<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Al-Khatib S</submitter><funding>Jordan University of Science and Technology</funding><pagination>e0272312</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC9337659</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>17(7)</volume><pubmed_abstract>Mature B-cell neoplasms are typically divided into Hodgkin and Non-Hodgkin Lymphomas. Hodgkin Lymphoma is characterized by the neoplastic Reed-Sternberg cells, usually harbored in an inflammatory background, with a frequent clinical presentation of mediastinal lymphadenopathy. Many studies link between autoimmunity and lymphomagenesis, a large proportion of these studies evidently trace the pathogenesis back to the misdirected detection of self-derived nucleic acids by Toll-Like Receptors (TLRs), especially those of the intracellular type. In this study, we analyzed the relationship between a selected SNP in TLR9 (TLR9-1237T>C; rs5743836) and the risk and overall survival of HL patients in a Jordanian Arab population. A total of 374 subjects; 136 cases of Hodgkin lymphoma and 238 matched healthy controls were incorporated in this study. Genomic DNA was extracted from formalin-fixed paraffin-embedded tissues. Genotyping of the genetic polymorphisms was conducted using a sequencing protocol. The results show a statistically significant higher distribution of the rs5743836 (TLR9-1237T>C) allele among the case population, with a p-value of 0.031 (&lt;0.05). This distribution proved significant when studied in the codominant (only significant in the T/C genotype, p-value = 0.030), dominant (p-value = 0.025), and overdominant (p-value = 0.035) models. None of the models showed any statistically significant difference in survival associated with the rs5743836 (TLR9-1237T>C) SNP.</pubmed_abstract><journal>PloS one</journal><pubmed_title>Association of TLR9-1237T>C; rs5743836 polymorphism with increased risk of Hodgkin's lymphoma: A case-control study.</pubmed_title><pmcid>PMC9337659</pmcid><funding_grant_id>20170225</funding_grant_id><pubmed_authors>Al-Khatib S</pubmed_authors><pubmed_authors>Khader Y</pubmed_authors><pubmed_authors>Shabaneh A</pubmed_authors><pubmed_authors>Al-Eitan L</pubmed_authors><pubmed_authors>Abdo N</pubmed_authors><pubmed_authors>Al-Mistarehi AH</pubmed_authors></additional><is_claimable>false</is_claimable><name>Association of TLR9-1237T>C; rs5743836 polymorphism with increased risk of Hodgkin's lymphoma: A case-control study.</name><description>Mature B-cell neoplasms are typically divided into Hodgkin and Non-Hodgkin Lymphomas. Hodgkin Lymphoma is characterized by the neoplastic Reed-Sternberg cells, usually harbored in an inflammatory background, with a frequent clinical presentation of mediastinal lymphadenopathy. Many studies link between autoimmunity and lymphomagenesis, a large proportion of these studies evidently trace the pathogenesis back to the misdirected detection of self-derived nucleic acids by Toll-Like Receptors (TLRs), especially those of the intracellular type. In this study, we analyzed the relationship between a selected SNP in TLR9 (TLR9-1237T>C; rs5743836) and the risk and overall survival of HL patients in a Jordanian Arab population. A total of 374 subjects; 136 cases of Hodgkin lymphoma and 238 matched healthy controls were incorporated in this study. Genomic DNA was extracted from formalin-fixed paraffin-embedded tissues. Genotyping of the genetic polymorphisms was conducted using a sequencing protocol. The results show a statistically significant higher distribution of the rs5743836 (TLR9-1237T>C) allele among the case population, with a p-value of 0.031 (&lt;0.05). This distribution proved significant when studied in the codominant (only significant in the T/C genotype, p-value = 0.030), dominant (p-value = 0.025), and overdominant (p-value = 0.035) models. None of the models showed any statistically significant difference in survival associated with the rs5743836 (TLR9-1237T>C) SNP.</description><dates><release>2022-01-01T00:00:00Z</release><publication>2022</publication><modification>2026-04-08T11:46:26.364Z</modification><creation>2025-04-19T22:47:36.778Z</creation></dates><accession>S-EPMC9337659</accession><cross_references><pubmed>35905120</pubmed><doi>10.1371/journal.pone.0272312</doi></cross_references></HashMap>