LINE-1 (L1) retrotransposons are potent endogenous insertional mutagens. L1 copies are largely repressed in the soma, but are considered a hallmark of cancer, and a source of evolutionary variation within populations. The mechanism of L1 de-repression in cancer is mostly unknown, though epigenetic regulation is thought to play an important role. Until recently, identifying de novo retrotransposon insertions and their epigenetic status was difficult due to the non-unique mapping of short sequencing reads to recently-integrated repetitive elements. We propose the novel use of long-read sequencing techniques to overcome these obstacles in a single experiment. Long reads ameliorate mapping issues, while the simultaneous detection of base modifications allows determination of epigenetic state and chromatin accessibility. In pilot data generated from liver tumors and matched controls using the Oxford Nanopore system, we observed a striking de-repression of an intronic L1 copy located in the TTC28 gene on chromosome 22 in histologically normal liver. This L1 is known to be mobile in numerous cancers and this result suggests its activation may precede tumorigenesis. Long-read (PacBio) transcriptomic analysis showed that the TTC28 L1 copy is highly expressed in cancer cell lines and may be transcribed from a promoter located in an adjacent upstream SINE Alu retrotransposon copy. While dual luciferase reporter assays indicated the Alu could moderately promote L1 transcription, this effect was much stronger when the Alu was tested as an enhancer. The presence of an SINE-derived enhancer may explain why the TTC28 L1 copy is unusually active. Genome-wide analyses uncovered several other young human L1 copies active in cancers, flanked by an upstream SINE element. This study reveals that upstream SINEs can hyperactivate L1 copies by acting as enhancers, and demonstrates the power of long read sequencing to resolve the structure and function of the repetitive genome.