The DNA methylation landscape of small cell lung cancer suggests a differentiation defect of neuroendocrine cells
Oncogene, 08/21/2012
Kalari S et al. – The authors hypothesize that two potential mechanisms, loss of cell fate–determining transcription factors by methylation of their promoters and functional inactivation of their corresponding genomic–binding sites by DNA methylation, can promote a differentiation defect of neuroendocrine cells thus enhancing the ability of tumor progenitor cells to transition toward Small cell lung cancer (SCLC).
