{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,15]],"date-time":"2026-10-15T21:30:52Z","timestamp":1792099852459,"version":"4.4.0"},"reference-count":0,"publisher":"S. Karger AG","issue":"5","license":[{"start":{"date-parts":[[2017,1,1]],"date-time":"2017-01-01T00:00:00Z","timestamp":1483228800000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/www.karger.com\/Services\/SiteLicenses"},{"start":{"date-parts":[[2017,1,1]],"date-time":"2017-01-01T00:00:00Z","timestamp":1483228800000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/www.karger.com\/Services\/SiteLicenses"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Pathobiology"],"published-print":{"date-parts":[[2017]]},"abstract":"<b><i>Objectives:<\/i><\/b> Clonal selection in the follicular germinal centers in lymphatic tissues is accompanied by an intense proliferation of polyclonal B cells in a precisely regulated fashion. In contrast, B-cell neoplasias proliferate autonomously due to endogenous stimuli. The cell kinetic activity is obvious at many levels including progressive chromatin modification and elevated mitotic rates. We asked if there are differences in the kinetics of histone H3S10 phosphorylation required for mitotic entry between highly proliferating B cells of reactive germinal centers and in B-cell lymphomas with different proliferative capacity. <b><i>Material and Methods:<\/i><\/b> Phospho-H3 histone (pH3S10)-specific immunohistochemistry was applied to cultivated cell, reactive and selected indolent and aggressive lymphoma samples (diffuse large B-cell lymphoma, Burkitt lymphoma, lymphoblastic lymphoma, follicular lymphoma and small lymphocytic lymphoma). Microscopic quantification of the \u201cdot-type\u201d (representing late G<sub>2<\/sub> phase) and \u201cmitotic\u201d immunolabeling patterns per field of view was performed and compared with classical cell proliferation markers. <b><i>Results:<\/i><\/b> In addition to the dense homogeneous chromatin labeling highlighting mitotic figures, we stated a selective dot-type nuclear labeling representing ongoing chromatin condensation in premitotic G<sub>2<\/sub> phase cells. While cell proliferation and mitotic counts correlated in general with histology, statistical analysis indicated an accumulation of G<sub>2<\/sub> phase pH3S10 pattern in the reactive germinal centers in contrast to lymphomas. The dot-type G<sub>2<\/sub> staining pattern was surprisingly overrepresented (1,321.7 \u00b1 356.5\/10 HPF) in the reactive germinal centers compared to aggressive lymphomas (101.3 \u00b1 33.1) (<i>p<\/i> < 0.005). The relative G<sub>2<\/sub>\/M value was significantly higher (4.6 \u00b1 0.6) in reactive germinal center B cells than in any lymphoma entity evaluated (0.7 \u00b1 0.2 in Burkitt lymphoma, 0.9 \u00b1 0.4 in grade 3b follicular lymphoma, 1.3 \u00b1 1.1 in diffuse large B-cell lymphoma, 1.5 \u00b1 0.6 in lymphoblastic lymphoma, and 0.9 \u00b1 0.2 in small lymphocytic lymphoma). <b><i>Conclusions:<\/i><\/b> pH3S10 immunohistochemistry enabled the presentation of significant differences in the cell cycle kinetics between reactive and neoplastic B-cell lymphoproliferations. Accumulation of G<sub>2<\/sub> phase B cells in reactive folliculi directs to physiological G<sub>2<\/sub>\/M checkpoint blockade. In contrast, accelerated G<sub>2<\/sub>\/M transition in lymphomas is potentially associated with impaired genomic repair and cell death mechanisms.<\/jats:p>","DOI":"10.1159\/000477737","type":"journal-article","created":{"date-parts":[[2017,7,17]],"date-time":"2017-07-17T17:01:16Z","timestamp":1500310876000},"page":"243-250","source":"Crossref","is-referenced-by-count":5,"title":["Distinct Dynamics of Mitotic Transition in B-Cell Lymphoma and Reactive B-Cell Lymphoproliferations Determined by H3S10 Phosphohistone Immunolabeling"],"prefix":"10.1159","volume":"84","author":[{"given":"G\u00e1bor","family":"M\u00e9hes","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Katalin","family":"Hegyi","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ravi","family":"Jobanputra","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"L\u00edvia","family":"Beke","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Gy\u00f6rgy","family":"Vereb","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Judit","family":"Bedekovics","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"127","published-online":{"date-parts":[[2017,7,18]]},"container-title":["Pathobiology"],"original-title":[],"language":"en","link":[{"URL":"https:\/\/www.karger.com\/Article\/Pdf\/477737","content-type":"application\/pdf","content-version":"vor","intended-application":"text-mining"},{"URL":"https:\/\/www.karger.com\/Article\/Pdf\/477737","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2025,4,23]],"date-time":"2025-04-23T12:33:04Z","timestamp":1745411584000},"score":1,"resource":{"primary":{"URL":"https:\/\/karger.com\/article\/doi\/10.1159\/000477737"}},"subtitle":[],"short-title":[],"issued":{"date-parts":[[2017]]},"references-count":0,"journal-issue":{"issue":"5","published-online":{"date-parts":[[2017,12,7]]}},"URL":"https:\/\/doi.org\/10.1159\/000477737","archive":["Portico"],"relation":{},"ISSN":["1015-2008","1423-0291"],"issn-type":[{"value":"1015-2008","type":"print"},{"value":"1423-0291","type":"electronic"}],"subject":[],"published":{"date-parts":[[2017]]}}}