Lyme disease (LD), caused by Borrelia burgdorferi, is the most common tick-borne infectious disease in the United States. We examined gene expression patterns in the blood of individuals with early disseminated LD at the time of diagnosis (Acute LD) and also at approximately 1 month and 6 months following antibiotic treatment. A distinct acute LD profile was observed that was sustained during early convalescence (1 month) but returned to control levels six months after treatment. Using a computer learning algorithm, we identified sets of 20 classifier genes that discriminate LD from other bacterial and viral infections. In addition, these novel LD biomarkers are highly acurate in distinvuishing patients with acute LD from healthy subjects and in discriminating between individuals with active and resolved infecitons. This computational approach offers the potential for more accurate diagnosis of early dissminated Lyme disease. It may also allow improved monitoring of treatment efficacy and disease resolution.
Global Transcriptome Analysis Identifies a Diagnostic Signature for Early Disseminated Lyme Disease and Its Resolution.
Disease, Disease stage
View SamplesWe compared gene expression differences in Atxn1L knockout vs wildtype HSCs
Ataxin1L is a regulator of HSC function highlighting the utility of cross-tissue comparisons for gene discovery.
Specimen part
View SamplesWe compared gene expression differences in Lyl-1 knockout vs wildtype LMPPs
The transcription factor Lyl-1 regulates lymphoid specification and the maintenance of early T lineage progenitors.
Specimen part
View Samplescharacterize the molecular signature of PB-IMC in different stages of tumor development, thus possibly leading to a novel, sensitive and elegant approach for early cancer detection and surveillance. Overall design: Two types of cancer. For each type 4 groups (day 0, day 4, day 8, day 11), for each group 3 biological repeats
The transcriptional profile of circulating myeloid derived suppressor cells correlates with tumor development and progression in mouse.
Specimen part, Cell line, Subject
View SamplesMultiple myeloma (MM) is a clonal plasma cell disorder frequently accompanied by hematopoietic impairment. Genomic profiling of distinct HSPC subsets revealed a consistent deregulation of signaling cascades, including TGF beta signaling, p38MAPK signaling and pathways involved in cytoskeletal organization, migration, adhesion and cell cycle regulation in MM patients.
Multiple myeloma-related deregulation of bone marrow-derived CD34(+) hematopoietic stem and progenitor cells.
Specimen part, Disease, Disease stage
View Samples