On Epigenetic Plasticity and Genome Topology
Lazaris, Charalampos, Iannis Aifantis, and Aristotelis Tsirigos. 2020. “On Epigenetic Plasticity and Genome Topology”. Trends Cancer 6: 177-80.
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Role of Dysregulated Cytokine Signaling and Bacterial Triggers in the Pathogenesis of Cutaneous T-Cell Lymphoma
Fanok, Melania H., Amy Sun, Laura K. Fogli, Vijay Narendran, Miriam Eckstein, Kasthuri Kannan, Igor Dolgalev, et al. 2018. “Role of Dysregulated Cytokine Signaling and Bacterial Triggers in the Pathogenesis of Cutaneous T-Cell Lymphoma”. J Invest Dermatol 138: 1116-25.
FBXW7 Modulates Cellular Stress Response and Metastatic Potential Through HSF1 Post-translational Modification
Kourtis, Nikos, Rana S. Moubarak, Beatriz Aranda-Orgilles, Kevin Lui, Iraz T. Aydin, Thomas Trimarchi, Farbod Darvishian, et al. 2015. “FBXW7 Modulates Cellular Stress Response and Metastatic Potential Through HSF1 Post-Translational Modification”. Nat Cell Biol 17: 322-32.
Epstein-Barr-virus-encoded LMP2A induces primary epithelial cell migration and invasion: possible role in nasopharyngeal carcinoma metastasis
Pegtel, D. M., A. Subramanian, T. S. Sheen, C. H. Tsai, T. R. Golub, and D. A. Thorley-Lawson. 2005. “Epstein-Barr-Virus-Encoded LMP2A Induces Primary Epithelial Cell Migration and Invasion: Possible Role in Nasopharyngeal Carcinoma Metastasis”. J Virol 79: 15430-42.
In vitro differentiation of epithelial cells from cervical neoplasias resembles in vivo lesions
Rader, J. S., T. R. Golub, J. B. Hudson, D. Patel, M. A. Bedell, and L. A. Laimins. 1990. “In Vitro Differentiation of Epithelial Cells from Cervical Neoplasias Resembles in Vivo Lesions”. Oncogene 5: 571-6.
Selective killing of cancer cells by a small molecule targeting the stress response to ROS
Raj, L., T. Ide, A. U. Gurkar, M. Foley, M. Schenone, X. Li, N. J. Tolliday, et al. 2011. “Selective Killing of Cancer Cells by a Small Molecule Targeting the Stress Response to ROS”. Nature 475: 231-4.
Integrated genomic analysis illustrates the central role of JAK-STAT pathway activation in myeloproliferative neoplasm pathogenesis
Rampal, R., F. Al-Shahrour, O. Abdel-Wahab, J. P. Patel, J. P. Brunel, C. H. Mermel, A. J. Bass, et al. 2014. “Integrated Genomic Analysis Illustrates the Central Role of JAK-STAT Pathway Activation in Myeloproliferative Neoplasm Pathogenesis”. Blood 123: e123-33.
Tumor necrosis factor-alpha suppresses adipocyte-specific genes and activates expression of preadipocyte genes in 3T3-L1 adipocytes: nuclear factor-kappaB activation by TNF-alpha is obligatory
Ruan, H., N. Hacohen, T. R. Golub, L. Van Parijs, and H. F. Lodish. 2002. “Tumor Necrosis Factor-Alpha Suppresses Adipocyte-Specific Genes and Activates Expression of Preadipocyte Genes in 3T3-L1 Adipocytes: Nuclear Factor-KappaB Activation by TNF-Alpha Is Obligatory”. Diabetes 51: 1319-36.
Tight coordination of protein translation and HSF1 activation supports the anabolic malignant state
Santagata, S., M. L. Mendillo, Y. C. Tang, A. Subramanian, C. C. Perley, S. P. Roche, B. Wong, et al. 2013. “Tight Coordination of Protein Translation and HSF1 Activation Supports the Anabolic Malignant State”. Science 341: 1238303.
A zebrafish bmyb mutation causes genome instability and increased cancer susceptibility
Shepard, J. L., J. F. Amatruda, H. M. Stern, A. Subramanian, D. Finkelstein, J. Ziai, K. R. Finley, et al. 2005. “A Zebrafish Bmyb Mutation Causes Genome Instability and Increased Cancer Susceptibility”. Proc Natl Acad Sci U S A 102: 13194-9.