<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Tsai HJ</submitter><funding>National Taiwan University Hospital</funding><funding>National Science and Technology Council</funding><pagination>383</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC11575159</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>24(1)</volume><pubmed_abstract>&lt;h4>Background&lt;/h4>This study aimed to explore whether cytotoxin-associated gene A (CagA) can inhibit cell cycle progression by activating nuclear factor of activated T cells (NFAT) in lymphoma B cells and contribute to Helicobacter pylori eradication (HPE) responsiveness (complete remission [CR] after HPE) in gastric mucosa-associated lymphoid tissue (MALT) lymphoma.&lt;h4>Materials and methods&lt;/h4>We co-cultured three B-lymphoma cell lines (MA-1, OCI-Ly3, and OCI-Ly7) with HP strains (derived from HPE-responsive gastric MALT lymphoma) and evaluated the expression patterns of CagA, phosphorylated (p)-CagA (CagA&lt;sup>P-Tyr&lt;/sup>), and CagA-signaling molecules, cell-cycle inhibitors, p-NFATc1 (Ser&lt;sup>172&lt;/sup>), and NFATc1 using western blotting. Furthermore, we evaluated the association betwe</pubmed_abstract><journal>Cancer cell international</journal><pubmed_title>Cooperative participation of CagA and NFATc1 in the pathogenesis of antibiotics-responsive gastric MALT lymphoma.</pubmed_title><pmcid>PMC11575159</pmcid><funding_grant_id>No. 110-2314-B-002-219-MY3, No. 112-2314-B-002-097-MY3, No. 112-2811-B-002-092-, and No. 113-2811-B-002-142</funding_grant_id><funding_grant_id>No. NTUH 113-S0087</funding_grant_id><pubmed_authors>Chen LT</pubmed_authors><pubmed_authors>Shun CT</pubmed_authors><pubmed_authors>Wang HP</pubmed_authors><pubmed_authors>Lin CW</pubmed_authors><pubmed_authors>Wei MF</pubmed_authors><pubmed_authors>Kuo SH</pubmed_authors><pubmed_authors>Zeng YS</pubmed_authors><pubmed_authors>Hsu PN</pubmed_authors><pubmed_authors>Tsai HJ</pubmed_authors><pubmed_authors>Wu MS</pubmed_authors><pubmed_authors>Liou JM</pubmed_authors><pubmed_authors>Yeh KH</pubmed_authors><pubmed_authors>Cheng AL</pubmed_authors></additional><is_claimable>false</is_claimable><name>Cooperative participation of CagA and NFATc1 in the pathogenesis of antibiotics-responsive gastric MALT lymphoma.</name><description>&lt;h4>Background&lt;/h4>This study aimed to explore whether cytotoxin-associated gene A (CagA) can inhibit cell cycle progression by activating nuclear factor of activated T cells (NFAT) in lymphoma B cells and contribute to Helicobacter pylori eradication (HPE) responsiveness (complete remission [CR] after HPE) in gastric mucosa-associated lymphoid tissue (MALT) lymphoma.&lt;h4>Materials and methods&lt;/h4>We co-cultured three B-lymphoma cell lines (MA-1, OCI-Ly3, and OCI-Ly7) with HP strains (derived from HPE-responsive gastric MALT lymphoma) and evaluated the expression patterns of CagA, phosphorylated (p)-CagA (CagA&lt;sup>P-Tyr&lt;/sup>), and CagA-signaling molecules, cell-cycle inhibitors, p-NFATc1 (Ser&lt;sup>172&lt;/sup>), and NFATc1 using western blotting. Furthermore, we evaluated the association betwe</description><dates><release>2024-01-01T00:00:00Z</release><publication>2024 Nov</publication><modification>2026-07-17T01:08:14.01Z</modification><creation>2025-04-04T20:38:48.117Z</creation></dates><accession>S-EPMC11575159</accession><cross_references><pubmed>39558403</pubmed><doi>10.1186/s12935-024-03552-6</doi></cross_references></HashMap>