MicroRNA-cancer connection: the beginning of a new tale.

By George A. Calin, Carlo Maria Croce. Cancer Research, 2006

1,075 citations recorded by the source corpus.

Subfields: Cancer Research, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/47b3fae370d488eb91f75293f105d1939e1f6c85

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Citations in the corpus

MicroRNA signatures in human cancers (2006, background): “In a specific tumour, abnormalities both in protein-coding genes and miRNAs can be identifie”
MicroRNA signatures of tumor-derived exosomes as diagnostic biomarkers of ovarian cancer. (2008, background): “All tumors analyzed by microRNA profiling have exhibited significantly distinct microRNA signatures, compared with normal cells from the same tissue [4,6,10].”
miR2Disease: a manually curated database for microRNA deregulation in human disease (2008, background): “First, microRNAs are located in the diseasecausing genomic loci, including minimal regions of loss of heterozygosity, minimal amplicon, or breakpoint cluster regions (19,25).”
MicroRNAs — the micro steering wheel of tumour metastases (2009, background): “Recent studies show that miRNAs may be members of the still elusive class of cancer-predisposing genes and that other types of ncRNAs also participate in the genetic puzzle giving rise to the malignant phenotype (for reviews see Ref”
MicroRNA signature predicts survival and relapse in lung cancer. (2008, methodology): “MicroRNAs can posttranscriptionally regulate the expression of hundreds of their target genes, thereby controlling a wide range of biological functions such as cellular proliferation, differentiation, and apoptosis (Calin and Croce, 2006b).”
Normalization of microRNA expression levels in quantitative RT-PCR assays: identification of suitable reference RNA targets in normal and cancerous human solid tissues. (2008, background): “It has been suggested that the capability of miRNAs to regulate multiple targets within the same pathway can amplify their biological effects (Calin and Croce 2006b).”
MicroRNA function in cancer: oncogene or a tumor suppressor? (2009, background): “Furthermore, the let-7 family members that target RAS oncogenes in lung cancer, like miR-15a and miR 16-1, which target BCL2 oncogene in chronic lymphocytic leukemia, contribute to oncogenesis by functioning as down-regulated tumor suppressors [54].”
Characterization of a germ-line deletion, including the entire INK4/ARF locus, in a melanoma-neural system tumor family: identification of ANRIL, an antisense noncoding RNA whose expression coclusters with ARF. (2007, background): “Moreover, we cannot rule out the possibility that ANRIL gene could be able to produce mature miRNAs (19) or encode a small peptide (20).”