Retrovirus insertion site analysis of LGL leukemia patient genomes.
Weiling LiLei YangRobert S HarrisLin LinThomas L OlsonCait E HameleDavid J FeithThomas P LoughranMary PossPublished in: BMC medical genomics (2019)
Our study confirms that the clonal expansion of LGL cells in LGL leukemia is not driven by the integration of a new infectious or endogenous retrovirus, although we do not rule out that these cells are responding to retroviral antigens produced in other cell types. However, our computational analyses revealed that the genomes of LGL leukemia patients carry a higher burden of polymorphic HERV-K proviruses compare to individuals from KGP of European ancestry. Our research emphasizes the merits of comprehensive genomic assessment of HERV-K in cancer samples and suggests that further analyses to determine contributions of HERV-K to LGL leukemia are warranted.
Keyphrases
- acute myeloid leukemia
- induced apoptosis
- bone marrow
- cell cycle arrest
- end stage renal disease
- single cell
- newly diagnosed
- ejection fraction
- chronic kidney disease
- papillary thyroid
- endoplasmic reticulum stress
- squamous cell carcinoma
- immune response
- case report
- prognostic factors
- signaling pathway
- cell therapy
- risk factors
- mesenchymal stem cells
- cell proliferation
- patient reported outcomes
- squamous cell
- patient reported