Search Results - "Ford, Heide L."

Epithelial-Mesenchymal Transition in Cancer: Parallels Between Normal Development and Tumor Progression by Micalizzi, Douglas S, Farabaugh, Susan M, Ford, Heide L

“…From the earliest stages of embryonic development, cells of epithelial and mesenchymal origin contribute to the structure and function of developing organs…”
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Epithelial―Mesenchymal Transition and Tumor Suppression Are Controlled by a Reciprocal Feedback Loop between ZEB1 and Grainyhead-like-2 by CIEPLY, Benjamin, FARRIS, Joshua, DENVIR, James, FORD, Heide L, FRISCH, Steven M

“…Epithelial-mesenchymal transition (EMT) in carcinoma cells enhances malignant progression by promoting invasion and survival. EMT is induced by…”
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EMT cells increase breast cancer metastasis via paracrine GLI activation in neighbouring tumour cells by Neelakantan, Deepika, Zhou, Hengbo, Oliphant, Michael U. J., Zhang, Xiaomei, Simon, Lukas M., Henke, David M., Shaw, Chad A., Wu, Meng-Fen, Hilsenbeck, Susan G., White, Lisa D., Lewis, Michael T., Ford, Heide L.

“…Recent fate-mapping studies concluded that EMT is not required for metastasis of carcinomas. Here we challenge this conclusion by showing that these studies…”
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Eya3 partners with PP2A to induce c-Myc stabilization and tumor progression by Zhang, Lingdi, Zhou, Hengbo, Li, Xueni, Vartuli, Rebecca L, Rowse, Michael, Xing, Yongna, Rudra, Pratyaydipta, Ghosh, Debashis, Zhao, Rui, Ford, Heide L

“…Eya genes encode a unique family of multifunctional proteins that serve as transcriptional co-activators and as haloacid dehalogenase-family Tyr phosphatases…”
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Breast cancer epithelial-to-mesenchymal transition: examining the functional consequences of plasticity by Drasin, David J, Robin, Tyler P, Ford, Heide L

“…The epithelial-to-mesenchymal transition (EMT) is a critical developmental process that has recently come to the forefront of cancer biology. In breast…”
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Cellular Plasticity in Breast Cancer Progression and Therapy by Kong, Deguang, Hughes, Connor J, Ford, Heide L

“…With the exception of non-melanoma skin cancer, breast cancer is the most frequently diagnosed malignant disease among women, with the majority of mortality…”
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SIX1 and EWS/FLI1 co-regulate an anti-metastatic gene network in Ewing Sarcoma by Hughes, Connor J., Fields, Kaiah M., Danis, Etienne P., Hsu, Jessica Y., Neelakantan, Deepika, Vincent, Melanie Y., Gustafson, Annika L., Oliphant, Michael J., Sreekanth, Varsha, Zaberezhnyy, Vadym, Costello, James C., Jedlicka, Paul, Ford, Heide L.

“…Ewing sarcoma (ES), which is characterized by the presence of oncogenic fusion proteins such as EWS/FLI1, is an aggressive pediatric malignancy with a high…”
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Negative regulation of endothelin signaling by SIX1 is required for proper maxillary development by Tavares, Andre L P, Cox, Timothy C, Maxson, Robert M, Ford, Heide L, Clouthier, David E

“…Jaw morphogenesis is a complex event mediated by inductive signals that establish and maintain the distinct developmental domains required for formation of…”
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Homeoprotein Six2 promotes breast cancer metastasis via transcriptional and epigenetic control of E-cadherin expression by Wang, Chu-An, Drasin, David, Pham, Catherine, Jedlicka, Paul, Zaberezhnyy, Vadym, Guney, Michelle, Li, Howard, Nemenoff, Raphael, Costello, James C, Tan, Aik-Choon, Ford, Heide L

“…Misexpression of developmental transcription factors occurs often in human cancers, where embryonic programs may be reinstated in a context that promotes or…”
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Transcriptional Differences between Normal and Glioma-Derived Glial Progenitor Cells Identify a Core Set of Dysregulated Genes by Auvergne, Romane M., Sim, Fraser J., Wang, Su, Chandler-Militello, Devin, Burch, Jaclyn, Al Fanek, Yazan, Davis, Danielle, Benraiss, Abdellatif, Walter, Kevin, Achanta, Pragathi, Johnson, Mahlon, Quinones-Hinojosa, Alfredo, Natesan, Sridaran, Ford, Heide L., Goldman, Steven A.

“…Glial progenitor cells (GPCs) are a potential source of malignant gliomas. We used A2B5-based sorting to extract tumorigenic GPCs from human gliomas spanning…”
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Epithelial-mesenchymal transition in development and cancer by Micalizzi, Douglas S, Ford, Heide L

“…The epithelial-mesenchymal transition (EMT) is a critical developmental process from the earliest events of embryogenesis to later morphogenesis and organ…”
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The Six1 oncoprotein downregulates p53 via concomitant regulation of RPL26 and microRNA-27a-3p by Towers, Christina G., Guarnieri, Anna L., Micalizzi, Doug S., Harrell, J. Chuck, Gillen, Austin E., Kim, Jihye, Wang, Chu-An, Oliphant, Michael U.J., Drasin, David J., Guney, Michelle A., Kabos, Peter, Sartorius, Carol A., Tan, Aik-Choon, Perou, Charles M., Espinosa, Joaquin M., Ford, Heide L.

“…TP53 is mutated in 50% of all cancers, and its function is often compromised in cancers where it is not mutated. Here we demonstrate that the…”
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CD147: a small molecule transporter ancillary protein at the crossroad of multiple hallmarks of cancer and metabolic reprogramming by Kendrick, Agnieszka A, Schafer, Johnathon, Dzieciatkowska, Monika, Nemkov, Travis, D'Alessandro, Angelo, Neelakantan, Deepika, Ford, Heide L, Pearson, Chad G, Weekes, Colin D, Hansen, Kirk C, Eisenmesser, Elan Z

“…Increased expression of CD147 in pancreatic cancer has been proposed to play a critical role in cancer progression via CD147 chaperone function for lactate…”
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Expression of Six1 in luminal breast cancers predicts poor prognosis and promotes increases in tumor initiating cells by activation of extracellular signal-regulated kinase and transforming growth factor-beta signaling pathways by Iwanaga, Ritsuko, Wang, Chu-An, Micalizzi, Douglas S, Harrell, J Chuck, Jedlicka, Paul, Sartorius, Carol A, Kabos, Peter, Farabaugh, Susan M, Bradford, Andrew P, Ford, Heide L

“…Mammary-specific overexpression of Six1 in mice induces tumors that resemble human breast cancer, some having undergone epithelial to mesenchymal transition…”
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Author Correction: Eya3 partners with PP2A to induce c-Myc stabilization and tumor progression by Zhang, Lingdi, Zhou, Hengbo, Li, Xueni, Vartuli, Rebecca L., Rowse, Michael, Xing, Yongna, Rudra, Pratyaydipta, Ghosh, Debashis, Zhao, Rui, Ford, Heide L.

“…In the original version of this Article, the title of the legend to Fig. 7 incorrectly read ‘Knockdown of B55α increases breast cancer metastasis’ instead of…”
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A Mechanism of Cyclin D1 Action Encoded in the Patterns of Gene Expression in Human Cancer by Lamb, Justin, Ramaswamy, Sridhar, Ford, Heide L., Contreras, Bernardo, Martinez, Robert V., Kittrell, Frances S., Zahnow, Cynthia A., Patterson, Nick, Golub, Todd R., Ewen, Mark E.

“…Here we describe how patterns of gene expression in human tumors have been deconvoluted to reveal a mechanism of action for the cyclin D1 oncogene…”
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Remembering Hypoxia: Uncovering the Long-Term Effects of Transient Oxygen Deprivation on IFN Signaling and Progression of Breast Cancer by Purdy, Stephen Connor, Ford, Heide L

“…Hypoxia occurs in 90% of solid tumors and is strongly associated with an increased propensity for metastasis. Hypoxia induces tumor progression largely through…”
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Six1 Overexpression in Mammary Cells Induces Genomic Instability and Is Sufficient for Malignant Transformation by COLETTA, Ricardo D, CHRISTENSEN, Kimberly L, ALICALIZZI, Douglas S, JEDLICKA, Paul, VARELLA-GARCIA, Marileila, FORD, Heide L

“…Homeoproteins are transcription factors that act as master regulators of development and are frequently dysregulated in cancers. During embryogenesis, the Six1…”
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Publisher Correction: EMT cells increase breast cancer metastasis via paracrine GLI activation in neighbouring tumour cells by Neelakantan, Deepika, Zhou, Hengbo, Oliphant, Michael U. J., Zhang, Xiaomei, Simon, Lukas M., Henke, David M., Shaw, Chad A., Wu, Meng-Fen, Hilsenbeck, Susan G., White, Lisa D., Lewis, Michael T., Ford, Heide L.

“…This Article contains an error in Figure 2. In panel a, the second lane of the western blot should have been labelled ‘siNT’. A correct version of Figure 2a…”
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Biochemical and Functional Characterization of Six SIX1 Branchio-oto-renal Syndrome Mutations by Patrick, Aaron N., Schiemann, Barbara J., Yang, Kui, Zhao, Rui, Ford, Heide L.

“…Branchio-oto-renal syndrome (BOR) is an autosomal dominant developmental disorder characterized by hearing loss, branchial arch defects, and renal anomalies…”
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