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MYC dysregulation is a key event in these cancers, yet MYC overexpression alone is often insufficient to initiate or sustain tumorigenesis.\n                    <jats:italic>Plasmocytoma variant translocation 1<\/jats:italic>\n                    (\n                    <jats:italic>PVT1<\/jats:italic>\n                    ), a long noncoding RNA (lncRNA) adjacent to\n                    <jats:italic>MYC<\/jats:italic>\n                    on chromosome 8q24, is frequently co-amplified with\n                    <jats:italic>MYC<\/jats:italic>\n                    in many of these cancers. Our prior work showed that\n                    <jats:italic>PVT1<\/jats:italic>\n                    potentiates MYC function, although the underlying mechanism has remained unclear. Here we show that, in addition to amplification with\n                    <jats:italic>MYC<\/jats:italic>\n                    , genomic rearrangements at\n                    <jats:italic>PVT1<\/jats:italic>\n                    frequently involve unbalanced translocations that asymmetrically enrich 5\u2032-\n                    <jats:italic>PVT1<\/jats:italic>\n                    while depleting 3\u2032-\n                    <jats:italic>PVT1<\/jats:italic>\n                    . The retained 5\u2032-\n                    <jats:italic>PVT1<\/jats:italic>\n                    region generates a circular RNA,\n                    <jats:italic>CircPVT1<\/jats:italic>\n                    , that encodes a novel protein we have named Firefox (FFX). We show that FFX is essential for MYC-mediated oncogenic signaling, as its depletion markedly reduces MYC protein abundance and transcriptional output. Mechanistically, FFX stimulates AKT\u2013mTORC1 signaling and enhances cap-dependent translational and biosynthetic capacity, thereby establishing a self-reinforcing oncogenic circuit that amplifies MYC activity. Inducible depletion of FFX in vivo significantly impairs tumor growth in MYC\n                    <jats:sup>+<\/jats:sup>\n                    xenograft models. These findings define FFX as a critical effector within the\n                    <jats:italic>MYC<\/jats:italic>\n                    -\n                    <jats:italic>PVT1<\/jats:italic>\n                    locus and reveal a therapeutically actionable vulnerability in MYC\n                    <jats:sup>+<\/jats:sup>\n                    cancers.\n                  <\/jats:p>","DOI":"10.1101\/gad.353355.125","type":"journal-article","created":{"date-parts":[[2026,8,19]],"date-time":"2026-08-19T14:15:24Z","timestamp":1787148924000},"page":"1688-1705","source":"Crossref","is-referenced-by-count":2,"title":["Firefox, a protein encoded by circular\n                    <i>PVT1<\/i>\n                    , is essential for MYC-driven oncogenesis"],"prefix":"10.1101","volume":"40","author":[{"given":"Ashutosh","family":"Tiwari","sequence":"first","affiliation":[{"name":"Cancer Genome and Epigenetics Program, National Cancer Institute Designated Cancer Center, Sanford Burnham Prebys Medical Discovery Institute, La Jolla, California 92037, USA;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Utkarsha","family":"Paithane","sequence":"additional","affiliation":[{"name":"Cancer Genome and Epigenetics Program, National Cancer Institute Designated Cancer Center, Sanford Burnham Prebys Medical Discovery Institute, La Jolla, California 92037, USA;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kojiro","family":"Tashiro","sequence":"additional","affiliation":[{"name":"Cancer Genome and Epigenetics Program, National Cancer Institute Designated Cancer Center, Sanford Burnham Prebys Medical Discovery Institute, La Jolla, California 92037, USA;"},{"name":"Department of Urology, Jikei University School of Medicine, Tokyo 105-8461, Japan;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Bryan","family":"Hall","sequence":"additional","affiliation":[{"name":"Cancer Genome and Epigenetics Program, National Cancer Institute Designated 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