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Table 1 Studies describing long interspersed nucleotide element (LINE)-1 hypomethylation in malignant tissues.

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

[96–98]

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

[101–103]

Urothelial carcinoma

L1 hypomethylation detected by Southern blot in most specimens

[104–106]