Identifying safeguards disabled by Epstein-Barr tumor virus infections in genomes from breast cancer patients: chromosomal bioinformatic analysis. (Preprint) DOI Creative Commons
Bernard Friedenson

JMIRx Med, Journal Year: 2024, Volume and Issue: 6, P. e50712 - e50712

Published: Nov. 20, 2024

The causes of breast cancer are poorly understood. A potential risk factor is Epstein-Barr virus (EBV), a lifelong infection nearly everyone acquires. EBV-transformed human mammary cells accelerate when transplanted into immunosuppressed mice, but the can disappear as malignant reproduce. If this model applies to cancers, then they should have genome damage characteristic EBV infection. This study tests hypothesis that predisposes one by causing permanent compromises safeguards. Publicly available data from approximately 2100 cancers and 25 ovarian were compared with proven associations EBV, including 70 nasopharyngeal 90 Burkitt lymphomas, 88 diffuse large B-cell 34 gastric cancers. Calculation algorithms make these comparisons developed. Chromosome breakpoints in clustered around EBV-associated Breakpoint distributions on some chromosomes not confidently distinguished (P>.05), differed controls unrelated Viral breakpoint clusters occurred high-risk, sporadic, other subgroups. disrupted gene functions essential for protection, which remain compromised even if disappears. As CRISPR (clustered regularly interspaced short palindromic repeats)-like reminders past during evolution, fragments found between Piwi-interacting RNA (piRNA) genes chromosome 6. Both had inactivated guard piRNA defenses major histocompatibility complex (MHC) locus. Breast variations converged highly polymorphic MHC. Not develops because MHC differences produce differing responses shattering mutation hot spots preferentially at incorporated viral sequences. On 17, those EBV-mediated linked estrogen effects. Other breaks affected sites where inhibits JAK-STAT SWI-SNF signaling pathways. EBV-cancer deletion shifts metabolism favor tumors was also These changes push metastasis survival metastatic cells. metastasis, Identifying pathogenic may improve screening, treatment, prevention. Immunizing children against protect breast, ovarian, potentially chronic unexplained diseases.

Language: Английский

Identifying safeguards disabled by Epstein-Barr tumor virus infections in genomes from breast cancer patients: chromosomal bioinformatic analysis. (Preprint) DOI Creative Commons
Bernard Friedenson

JMIRx Med, Journal Year: 2024, Volume and Issue: 6, P. e50712 - e50712

Published: Nov. 20, 2024

The causes of breast cancer are poorly understood. A potential risk factor is Epstein-Barr virus (EBV), a lifelong infection nearly everyone acquires. EBV-transformed human mammary cells accelerate when transplanted into immunosuppressed mice, but the can disappear as malignant reproduce. If this model applies to cancers, then they should have genome damage characteristic EBV infection. This study tests hypothesis that predisposes one by causing permanent compromises safeguards. Publicly available data from approximately 2100 cancers and 25 ovarian were compared with proven associations EBV, including 70 nasopharyngeal 90 Burkitt lymphomas, 88 diffuse large B-cell 34 gastric cancers. Calculation algorithms make these comparisons developed. Chromosome breakpoints in clustered around EBV-associated Breakpoint distributions on some chromosomes not confidently distinguished (P>.05), differed controls unrelated Viral breakpoint clusters occurred high-risk, sporadic, other subgroups. disrupted gene functions essential for protection, which remain compromised even if disappears. As CRISPR (clustered regularly interspaced short palindromic repeats)-like reminders past during evolution, fragments found between Piwi-interacting RNA (piRNA) genes chromosome 6. Both had inactivated guard piRNA defenses major histocompatibility complex (MHC) locus. Breast variations converged highly polymorphic MHC. Not develops because MHC differences produce differing responses shattering mutation hot spots preferentially at incorporated viral sequences. On 17, those EBV-mediated linked estrogen effects. Other breaks affected sites where inhibits JAK-STAT SWI-SNF signaling pathways. EBV-cancer deletion shifts metabolism favor tumors was also These changes push metastasis survival metastatic cells. metastasis, Identifying pathogenic may improve screening, treatment, prevention. Immunizing children against protect breast, ovarian, potentially chronic unexplained diseases.

Language: Английский

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