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000144514 0247_ $$2doi$$a10.1172/jci.insight.128435
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000144514 1001_ $$aScherger, Anna K$$b0
000144514 245__ $$aActivated gp130 signaling selectively targets B cell differentiation to induce mature lymphoma and plasmacytoma.
000144514 260__ $$aAnn Arbor, Michigan$$bJCI Insight$$c2019
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000144514 520__ $$aAberrant activity of the glycoprotein 130 130/JAK/STAT3 (gp130/JAK/STAT3) signaling axis is a recurrent event in inflammation and cancer. In particular, it is associated with a wide range of hematological malignancies, including multiple myeloma and leukemia. Novel targeted therapies have only been successful for some subtypes of these malignancies, underlining the need for developing robust mouse models to better dissect the role of this pathway in specific tumorigenic processes. Here, we investigated the role of selective gp130/JAK/STAT3 activation by generating a conditional mouse model. This model targeted constitutively active, cell-autonomous gp130 activity to B cells, as well as to the entire hematopoietic system. We found that regardless of the timing of activation in B cells, constitutively active gp130 signaling resulted in the formation specifically of mature B cell lymphomas and plasma cell disorders with full penetrance, only with different latencies, where infiltrating CD138+ cells were a dominant feature in every tumor. Furthermore, constitutively active gp130 signaling in all adult hematopoietic cells also led to the development specifically of largely mature, aggressive B cell cancers, again with a high penetrance of CD138+ tumors. Importantly, gp130 activity abrogated the differentiation block induced by a B cell-targeted Myc transgene and resulted in a complete penetrance of the gp130-associated, CD138+, mature B cell lymphoma phenotype. Thus, gp130 signaling selectively provides a strong growth and differentiation advantage for mature B cells and directs lymphomagenesis specifically toward terminally differentiated B cell cancers.
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000144514 7001_ $$aAl-Maarri, Mona$$b1
000144514 7001_ $$aMaurer, Hans Carlo$$b2
000144514 7001_ $$aSchick, Markus$$b3
000144514 7001_ $$aMaurer, Sabine$$b4
000144514 7001_ $$aÖllinger, Rupert$$b5
000144514 7001_ $$aGonzalez-Menendez, Irene$$b6
000144514 7001_ $$aMartella, Manuela$$b7
000144514 7001_ $$aThaler, Markus$$b8
000144514 7001_ $$0P:(DE-He78)1357588a5c7b2c3f249da63f694a0cdf$$aPechloff, Konstanze$$b9
000144514 7001_ $$0P:(DE-HGF)0$$aSteiger, Katja$$b10
000144514 7001_ $$0P:(DE-He78)3c4e3363a68498c72ad042b849e11f3a$$aSander, Sandrine$$b11
000144514 7001_ $$0P:(DE-HGF)0$$aRuland, Jürgen$$b12
000144514 7001_ $$0P:(DE-He78)340f7c2dcaedeae68e4a62c281c7350b$$aRad, Roland$$b13
000144514 7001_ $$aQuintanilla-Martinez, Leticia$$b14
000144514 7001_ $$aWunderlich, Frank T$$b15
000144514 7001_ $$aRose-John, Stefan$$b16
000144514 7001_ $$0P:(DE-HGF)0$$aKeller, Ulrich$$b17
000144514 773__ $$0PERI:(DE-600)2874757-4$$a10.1172/jci.insight.128435$$gVol. 4, no. 15, p. e128435$$n15$$pe128435$$tJCI insight$$v4$$x2379-3708$$y2019
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000144514 9141_ $$y2019
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