Research 03/2010; 70(7):2789-98. · 7.86 Impact Factor -
Article: p27kip1 controls cell morphology and motility by regulating microtubule-dependent lipid raft recycling.
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ABSTRACT: p27(kip1) (p27) is an inhibitor of cyclin/cyclin-dependent kinase complexes, whose nuclear loss indicates a poor prognosis in various solid tumors. When located in the cytoplasm, p27 binds Op18/stathmin (stathmin), a microtubule (MT)-destabilizing protein, and restrains its activity. This leads to MT stabilization, which negatively affects cell migration. Here, we demonstrate that this p27 function also influences morphology and motility of cells immersed in three-dimensional (3D)matrices. Cells lacking p27 display a decrease in MT stability, a rounded shape when immersed in 3D environments, and a mesenchymal-amoeboid conversion in their motility mode. Upon cell contact to extracellular matrix, the decreased MT stability observed in p27 null cells results in accelerated lipid raft trafficking and increased RhoA activity. Importantly, cell morphology, motility, MT network composition, and distribution of p27 null cells were rescued by the concomitant genetic ablation of Stathmin, implicating that the balanced expression of p27 and stathmin represents a crucial determinant for cytoskeletal organization and cellular behavior in 3D contexts.Molecular and cellular biology 03/2010; 30(9):2229-40. · 6.06 Impact Factor -
Article: Expression of mutated IGHV3-23 genes in chronic lymphocytic leukemia identifies a disease subset with peculiar clinical and biological features.
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ABSTRACT: B-cell chronic lymphocytic leukemia (CLL) is a clinically heterogeneous disease whose outcome can be foreseen by investigating the mutational status of immunoglobulin heavy chain variable (IGHV) genes. Moreover, a different prognosis was reported for CLL expressing specific IGHV genes in the context or not of stereotyped B-cell receptors. Here we investigated novel associations between usage of specific IGHV genes and clinical features in CLL. Among 1,426 CLL-specific IG-rearrangements, stereotyped B-cell receptor clusters never utilized the IGHV3-23 gene. Given this notion, this study was aimed at characterizing the IGHV3-23 gene in CLL, and identifying the properties of IGHV3-23-expressing CLL. IGHV3-23 was the second most frequently used (134 of 1,426) and usually mutated (M; 109 of 134) IGHV gene in our CLL series. In the vast majority of M IGHV3-23 sequences, the configuration of the 13 amino acids involved in superantigen recognition was consistent with superantigen binding. Clinically, M IGHV3-23 CLL had shorter time-to-treatment than other M non-IGHV3-23 CLL, and multivariate analyses selected IGHV3-23 gene usage, Rai staging, and chromosomal abnormalities as independent prognosticators for M CLL. Compared with M non-IGHV3-23 CLL, the gene expression profile of M IGHV3-23 CLL was deprived in genes, including the growth/tumor suppressor genes PDCD4, TIA1, and RASSF5, whose downregulation is under control of miR-15a and miR-16-1. Accordingly, relatively higher levels of miR-15a and miR-16-1 were found in M IGHV3-23 compared with M non-IGHV3-23 CLL. Altogether, expression of the IGHV3-23 gene characterizes a CLL subset with distinct clinical and biological features.Clinical Cancer Research 01/2010; 16(2):620-8. · 7.74 Impact Factor -
Article: SnapShot: MicroRNAs in Cancer.
Cell 06/2009; 137(3):586-586.e1. · 32.40 Impact Factor -
Article: MicroRNAs and cancer--new paradigms in molecular oncology.
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ABSTRACT: The 'classic' view of molecular oncology indicates that cancer is a genetic disease involving tumor suppressor and oncogenic proteins. However, in the recent years, it has been demonstrated that small regulatory non-coding RNAs (ncRNAs) named microRNAs (miRNAs) are involved in human tumorigenesis, thus revealing a new layer in the molecular architecture of human cancer. Gene expression studies revealed that hundreds of miRNAs are deregulated in cancer cells and functional studies clarified that miRNAs are involved in all the molecular and biological processes that drive tumorigenesis. Here, we summarize the recent advances in miRNA involvement in human cancer and illustrate the benefits of using these knowledge for medical practice. New diagnostic classifiers based on miRNAs will soon be available for medical practitioners and, even more importantly, miRNAs may become novel anti-cancer tools.Current opinion in cell biology 06/2009; 21(3):470-9. · 14.15 Impact Factor -
Article: MicroRNAs--the micro steering wheel of tumour metastases.
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ABSTRACT: Recently, microRNAs (miRNAs) have been discovered to have a role in metastasis. Here we describe how miRNAs are involved in advanced stages of tumour progression, stressing their roles as metastasis activators or suppressors, and discuss their possible use in the clinic as predictive markers and as therapeutic strategies for patients with metastases. Furthermore, we develop the concept that the same miRNAs could be involved both in the cancer stem cell phenotype and in the ability of specific cancer cells to produce metastases, thus representing a mechanistic link between the initial and the final steps of tumorigenesis.Nature Reviews Cancer 05/2009; 9(4):293-302. · 29.54 Impact Factor -
Article: MiRNAs - The Jack of All Trades
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ABSTRACT: Focusing on the pervasive role of microRNAs (miRNAs), we review the multiple steps of malignant transformation, outlining the common hallmarks of tumorigenesis: self-sufficiency in growth signals, insensitivity to growth-inhibitory signals, evasion of apoptosis, limitless replicative potential, sustained angiogenesis, and tissue invasion and metastasis. For each of these traits, we provide examples of miRNA contribution to the acquisition of a malignant phenotype. Finally, through an overview of the remarkable ability of miRNAs to regulate entire pathwaysas a result of the multiplicity of their targets, we highlight the attractive potential of developing miRNA-targeted therapies, which should affect all the aspects of tumorigenesisClinical Leukemia 02/2009; 3(1):20-32. -
Article: MicroRNA fingerprints identify miR-150 as a plasma prognostic marker in patients with sepsis.
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ABSTRACT: The physiopathology of sepsis continues to be poorly understood, and despite recent advances in its management, sepsis is still a life-threatening condition with a poor outcome. If new diagnostic markers related to sepsis pathogenesis will be identified, new specific therapies might be developed and mortality reduced. Small regulatory non-coding RNAs, microRNAs (miRNAs), were recently linked to various diseases; the aim of our prospective study was to identify miRNAs that can differentiate patients with early-stage sepsis from healthy controls and to determine if miRNA levels correlate with the severity assessed by the Sequential Organ Failure Assessment (SOFA) score. By using genome-wide miRNA profiling by microarray in peripheral blood leukocytes, we found that miR-150, miR-182, miR-342-5p, and miR-486 expression profiles differentiated sepsis patients from healthy controls. We also proved by quantitative reverse transcription-polymerase chain reaction that miR-150 levels were significantly reduced in plasma samples of sepsis patients and correlated with the level of disease severity measured by the SOFA score, but were independent of the white blood counts (WBC). We found that plasma levels of tumor necrosis factor alpha, interleukin-10, and interleukin-18, all genes with sequence complementarity to miR-150, were negatively correlated with the plasma levels of this miRNA. Furthermore, we identified that the plasma levels ratio for miR-150/interleukin-18 can be used for assessing the severity of the sepsis. We propose that miR-150 levels in both leukocytes and plasma correlate with the aggressiveness of sepsis and can be used as a marker of early sepsis. Furthermore, we envision miR-150 restoration as a future therapeutic option in sepsis patients.PLoS ONE 01/2009; 4(10):e7405. · 4.09 Impact Factor -
Article: MicroRNAs: new players in AML pathogenesis.
Cancer treatment and research 01/2009; 145:169-81. -
Article: A microRNA DNA methylation signature for human cancer metastasis.
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ABSTRACT: MicroRNAs (miRNAs) are small, noncoding RNAs that can contribute to cancer development and progression by acting as oncogenes or tumor suppressor genes. Recent studies have also linked different sets of miRNAs to metastasis through either the promotion or suppression of this malignant process. Interestingly, epigenetic silencing of miRNAs with tumor suppressor features by CpG island hypermethylation is also emerging as a common hallmark of human tumors. Thus, we wondered whether there was a miRNA hypermethylation profile characteristic of human metastasis. We used a pharmacological and genomic approach to reveal this aberrant epigenetic silencing program by treating lymph node metastatic cancer cells with a DNA demethylating agent followed by hybridization to an expression microarray. Among the miRNAs that were reactivated upon drug treatment, miR-148a, miR-34b/c, and miR-9 were found to undergo specific hypermethylation-associated silencing in cancer cells compared with normal tissues. The reintroduction of miR-148a and miR-34b/c in cancer cells with epigenetic inactivation inhibited their motility, reduced tumor growth, and inhibited metastasis formation in xenograft models, with an associated down-regulation of the miRNA oncogenic target genes, such as C-MYC, E2F3, CDK6, and TGIF2. Most important, the involvement of miR-148a, miR-34b/c, and miR-9 hypermethylation in metastasis formation was also suggested in human primary malignancies (n = 207) because it was significantly associated with the appearance of lymph node metastasis. Our findings indicate that DNA methylation-associated silencing of tumor suppressor miRNAs contributes to the development of human cancer metastasis.Proceedings of the National Academy of Sciences 10/2008; 105(36):13556-61. · 9.68 Impact Factor -
Article: Stathmin activity influences sarcoma cell shape, motility, and metastatic potential.
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ABSTRACT: The balanced activity of microtubule-stabilizing and -destabilizing proteins determines the extent of microtubule dynamics, which is implicated in many cellular processes, including adhesion, migration, and morphology. Among the destabilizing proteins, stathmin is overexpressed in different human malignancies and has been recently linked to the regulation of cell motility. The observation that stathmin was overexpressed in human recurrent and metastatic sarcomas prompted us to investigate stathmin contribution to tumor local invasiveness and distant dissemination. We found that stathmin stimulated cell motility in and through the extracellular matrix (ECM) in vitro and increased the metastatic potential of sarcoma cells in vivo. On contact with the ECM, stathmin was negatively regulated by phosphorylation. Accordingly, a less phosphorylable stathmin point mutant impaired ECM-induced microtubule stabilization and conferred a higher invasive potential, inducing a rounded cell shape coupled with amoeboid-like motility in three-dimensional matrices. Our results indicate that stathmin plays a significant role in tumor metastasis formation, a finding that could lead to exploitation of stathmin as a target of new antimetastatic drugs.Molecular biology of the cell 06/2008; 19(5):2003-13. · 5.98 Impact Factor -
Article: E2F1-regulated microRNAs impair TGFbeta-dependent cell-cycle arrest and apoptosis in gastric cancer.
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ABSTRACT: Deregulation of E2F1 activity and resistance to TGFbeta are hallmarks of gastric cancer. MicroRNAs (miRNAs) are small noncoding RNAs frequently misregulated in human malignancies. Here we provide evidence that the miR-106b-25 cluster, upregulated in a subset of human gastric tumors, is activated by E2F1 in parallel with its host gene, Mcm7. In turn, miR-106b and miR-93 regulate E2F1 expression, establishing a miRNA-directed negative feedback loop. Furthermore, upregulation of these miRNAs impairs the TGFbeta tumor suppressor pathway, interfering with the expression of CDKN1A (p21(Waf1/Cip1)) and BCL2L11 (Bim). Together, these results suggest that the miR-106b-25 cluster is involved in E2F1 posttranscriptional regulation and may play a key role in the development of TGFbeta resistance in gastric cancer.Cancer cell 04/2008; 13(3):272-86. · 25.29 Impact Factor -
Article: MicroRNA involvement in brain tumors: from bench to bedside.
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ABSTRACT: MicroRNAs (miRNAs), a novel class of small non-coding RNAs, are effective post-transcriptional regulators of gene expression, exhibiting, when altered in human tumors, both oncogenic and tumor suppressive potential. Recently, miRNA involvement in the pathophysiology of brain cancer has been assessed. Aberrant gene expression is the main mechanism of miRNAs dysfunction in cancer, with abnormal expression levels of mature and/or precursor miRNA expression in tumor samples versus normal. MiRNA germline and somatic mutations or polymorphisms in the protein coding messenger RNA targeted by miRNAs may also occur, contributing to cancer predisposition, initiation and/or progression. If present in somatic cells, miRNA alterations may play a role in tumor initiation, while if present in germ line cells they could constitute a cancer predisposing event. MiRNA expression profiling of human tumors has led to the identification of signatures correlated with the tumor diagnosis, staging, progression, prognosis and response to treatment. MiRNA fingerprinting can therefore be added to the diagnostic and prognostic tools used by medical oncologists. Furthermore, new therapeutic strategies involving miRNA silencing or miRNA mimics could be proposed based on the roles of these small non-coding RNAs as oncogenes and tumor suppressors in brain tumors.Brain Pathology 02/2008; 18(1):122-9. · 3.99 Impact Factor -
Article: MicroRNAs as new biomarkers in oncology.
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ABSTRACT: MicroRNAs (miRNAs) represent a new class of small non-coding RNAs ∼ 22 nucleotides in length that are involved in fine-tuning of gene expression. An increasing number of papers are identifying a link between miRNAs and cancer. The discovery of miRNA expression signatures able to discriminate tumor from normal cells and between various categories of patients with the same type of cancer suggests the possible application of miRNAs as new biomarkers in molecular oncology. In this review, the authors describe the different techniques used to detect miRNAs in tumor samples and their potential for clinical use. The authors review the published evidence testing miRNAs as novel cancer biomarkers and describe the steps necessary to move forward in the application of miRNAs as biomarkers. Finally, the authors consider the utility of miRNAs as tumor predisposition markers in cancer screening programs.Expert Opinion on Medical Diagnostics 02/2008; 2(2):115-27. -
Article: MicroRNAs in the pathogeny of chronic lymphocytic leukaemia.
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ABSTRACT: MicroRNAs (miRNAs) have been linked to the initiation and progression of chronic lymphocytic leukaemia (CLL). The main molecular alterations are represented by variations in gene expression, usually mild and with consequences for a vast number of target protein-coding genes. Recent studies have shown that miRNAs are the main candidates for the elusive class of CLL predisposing genes. These discoveries could be exploited for the development of useful markers for diagnosis and prognosis, as well as for the development of new RNA-based cancer therapies.British Journal of Haematology 01/2008; 139(5):709-16. · 4.94 Impact Factor
Top co-authors
Top Journals
- PLoS ONE (3)
- Cancer Research (2)
- Cancer Cell (2)
- Cancer treatment and research (1)
- Oncogene (1)
Institutions
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2008–2012
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University of Texas MD Anderson Cancer Center
- Department of Experimental Therapeutics
Houston, TX, USA
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2006–2011
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The Ohio State University
- Department of Molecular Virology, Immunology and Medical Genetics
Columbus, OH, USA
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2009
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Institutul Clinic Fundeni
Bucharest, Bucuresti, Romania -
Universita degli studi di Ferrara
- Department of Morphology, Surgery and Experimental Medicine
Ferrara, Emilia-Romagna, Italy
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