From: Mobilizing diversity: transposable element insertions in genetic variation and disease
Tumor | Evidence for LINE hypomethylation | Reference |
---|---|---|
Breast cancer | 5' flanking sequences of hypomethylated L1 homo sapien elements were isolated from T-47 D cells by inverse polymerase chain reaction (PCR) | [94] |
Chronic myeloid leukaemia (blast phase) | Methylation-specific PCR of primary samples; hypomethylation associated with blast crisis, high levels of BCR-ABL messenger RNA, resistance to tyrosine kinase inhibitor chemotherapy | [95] |
Chronic lymphocytic leukaemia | A variety of primary specimens analysed by Hpa II restriction enzyme digest and Southern blot analysis | [96] |
Colorectal adenocarcinoma | As compared to neighbouring normal colon; colorectal carcinomas with sporadic microsatellite instability a noted exception; alternative progression pathways proposed | |
Hepatocellular carcinoma | Hepatocellular carcinomas compared to surrounding cirrhotic liver; Hpa II restriction enzyme digest | [99] |
Neuroendocrine tumours | Well-differentiated pancreatic endocrine and carcinoid tumours compared to surrounding tissue; LINE hypomethylation correlates with lymph node metastasis and cytogenetic aberrations | [100] |
Prostate cancer | Adenocarcinoma compared to surrounding tissue; hypomethylation of L1 s associated with preoperative PSA, Gleason grade, and clinical stage; associated independently with cytogenetic abnormalities | |
Urothelial carcinoma | L1 hypomethylation detected by Southern blot in most specimens |