Baylin

Stephen Baylin, M.D.

Professor of Oncology, Deputy Director of the Cancer Center

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Contact Information

Suite 544, Bunting Blaustein Cancer Research Building
410-955-8506
410-614-9884 (Fax)
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Research Interests

Scientific Summary

The Baylin laboratory, in close collaboration with the Herman laboratory, seeks to uncover the molecular basis for a change in the DNA of cancer cells which causes impaired function of important regulatory genes which are necessary to prevent the formation of tumors. Many such losses of gene function in cancer are caused by gene mutations, which cause the cell to produce defective proteins from these genes. These genetic changes are permanent in the DNA and cannot be reversed. The change studied by the Baylin and Herman labs is an alternative way in which cancer cells inactivate genes by adding methyl groups to the start regions of genes and this is associated with a "silencing" of the gene. This process prevents the gene from making any protein and, over the past several years, is being recognized as a very frequent abnormality in all types of human cancer. Unlike DNA mutations, DNA methylation abnormalities are reversible by drugs in a laboratory setting and this reversal allows cancer cells to reactivate the silenced genes and produce normal protein. Understanding how the abnormal DNA methylation arises in cancer cells, and how this change leads to silencing of genes, is extremely important for enriching the possibility of reversing this process as a strategy to prevent and/or treat cancer. Clinical trials are already underway at Hopkins and other institutions with some of the drugs that can potentially accomplish these goals. The Baylin and Herman labs work closely with clinicians to monitor these trials and to improve the approaches for ultimate success.

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General Summary

The Baylin laboratory, in close collaboration with the Herman laboratory, seeks to uncover the molecular basis for a change in the DNA of cancer cells which causes impaired function of important regulatory genes which are necessary to prevent the formation of tumors. Many such losses of gene function in cancer are caused by gene mutations, which cause the cell to produce defective proteins from these genes. These genetic changes are permanent in the DNA and cannot be reversed. The change studied by the Baylin and Herman labs is an alternative way in which cancer cells inactivate genes by adding methyl groups to the start regions of genes and this is associated with a "silencing" of the gene. This process prevents the gene from making any protein and, over the past several years, is being recognized as a very frequent abnormality in all types of human cancer. Unlike DNA mutations, DNA methylation abnormalities are reversible by drugs in a laboratory setting and this reversal allows cancer cells to reactivate the silenced genes and produce normal protein. Understanding how the abnormal DNA methylation arises in cancer cells, and how this change leads to silencing of genes, is extremely important for enriching the possibility of reversing this process as a strategy to prevent and/or treat cancer. Clinical trials are already underway at Hopkins and other institutions with some of the drugs that can potentially accomplish these goals. The Baylin and Herman labs work closely with clinicians to monitor these trials and to improve the approaches for ultimate success.

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Selected Publications

Chen W-Y, Zeng X, Carter MG, Morrell CN, Yen R-YC, Esteller M, Watkins DN, Herman JG, Mankowski JL, Baylin SB. Epigenetic and genetic loss of Hic1 function accentuates the role of p53 in tumorigenesis. Cancer Cell 6:387-298, 2004.

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Chen W-Y, Wang DH, Yen R-WC, Yen Luo J, Gu W, Baylin SB. Tumor Suppressor HIC1 Directly Regulates SIRT1 and Modulates p53 Dependent Apoptotic DNA Damage Responses. Cell 123:437-448, 2005.

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Jones PA, Baylin SB.  The Epigenomics of Cancer.  Cell 128:683-692, 2007.

 

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Ohm JE, McGarvey KM, Yu X, Cheng L, Schuebel KE, Cope L, Mohammad HP, Chen W, Daniel VC, Yu W, Berman  DM, Jenuwein T, Pruitt K, Sharkis SJ, Watkins DN, Herman JG, Baylin SB. A Stem Cell-Like Chromatin Pattern May Predispose Tumor Suppressor Genes to DNA Hypermethylation and Silencing in Adult Cancers. Nature Genetics 39:237-242, 2007.

 

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Tiwari VK, McGarvey KM, Licchesi JD, Ohm JE, Herman JG, Schübeler D, Baylin SB. PcG proteins, DNA methylation, and gene repression by chromatin looping. PLoS Biol 6(12):2911-27. 2008.

 

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McGarvey KM, Van Neste L, Cope L, Ohm J.E, Herman JG , Van Criekinge W, Schuebel KE, Baylin SB. Defining a Chromatin Pattern Which Characterizes DNA Hypermethylated Genes in Colon Cancer Cells. Cancer Res 68:5753-5759, 2008.

 

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O’Hagan HM, Mohammad HP, Baylin SB. Double Strand Breaks Can Initiate Gene Silencing and SIRT1 Dependent Onset of DNA Methylation in an Exogenous Promoter CpG Island. PLoS Genet. 4(8):e1000155, 2008.

 

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Easwaran HP, Van Neste L, Cope L, Sen S, Mohammad HP, Pageau GJ, Lawrence JB, Herman JG, Schuebel KE, Baylin SB. Aberrant silencing of cancer-related genes by CpG hypermethylation occurs independently of their spatial organization in the nucleus. Cancer Res 70(20):8015-24, 2010.

 

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Baylin SB, Jones PA.  A Decade of Visualizing the Evolution, Structure, and Translational Potential of the Cancer Epigenome. Nat Rev Cancer 11(10):726-34, 2011.

 

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O’Hagan HM, Wang W, Sen S, Destefano Shields C, Lee SS, Zhang Y, Clements EG, Cai Y, Van Neste L, Easwaran H, Casero RA, Sears CL, Baylin SB. Oxidative Damage Targets Complexes Containing DNA Methyltransferases, SIRT1 and Polycomb Members to Promoter CpG Islands. Cancer Cell Cancer Cell, 20(5):606-19, 2011.

 

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Juergens RA, Wrangle J, Vendetti FP, Murphy SC, Zhao M, Coleman B, Sebree R, Rodgers K, Hooker CM, Franco N, Lee B, Tsai S, Espinoza Delgado I, Rudek MA, Belinsky SA, Herman JG, Baylin SB, Brock MV, Rudin CM. Combination Epigenetic Therapy Has Efficacy in Patients with Refractory Advanced Non–Small Cell Lung Cancer.  Cancer Discovery, 2012.

 

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Tsai H-C, Li H, Van Neste L, Cai Y, Robert C, Rassool FV, Shin JJ, Harbom KM, Beaty R, Pappou E, Harris J, Yen RWC, Ahuja N, Brock MV, Stearns V, Feller-Kopman D, Yarmus LB, Lin YC, Welm AL, Issa JP, Minn I, Matsui W, Jang YY, Sharkis, SJ, Baylin SB, Zahnow CA. Transient Low Doses of DNA Demethylating Agents Exert Durable Anti-tumor Effects on Hematological and Epithelial Tumor Cells. Cancer Cell,  2012.

 

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