scholarly journals Erratum: Loss in MCL-1 function sensitizes non-Hodgkin’s lymphoma cell lines to the BCL-2-selective inhibitor venetoclax (ABT-199)

2016 ◽  
Vol 6 (3) ◽  
pp. e403-e403 ◽  
Author(s):  
D C Phillips ◽  
Y Xiao ◽  
L T Lam ◽  
E Litvinovich ◽  
L Roberts-Rapp ◽  
...  
1995 ◽  
Vol 19 (1-2) ◽  
pp. 165-171 ◽  
Author(s):  
Hong Chang ◽  
John A. Blondal ◽  
Sam Benchimol ◽  
Mark D. Minden ◽  
Hans A. Messner

2015 ◽  
Vol 5 (11) ◽  
pp. e368-e368 ◽  
Author(s):  
D C Phillips ◽  
Y Xiao ◽  
L T Lam ◽  
E Litvinovich ◽  
L Roberts-Rapp ◽  
...  

Abstract As a population, non-Hodgkin’s lymphoma (NHL) cell lines positive for the t(14;18) translocation and/or possessing elevated BCL2 copy number (CN; BCL2 High ) are exquisitely sensitive to navitoclax or the B-cell lymphoma protein-2 (BCL-2)-selective inhibitor venetoclax. Despite this, some BCL2 High cell lines remain resistant to either agent. Here we show that the MCL-1-specific inhibitor A-1210477 sensitizes these cell lines to navitoclax. Chemical segregation of this synergy with the BCL-2-selective inhibitor venetoclax or BCL-XL-selective inhibitor A-1155463 indicated that MCL-1 and BCL-2 are the two key anti-apoptotic targets for sensitization. Similarly, the CDK inhibitor flavopiridol downregulated MCL-1 expression and synergized with venetoclax in BCL2 High NHL cell lines to a similar extent as A-1210477. A-1210477 also synergized with navitoclax in the majority of BCL2 Low NHL cell lines. However, chemical segregation with venetoclax or A-1155463 revealed that synergy was driven by BCL-XL inhibition in this population. Collectively these data emphasize that BCL2 status is predictive of venetoclax potency in NHL not only as a single agent, but also in the adjuvant setting with anti-tumorigenic agents that inhibit MCL-1 function. These studies also potentially identify a patient population (BCL2 Low ) that could benefit from BCL-XL (navitoclax)-driven combination therapy.


2005 ◽  
Vol 28 (8-9) ◽  
pp. 415-420 ◽  
Author(s):  
Frauke Hugo ◽  
Thomas Dittmar ◽  
Eva K. Treutler ◽  
Kurt S. Zänker ◽  
Jürgen J. Kuehn

2010 ◽  
Vol 2010 ◽  
pp. 1-9 ◽  
Author(s):  
Daniel P. Widney ◽  
Dorina Gui ◽  
Laura M. Popoviciu ◽  
Jonathan W. Said ◽  
Elizabeth C. Breen ◽  
...  

Background. The homeostatic chemokine, CXCL13 (BLC, BCA-1), helps direct the recirculation of mature, resting B cells, which express its receptor, CXCR5. CXCL13/CXCR5 are expressed, and may play a role, in some non-AIDS-associated B cell tumors.Objective. To determine if CXCL13/CXCR5 are associated with AIDS-related non-Hodgkin's lymphoma (AIDS-NHL).Methods. Serum CXCL13 levels were measured by ELISA in 46 subjects who developed AIDS-NHL in the Multicenter AIDS Cohort Study and in controls. The expression or function of CXCL13 and CXCR5 was examined on primary AIDS-NHL specimens or AIDS-NHL cell lines.Results. Serum CXCL13 levels were significantly elevated in the AIDS-NHL group compared to controls. All primary AIDS-NHL specimens showed CXCR5 expression and most also showed CXCL13 expression. AIDS-NHL cell lines expressed CXCR5 and showed chemotaxis towards CXCL13.Conclusions. CXCL13/CXCR5 are expressed in AIDS-NHL and could potentially be involved in its biology. CXCL13 may have potential as a biomarker for AIDS-NHL.


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