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| lymphoma [2026/05/10 21:02] – [Hodgkin's lymphoma] wh | lymphoma [2026/05/10 21:02] (current) – [risk factors] wh |
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| *FH NHL => 2x risk | *FH NHL => 2x risk |
| *FH coeliac disease in a sibling => increased risk | *FH coeliac disease in a sibling => increased risk |
| *POT1 mutation | *[[POT1_mutation|POT1 mutation]] |
| * "predisposes to pan-lymphoid malignancy syndrome associated with melanoma, sarcoma, and myeloproliferative neoplasms associated with long telemore (TL) and ageing of lymphocytes, sustaining lymphocyte clonal evolution especially in B cells. UK Biobank participants with pathogenic POT1 variants had long TL and higher lymphoid malignancy rates (45% by the age of 80 years; hazard ratio, 8.28; 95% confidence interval, 5.29-13.0). Haploinsufficient mutations in POT1 lead to an autosomal dominant cancer-prone syndrome mediated by long TL.7,13-15 POT1 binds single-stranded telomeric DNA and is essential for telomere protection,16 but POT1 heterozygous loss of function is permissive of telomerase elongation in the absence of a detectable DNA damage response. The prevalence of POT1 mutations in cancer has been limited to single-disease studies, and mutations have been identified consistently in ∼0.5% to 1% of multiple cancers."(([[https://ashpublications.org/blood/article/147/19/2226/566170/Lymphoid-malignancy-and-clonality-in-the-POT1|2026: Lymphoid malignancy and clonality in the POT1-mediated long telomere syndrome ]])) | * "predisposes to pan-lymphoid malignancy syndrome associated with melanoma, sarcoma, and myeloproliferative neoplasms associated with long telemore (TL) and ageing of lymphocytes, sustaining lymphocyte clonal evolution especially in B cells. UK Biobank participants with pathogenic POT1 variants had long TL and higher lymphoid malignancy rates (45% by the age of 80 years; hazard ratio, 8.28; 95% confidence interval, 5.29-13.0). Haploinsufficient mutations in POT1 lead to an autosomal dominant cancer-prone syndrome mediated by long TL.7,13-15 POT1 binds single-stranded telomeric DNA and is essential for telomere protection,16 but POT1 heterozygous loss of function is permissive of telomerase elongation in the absence of a detectable DNA damage response. The prevalence of POT1 mutations in cancer has been limited to single-disease studies, and mutations have been identified consistently in ∼0.5% to 1% of multiple cancers."(([[https://ashpublications.org/blood/article/147/19/2226/566170/Lymphoid-malignancy-and-clonality-in-the-POT1|2026: Lymphoid malignancy and clonality in the POT1-mediated long telomere syndrome ]])) |
| *carcinogens: | *carcinogens: |
