OncomiR addiction in an in vivo model of microRNA-21-induced pre-B-cell lymphoma

By P. Medina, M. Nolde, Frank J. Slack. Nature, 2010

993 citations recorded by the source corpus.

Subfields: Cancer Research, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/cf348a0cefe0fedd7d15bf8a2b58725dbcaf5c30

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Citations in the corpus

microRNAs in cancer (2013, background): “Several strains of mice lacking or overexpressing cancer-associated miRNAs have been developed and characterized, including the germ-line transgenic or knockout mice of miR155 (39), miR-17/92 and its paralogs (60–62), miR-21 (40), miR-221 (63), the miR-15/16-1 cluster (64), miR-122 (65, 66), and miR”
OncomiR or Tumor Suppressor? The Duplicity of MicroRNAs in Cancer (2016, positive): “It is even possible for cancers to become completely reliant upon, or "addicted", to an oncomiR, such that suppression of the oncomiR results in complete regression of the cancer (1).”
MicroRNA dysregulation in cancer: diagnostics, monitoring and therapeutics. A comprehensive review (2012, neutral): “More recently, Slack’s group (Medina et al, 2010) has shown that mice conditionally expressing miR-21 develop a pre-B malignant lymphoid-like phenotype, thus demonstrating that miR-21 is a genuine oncogene. miR-17-92 cluster and miR-155, both discovered to be overexpressed in lymphoproliferative…”
Non-coding RNAs in human disease (2011, background): “A good example is a mouse model that conditionally expresses miR-21, which revealed the function of this miRNA as a genuine oncogen”
MicroRNAs en route to the clinic: progress in validating and targeting microRNAs for cancer therapy (2011, neutral): “, three groups generated mir-21 -knockout or mir-21 -overexpressing mic”
Exosome Uptake through Clathrin-mediated Endocytosis and Macropinocytosis and Mediating miR-21 Delivery* (2014, background): “miR-21 is a unique miRNA that is overexpressed in most tumor types (31).”
MicroRNAs in stress signaling and human disease (2012, background): “, 2006) or miR-21 (Medina et al., 2010) is sufficient to initiate lymphomagenesis in mice.”
miRNAs in human cancer (2010, background): “Over-expression of another oncogene, mir-21, frequently highly expressed in solid and haematological malignancies, resulted in a pre-B malignant lymphoid-like phenotype, whereas subsequent mir-21 inactivation in the same model led to apoptosis and tumour regression [158].”
MicroRNAs in human cancer. (2013, background): “Overexpression of another oncogene, miR-21, frequently highly expressed in solid and hematologic malignancies, resulted in a pre-B malignant lymphoid like phenotype whereas subsequent miR-21 inactivation in the same model led to apoptosis and tumor regression [ 174 ] .”
Improved classification of breast cancer by analysis of genetic alterations and gene expression profiling (2011, background): “We noted the drastic up-regulation of miR-21 in carcinomas, recently identified as an oncogene in mouse models (45, 46).”