Table S3. Probeset centric RMA normalized Affymetrix expression data is shown for the 180 prioritized genes across the mixed-tumor and melanoma cell panels.

Supplementary Table 2. List of genes commonly down-regulated in at least two resistant cell lines and re-activated by 5-Aza-dC

Supplementary Table 2b: Genes overexpressed in the gene expression signature

Supplementary Table 2a: Genes in the 97-gene expression signature

SuppTable 2a. Comparison of LCH Array Gene Expression to Previous Reports.  CD207Array (LCH Lesion CD207+ vs Skin Control CD207+) Langerhans cell histiocytosis (LCH) is a rare disease characterized by heterogeneous lesions containing CD207+ Langerhans cells (LCs) and lymphocytes that can arise in almost any tissue and cause significant morbidity and mortality. After decades of research, the cause of LCH remains speculative. Results from this study support a model of LCH pathogenesis in which lesions do not arise from epidermal LCs but from accumulation of bone marrow-derived immature myeloid dendritic cells that recruit activated lymphocytes.

SuppTable 2. LCH Lesion CD3 vs LCH Peripheral CD3 Array Results (L-CD3/P-CD3). Langerhans cell histiocytosis (LCH) is a rare disease characterized by heterogeneous lesions containing CD207+ Langerhans cells (LCs) and lymphocytes that can arise in almost any tissue and cause significant morbidity and mortality. After decades of research, the cause of LCH remains speculative. Results from this study support a model of LCH pathogenesis in which lesions do not arise from epidermal LCs but from accumulation of bone marrow-derived immature myeloid dendritic cells that recruit activated lymphocytes.

SuppTable 1. LCH CD207 vs Control Skin CD207 - Expression Array Results (LCH CD207/Skin CD207). Langerhans cell histiocytosis (LCH) is a rare disease characterized by heterogeneous lesions containing CD207+ Langerhans cells (LCs) and lymphocytes that can arise in almost any tissue and cause significant morbidity and mortality. After decades of research, the cause of LCH remains speculative. Results from this study support a model of LCH pathogenesis in which lesions do not arise from epidermal LCs but from accumulation of bone marrow-derived immature myeloid dendritic cells that recruit activated lymphocytes.