Unlike X-inactivation in somatic cells, the choice of which set of rRNA genes to silence is not random but instead involves silencing of rRNA genes inherited from the same progenitor, independent of maternal or paternal effects. Several lines of evidence implicate the chromatin environment of rRNA genes in the control of nucleolar dominance. In Brassica or Arabidopsis allopolyploid hybrids, underdominant rRNA genes transfected into protoplasts are transcribed even though their endogenous, Sulfamethazine chromosomal counterparts are silenced. These experiments indicate that the necessary transcription factors are available in the cell but that chromosomal genes are denied access to them. The repression of the silenced chromosomal rRNA genes is mediated by chromatin Clindamycin modifications that include cytosine methylation, histone deacetylation and histone H3 lysine 9 dimethylation and can be reversed by chemical inhibitors of DNA methylation or histone deacetylation or by genetic knockdown of specific chromatin modifying activities, such as histone deacetylases HDT1 and HDA6. Small cell lung cancer is the most aggressive type of lung cancer and has a uniformly poor prognosis. Metastases develop quickly, primarily to bone marrow and brain, and are usually present at the time of diagnosis. In untreated patients, median survival is two months from the onset of symptoms. In several types of tumors increased levels of urokinase plasminogen activator and its receptor uPAR strongly correlate with poor prognosis and unfavorable clinical outcome. uPA and uPAR are instrumental in controlling membrane-associated extracellular proteolysis and transmembrane signaling, thus affecting cell migration and invasion under physiological and pathological conditions. uPAR over-expression in malignant cells results from activation of several oncogenic pathways, including MAPK, RTK, ERK2 and FAK. Multiple oncogenic mutations, including p53 in cancer cells lead to uncontrolled expression of uPA/uPAR. Inhibition of uPAR in a mouse model of non-small cell lung cancer and other tumors inhibited tumor growth, invasion, angiogenesis and metastasis.