Syndax Pharmaceuticals Key Publications


Epigenetics

Jones, P.A. and S. Baylin (2007). Cell 128:683-92.

Baylin, S. and P.A. Jones (2010). Science Mag. 330:576-578.

HDACi

Witt, O., H.E. Deubzer, et al (2009). "HDAC family: What are the cancer relevant targets?" Cancer Lett. article in-press

Lane, A.A. and B.A. Bradner (2009). "Histone deacetylase inhibitors in cancer therapy." J Clin Onc. 27(32):5459-68.

Bradner, J.E., N. West, et al (2010). "Chemical phylogenetics of histone deacetylases." Nat Chem Biol. 6(March): 238-43.

HDACi/DNMTi

Ganesan, A., L. Nolan, et al (2009). " Epigenetic Therapy: Histone Acetylation, DNA Methylation and Anti-Cancer Drug Discovery." Curr Cancer Drug Targets. 9:963-81.

Gore, Steven D. (2009). "In vitro basis for treatment with hypomethylating agents and histone deacetylase inhibitors: can epigenetic changes be used to monitor treatment?" Leuk Res 33(Suppl.2): S2–S6.

Stearns, V., Q. Zhou, et al (2007). "Epigenetic Regulation as a New Target for Breast Cancer Therapy." Canc Invest. 25:659–65.

Cameron, E.E., K.E. Bachman, et al. (1999). "Synergy of demethylation and histone deacetylase inhibition in the re-expression of genes silenced in cancer." Nature Gen. 21:103-07.

Zhou, Q., A.T. Agoston, et al. (2008). "Inhibition of histone deacetylases promotes ubiquitin-dependent proteasomal degradation of DNA methyltransferase 1 in human breast cancer cells." Mol Cancer Res. 6(5):873-83.

Lee, M.J., A. Adjei, et al. (2009). "Pharmacokinetic and pharmacodynamic analysis of patients treated with the histone deacetylase inhibitor entinostat in combination with erlotinib." AACR Mol Targets Meeting Poster B206.

Kaiser, J. (2010) "Epigenetics drugs take on cancer." Science. 330:576-78.

Belinsky, S., M. Grimes, et al. (2011) "Combination therapy with vidaza and entinostat suppresses tumor growth and reprograms the epigenome in an orthotopic lung cancer model." Cancer Res. 71(2):OF1-9.

HDACi/EGFR

Lee, M.J., Y.S. Kim, et al (2008). "Histone deacetylase inhibitors in cancer therapy." Curr Opin Oncol. 20(6):639-49.

Kakihana, M., T. Ohira, et al. (2009). "Induction of E-cadherin in lung cancer and interaction with growth suppression by histone deacetylase inhibition." J Thor Oncology. 4(12):1455-65.

Witta, S.E., R.M. Gemmill, et al. (2006). "Restoring E-cadherin expression increases sensitivity to epidermal growth factor receptor inhibitors in lung cancer cell lines." Cancer Res 66(2): 944-50.

Witta, S.E., R. Dziadziuszko, et al. (2009). "ErbB-3 expression is associated with E-cadherin and their coexpression restores response to gefitinib in non-small-cell lung cancer SCLC)." Annals Onc. 1-7.

Sharma, S.V., D.Y. Lee, et al. (2010). "A chromatin-mediated reversible drug-tolerant state in cancer cell subpopulations." Cell. 141:69-80.

Yauch, R.L., T. Januario, et al. (2005). "Epithelial versus mesenchymal phenotype determines in vitro sensitivity and predicts clinical activity of erlotinib in lung cancer patients." Clin Cancer Res. 11(24):8686-98.

Coldren, C.D., B.A. Helfrich, et al. (2006). "Baseline gene expression predicts sensitivity to gefitinib in non–small cell lung cancer cell lines." Mol Cancer Res. 4(8):521-28.

Thomson, et al. (2005). "Epithelial to mesenchymal transition is a determinant of sensitivity of non–small-cell lung carcinoma cell lines and xenografts to epidermal growth factor receptor inhibition." Cancer Res. 65(20):9455-62.

Dannenberg, J-H. and A. Berns (2010). "Drugging drug resistance." Cell. 141:18-20.

Workman, P. and J. Travers. (2010). "Drug-tolerant insurgents." Nature. 464:844-85.

HDACi Endocrine Therapy

Brodie, A., L. Macedo, et al. (2010). "Aromatase resistance mechanisms in model systems in vivo." J Steroid Biochem Mol Biol. 118:283-87.

Chumsri, S., T. Howes, et al. (2010). "Aromatase, Aromatase Inhibitors, and Breast Cancer." J Steroid Biochem Mol Biology. doi:10.1016/j.jsbmb.2011.02.001

Lustberg, M.B. and B. Ramaswamy. (2009). "Epigenetic targeting in breast cancer: therapeutic impact and future direction." Drug News Perspect. 22(7):369-81.

Stearns, V., Q. Zhou, et al (2007). "Epigenetic Regulation as a New Target for Breast Cancer Therapy." Canc Invest. 25:659–65.

Bicaku, E., D.C. Marchion, et al. (2008). "Selective inhibition of histone deacetylase 2 silences progesterone receptor-mediated signaling." Cancer Res. 68(5):1513-9.

Hodges-Gallagher, L., C.D. Valentine, et al. (2007). "Inhibition of histone deacetylase enhances the anti-proliferative action of antiestrogens on breast cancer cells and blocks tamoxifen-induced proliferation of uterine cells." Breast Cancer Res Treat. 105(3):297-309.

Sabnis, G., O. Goloubeva, et al. (2011). "Functional activation of the estrogen receptor-a and aromatase by the HDAC inhibitor entinostat sensitizes ER-negative tumors to letrozole." Cancer Res. Mar 1;71(5):1893-903. Epub 2011 Jan 18.

Sabnis, G., O. Golobeva, et al. (2010). "HDAC inhibitor entinostat restores responsiveness of letrozole resistant MCF-7Ca xenografts to AIs through Modulation of Her-2." SABCS poster.

Thomas, S. and P.N. Munster. (2009). "Histone deacetylase inhibitor induced modulation of anti-estrogen therapy." Cancer Lett. 280:184-91.

HDACi/Hodgkin's Lymphoma

Buglio, D., G.V. Georgakis, et al. (2008). "Vorinostat inhibits STAT6-mediated TH2 cytokine and TARC production and induces cell death in Hodgkin lymphoma cell lines." Blood 112(4):1424-33.

Ashraf, U., M.S. Czuczman, et al. (2009). "Entinostat (SNDX-275), a novel DAC inhibitor, is highly effective in rituximab-[chemotherapy]-sensitive or rituximab-[chemotherapy]-resistant lymphomas and has synergistic anti-tumor activity when combined with bortezomib." ASH Meeting Poster.

Kashkhely, N., D. Buglio, et al. (2009). "The histone deacetylase (HDAC) inhibitor entinostat (SNDX-275) targets Hodgkin lymphoma through a dual mechanism of immune modulation and apoptosis induction." ASH Meeting Poster.

Buglio, D., N. Kashkhely, et al. (2011). "HDAC11 plays an essential role in regulating OX40 ligand expression in Hodgkin lymphoma." Blood. Online.

Entinostat

Jotte ,R., S. Witta, et al. (2010). “Molecular analysis identifies a subset of non-small cell lung cancer patients with differential sensitivity to histone deacetylase inhibitor (hdaci) /epidermal growth factor receptor tyrosine kinase inhibitor (egfr-tki) treatment.” 2010 Chicago Multidisciplinary Symposium in Thoracic Oncology. LBOA3 presentation.

Hess-Stumpp, H., T.U. Bracker, et al. (2007). "MS-275, a potent orally available inhibitor of histone deacetylases--the development of an anticancer agent." Int J Biochem Cell Biol. 39(7-8):1388-405.

Gojo, I., A. Jiemjit, et al. (2007) "Phase 1 and pharmacologic study of MS-275, a histone deacetylase inhibitor, in adults with refractory and relapsed acute leukemias." Blood. 109(7):2781-90.

Gore, L., M. Rothenberg, et al. (2008). "A phase I and pharmacokinetic study of the oral histone deacetylase inhibitor, MS-275, in patients with refractory solid tumors and lymphomas." Clin Cancer Res. 14(14):4517-25.

Hauschild, A., U. Trefzer, et al. (2008). "Multicenter phase II trial of the histone deacetylase inhibitor pyridylmethyl-N-{4-[(2-aminophenyl)-carbamoyl]-benzyl}-carbamate in pretreated metastatic melanoma." Melanoma Res. 18(4):274-78

Kummar, S., M. Gutierrez, et al. (2007). "Phase I trial of MS-275, a histone deacetylase inhibitor, administered weekly in refractory solid tumors and lymphoid malignancies." Clin Cancer Res 13(18):5411-17.

Ryan, Q.C., D. Headlee, et al. (2005). "Phase I and pharmacokinetic study of MS-275, a histone deacetylase inhibitor, in patients with advanced and refractory solid tumors or lymphoma." J Clin Oncol. 23(17):3912–22.

Choudhary, C., C. Kumar, et al. (2009). "Lysine acetylation targets protein complexes and co-regulates major cellular functions." Sciencexpress. 1-16.