miRiad roles for the miR-17-92 cluster in development and disease.

By Joshua T. Mendell. Cell, 2008

1,143 citations recorded by the source corpus.

Subfields: Cancer Research, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/f6b539258fb967b1cbf95cfcea80657c1caf1bdf

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Cancer Research

In Molecular Biology

Citations in the corpus

The detection of differentially expressed microRNAs from the serum of ovarian cancer patients using a novel real-time PCR platform. (2009, background): “Over-expressed miRNAs such as mir-21 and the cluster mir-17–92, are oncogenes (oncomirs), targeting tumor suppressors PTEN and E2F1 in solid and hematologic malignancies respectively [10,11].”
MicroRNAs in human cancer. (2013, positive): “mir-17-92 cluster Ubiquitous Multiple members (chromosomes 7, 13, X) OG Lymphoma [ 143 ] , multiple myeloma [ 9 ] , lung [ 139 ] , colon [ 143 ] , medulloblastoma [ 144 ] , breast [ 140 ] , prostate [ 145 ]”
Heat shock factors: integrators of cell stress, development and lifespan (2010, background): “Targeting of HSF2 in spermatogenesis reveals the first physiological role for miR-18, which belongs to the oncomir-1 cluster associated mainly with tumour progressio”
Differential expression of microRNAs in plasma of patients with colorectal cancer: a potential marker for colorectal cancer screening (2009, background): “Expression of miR-17-92 cluster promotes cell proliferation, suppresses apoptosis of cancer cells, and induces tumour angiogenesis.(29)”
MicroRNAs and cancer: short RNAs go a long way. (2009, background): “Another notable member of the family of oncogenic miRNAs is the miR-17~92 cluster (reviewed in Mendell, 2008).”
MicroRNA: Biogenesis, Function and Role in Cancer (2010, neutral): “conserved among all vertebrates examined [293].”
MicroRNAs in stress signaling and human disease (2012, background): “Oncogenic pathways also utilize miRNAs as effectors of their protumorigenic programs, as exemplified by the induction of the miR-17-92 cluster by the MYC oncogene (Figure 2A), which results in enhanced cellular proliferation, survival, and tumor angiogenesis (Mendell, 2008; O’Donnell et al., 2005).”
miRNAs in human cancer (2010, background): “2 TS CLL [124], lymphoma [9], multiple myeloma [9], pituitary adenoma [125], prostate [125], pancreatic [125] miR-17-92 family Ubiquitous Multiple members (chromosomes 7, 13, X) OG Lymphoma [126], multiple myeloma [9], lung [122], colon [126], medulloblastoma [127], breast [123], prostate [128] miR-”
Targeting brain cancer: advances in the molecular pathology of malignant glioma and medulloblastoma (2010, background): “It has recently been demonstrated that the oncogenic miRNA cluster, miR-17–92 , is a downstream target of MYC, the expression of which seems to be associated with a wide range of tumour type”
The integrated stress response (2016, positive): “Both ATF4 and NRF2 (which are directly phosphorylated by PERK) repress the miR-106b-25 cluster, which functions as an oncogene and whose overexpression has been documented in lung cancer, B-cell lymphoma, and gastric cancer [201,202].”
Physiological and pathological roles for microRNAs in the immune system (2010, background): “miR-17–92 is overexpressed by many human haematopoietic cell neoplasms, including acute lymphoblastic leukaemia (ALL), diffuse large B cell lymphoma (DLBCL) and chronic myeloid leukaemia (CML”