Mitochondrial priming of chronic lymphocytic leukemia patients associates Bcl-xL dependence with alvocidib response

Pierceall, William E.; Warner, Steven L.; Lena, Ryan J.; Doykan, Camille; Blake, Noel; Elashoff, Michael; Hoff, Daniel D. Von; Bearss, David J.; Cardone, Michael H.; Andritsos, Leslie A.; Byrd, John C.; Lanasa, Mark C.; Johnson, Amy J.

doi:10.1038/leu.2014.206

Cited by 2 publications

(2 citation statements)

References 16 publications

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“…Moreover, our study provides a proof-of-principle for the use of BH3 profiling to predict the efficacy of Bcl-2 family antagonists at eliminating specific persistent virus and cell infection combinations, which could have immediate impact on the treatment of diseases associated with latent herpesvirus infections. Since KSHV and EBV are oncogenic viruses and BH3 profiling is currently being used to predict tumor sensitivity to Bcl-2 inhibitors, BH3 profiling could be used to design effective chemotherapeutic regimens against the cancers induced by these viruses (61,62). In addition, BH3 profiling can be used to screen the efficacy of different Mcl-1 small-molecule inhibitors in inducing death of HCMV-infected monocytes and CD34 ϩ stem cells.…”

Section: Resultsmentioning

confidence: 99%

BH3 Profiling Reveals Selectivity by Herpesviruses for Specific Bcl-2 Proteins To Mediate Survival of Latently Infected Cells

Cojohari

Burrer

Peppenelli

et al. 2015

J Virol

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Herpesviruses, including human cytomegalovirus (HCMV), Epstein-Barr virus (EBV), and Kaposi’s sarcoma-associated herpesvirus, establish latency by modulating or mimicking antiapoptotic Bcl-2 proteins to promote survival of carrier cells. BH3 profiling, which assesses the contribution of Bcl-2 proteins towards cellular survival, was able to globally determine the level of dependence on individual cellular and viral Bcl-2 proteins within latently infected cells. Moreover, BH3 profiling predicted the sensitivity of infected cells to small-molecule inhibitors of Bcl-2 proteins.

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Section: Resultsmentioning

confidence: 99%

BH3 Profiling Reveals Selectivity by Herpesviruses for Specific Bcl-2 Proteins To Mediate Survival of Latently Infected Cells

Cojohari

Burrer

Peppenelli

et al. 2015

J Virol

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“…Several inhibitors targeting CDK2 have been identified over the years, and many of them are currently in different phases of drug discovery. Some of the early reported CDK2 inhibitors such as flavopiridol, dinaciclib, roscovitine, and staurosporine are in clinical trials (Aklilu et al., 2003; Burdette‐Radoux et al., 2004; Carlson et al., 1996; Chen et al., 2016; Dickson & Schwartz, 2009; Liu et al., 2011, 2015; Martin et al., 2013; Meijer et al., 1997; Monnerat et al., 2004; Pierceall et al., 2014). However, these are pan‐CDK inhibitors and display potential toxicity issues that restrict their clinical applicability (Whittaker et al., 2017).…”

Section: Introductionmentioning

confidence: 99%

Structural and binding studies of cyclin‐dependent kinase 2 with NU6140 inhibitor

et al. 2021

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Cell cycle dysregulation leads to uncontrolled cell proliferation and is one of the hallmarks of cancer. A set of protein kinases known as cyclin-dependent kinases (CDKs) tightly regulate the cell cycle through phosphorylation of their substrates, which are involved in various functions associated with cell growth. CDKs also play a critical role in transcription and differentiation; CDK family of proteins comprises around twenty kinases that are involved in different nodes of cell cycle regulation (Lim & Kaldis, 2013;Malumbres & Barbacid, 2005). Cyclin-dependent kinase 2 (CDK2) is a key cell cycle regulator kinase that is responsible for G1/S transition and S-phase progression (Sherr, 1994). CDK2 partners with cyclin A or cyclin E to facilitate specific functions during cell cycle progression. Phosphorylation of retinoblastoma protein facilitated by CDK2-cyclin E complex is required for G1/S transition. CDK2-cyclin A complex is required for orderly S-phase progression (Malumbres, 2014;Pines, 1991). Although CDK2 is dispensable for normal cell development, it is critically associated with tumor growth in multiple cancers. The overexpression of CDK2 is reported in several cancers, viz. glioblastoma, oral cancer, breast cancer, lung

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Mitochondrial priming of chronic lymphocytic leukemia patients associates Bcl-xL dependence with alvocidib response

Cited by 2 publications

References 16 publications

BH3 Profiling Reveals Selectivity by Herpesviruses for Specific Bcl-2 Proteins To Mediate Survival of Latently Infected Cells

BH3 Profiling Reveals Selectivity by Herpesviruses for Specific Bcl-2 Proteins To Mediate Survival of Latently Infected Cells

Structural and binding studies of cyclin‐dependent kinase 2 with NU6140 inhibitor

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