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808 results on '"Vousden, Karen H."'

205. PHD1 regulates p53-mediated colorectal cancer chemoresistance.

Author

Deschoemaeker, Sofie, Di Conza, Giusy, Lilla, Sergio, Martín‐Pérez, Rosa, Mennerich, Daniela, Boon, Lise, Hendrikx, Stefanie, Maddocks, Oliver DK, Marx, Christian, Radhakrishnan, Praveen, Prenen, Hans, Schneider, Martin, Myllyharju, Johanna, Kietzmann, Thomas, Vousden, Karen H, Zanivan, Sara, and Mazzone, Massimiliano

Abstract

Overcoming resistance to chemotherapy is a major challenge in colorectal cancer ( CRC) treatment, especially since the underlying molecular mechanisms remain unclear. We show that silencing of the prolyl hydroxylase domain protein PHD1, but not PHD2 or PHD3, prevents p53 activation upon chemotherapy in different CRC cell lines, thereby inhibiting DNA repair and favoring cell death. Mechanistically, PHD1 activity reinforces p53 binding to p38α kinase in a hydroxylation-dependent manner. Following p53-p38α interaction and chemotherapeutic damage, p53 can be phosphorylated at serine 15 and thus activated. Active p53 allows nucleotide excision repair by interacting with the DNA helicase XPB, thereby protecting from chemotherapy-induced apoptosis. In accord with this observation, PHD1 knockdown greatly sensitizes CRC to 5- FU in mice. We propose that PHD1 is part of the resistance machinery in CRC, supporting rational drug design of PHD1-specific inhibitors and their use in combination with chemotherapy. [ABSTRACT FROM AUTHOR]

Published
2015
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206. Hitting cancers’ weak spots: vulnerabilities imposed by p53 mutation.

Author

Gurpinar, Evrim and Vousden, Karen H.

Subjects
*GENETIC mutation, *P53 protein, *CANCER invasiveness, *TUMOR growth, *CANCER treatment
Abstract

The tumor suppressor protein p53 plays a critical role in limiting malignant development and progression. Almost all cancers show loss of p53 function, through either mutation in the p53 gene itself or defects in the mechanisms that activate p53. While reactivation of p53 can effectively limit tumor growth, this is a difficult therapeutic goal to achieve in the many cancers that do not retain wild type p53. An alternative approach focuses on identifying vulnerabilities imposed on cancers by virtue of the loss of or alterations in p53, to identify additional pathways that can be targeted to specifically kill or inhibit the growth of p53 mutated cells. These indirect ways of exploiting mutations in p53 – which occur in more than half of all human cancers – provide numerous exciting therapeutic possibilities. [ABSTRACT FROM AUTHOR]

Published
2015
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210. HDM2 phosphorylation by MAPKAP kinase 2

Author

Weber, Hans Oliver, primary, Ludwig, Robert L, additional, Morrison, Deborah, additional, Kotlyarov, Alexey, additional, Gaestel, Matthias, additional, and Vousden, Karen H, additional

Published
2005
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216. Molecular mechanisms of cell death: recommendations of the Nomenclature Committee on Cell Death 2018

Author

Galluzzi, Lorenzo, Vitale, Ilio, Aaronson, Stuart A., Abrams, John M., Adam, Dieter, Agostinis, Patrizia, Alnemri, Emad S., Altucci, Lucia, Amelio, Ivano, Andrews, David W., Annicchiarico-Petruzzelli, Margherita, Antonov, Alexey V., Arama, Eli, Baehrecke, Eric H., Barlev, Nickolai A., Bazan, Nicolas G., Bernassola, Francesca, Bertrand, Mathieu J. M., Bianchi, Katiuscia, Blagosklonny, Mikhail V., Blomgren, Klas, Borner, Christoph, Boya, Patricia, Brenner, Catherine, Campanella, Michelangelo, Candi, Eleonora, Carmona-Gutierrez, Didac, Cecconi, Francesco, Chan, Francis K.-M., Chandel, Navdeep S., Cheng, Emily H., Chipuk, Jerry E., Cidlowski, John A., Ciechanover, Aaron, Cohen, Gerald M., Conrad, Marcus, Cubillos-Ruiz, Juan R., Czabotar, Peter E., D’Angiolella, Vincenzo, Dawson, Ted M., Dawson, Valina L., De Laurenzi, Vincenzo, De Maria, Ruggero, Debatin, Klaus-Michael, DeBerardinis, Ralph J., Deshmukh, Mohanish, Di Daniele, Nicola, Di Virgilio, Francesco, Dixit, Vishva M., Dixon, Scott J., Duckett, Colin S., Dynlacht, Brian D., El-Deiry, Wafik S., Elrod, John W., Fimia, Gian Maria, Fulda, Simone, García-Sáez, Ana J., Garg, Abhishek D., Garrido, Carmen, Gavathiotis, Evripidis, Golstein, Pierre, Gottlieb, Eyal, Green, Douglas R., Greene, Lloyd A., Gronemeyer, Hinrich, Gross, Atan, Hajnoczky, Gyorgy, Hardwick, J. Marie, Harris, Isaac S., Hengartner, Michael O., Hetz, Claudio, Ichijo, Hidenori, Jäättelä, Marja, Joseph, Bertrand, Jost, Philipp J., Juin, Philippe P., Kaiser, William J., Karin, Michael, Kaufmann, Thomas, Kepp, Oliver, Kimchi, Adi, Kitsis, Richard N., Klionsky, Daniel J., Knight, Richard A., Kumar, Sharad, Lee, Sam W., Lemasters, John J., Levine, Beth, Linkermann, Andreas, Lipton, Stuart A., Lockshin, Richard A., López-Otín, Carlos, Lowe, Scott W., Luedde, Tom, Lugli, Enrico, MacFarlane, Marion, Madeo, Frank, Malewicz, Michal, Malorni, Walter, Manic, Gwenola, Marine, Jean-Christophe, Martin, Seamus J., Martinou, Jean-Claude, Medema, Jan Paul, Mehlen, Patrick, Meier, Pascal, Melino, Sonia, Miao, Edward A., Molkentin, Jeffery D., Moll, Ute M., Muñoz-Pinedo, Cristina, Nagata, Shigekazu, Nuñez, Gabriel, Oberst, Andrew, Oren, Moshe, Overholtzer, Michael, Pagano, Michele, Panaretakis, Theocharis, Pasparakis, Manolis, Penninger, Josef M., Pereira, David M., Pervaiz, Shazib, Peter, Marcus E., Piacentini, Mauro, Pinton, Paolo, Prehn, Jochen H.M., Puthalakath, Hamsa, Rabinovich, Gabriel A., Rehm, Markus, Rizzuto, Rosario, Rodrigues, Cecilia M.P., Rubinsztein, David C., Rudel, Thomas, Ryan, Kevin M., Sayan, Emre, Scorrano, Luca, Shao, Feng, Shi, Yufang, Silke, John, Simon, Hans-Uwe, Sistigu, Antonella, Stockwell, Brent R., Strasser, Andreas, Szabadkai, Gyorgy, Tait, Stephen W.G., Tang, Daolin, Tavernarakis, Nektarios, Thorburn, Andrew, Tsujimoto, Yoshihide, Turk, Boris, Vanden Berghe, Tom, Vandenabeele, Peter, Vander Heiden, Matthew G., Villunger, Andreas, Virgin, Herbert W., Vousden, Karen H., Vucic, Domagoj, Wagner, Erwin F., Walczak, Henning, Wallach, David, Wang, Ying, Wells, James A., Wood, Will, Yuan, Junying, Zakeri, Zahra, Zhivotovsky, Boris, Zitvogel, Laurence, Melino, Gerry, and Kroemer, Guido

Abstract

Over the past decade, the Nomenclature Committee on Cell Death (NCCD) has formulated guidelines for the definition and interpretation of cell death from morphological, biochemical, and functional perspectives. Since the field continues to expand and novel mechanisms that orchestrate multiple cell death pathways are unveiled, we propose an updated classification of cell death subroutines focusing on mechanistic and essential (as opposed to correlative and dispensable) aspects of the process. As we provide molecularly oriented definitions of terms including intrinsic apoptosis, extrinsic apoptosis, mitochondrial permeability transition (MPT)-driven necrosis, necroptosis, ferroptosis, pyroptosis, parthanatos, entotic cell death, NETotic cell death, lysosome-dependent cell death, autophagy-dependent cell death, immunogenic cell death, cellular senescence, and mitotic catastrophe, we discuss the utility of neologisms that refer to highly specialized instances of these processes. The mission of the NCCD is to provide a widely accepted nomenclature on cell death in support of the continued development of the field.

Published
2018
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223. Phosphorylation of HDM2 by Akt

Author

Ashcroft, Margaret, primary, Ludwig, Robert L, additional, Woods, Douglas B, additional, Copeland, Terry D, additional, Weber, H Oliver, additional, MacRae, Elizabeth J, additional, and Vousden, Karen H, additional

Published
2002
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233. A common polymorphism acts as an intragenic modifier of mutant p53 behaviour

Author

Marin, Maria Carmen, primary, Jost, Christine A., additional, Brooks, Louise A., additional, Irwin, Meredith S., additional, O'Nions, Jenny, additional, Tidy, John A., additional, James, Nick, additional, McGregor, Jane M., additional, Harwood, Catherine A., additional, Yulug, Isik G., additional, Vousden, Karen H., additional, Allday, Martin J., additional, Gusterson, Barry, additional, Ikawa, Shuntaro, additional, Hinds, Philip W., additional, Crook, Tim, additional, and Kaelin, William G., additional

Published
2000
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237. Relation between infection with a subtype of HPV16 and cervical neoplasia

Author

Tidy, John A., Vousden, Karen H., and Farrell, Paul J.

Subjects
Cancer -- Causes of, Cervical cancer, Gene amplification -- Analysis, Medical screening -- Methods, Papillomaviruses -- Identification and classification, Papillomavirus infections -- Research, Polymerase chain reaction -- Research
Published
1989

238. Serine, but Not Glycine, Supports One-Carbon Metabolism and Proliferation of Cancer Cells.

Author

Labuschagne, Christiaan F., van den Broek, Niels J.F., Mackay, Gillian M., Vousden, Karen H., and Maddocks, Oliver D.K.

Abstract

Summary: Previous work has shown that some cancer cells are highly dependent on serine/glycine uptake for proliferation. Although serine and glycine can be interconverted and either might be used for nucleotide synthesis and one-carbon metabolism, we show that exogenous glycine cannot replace serine to support cancer cell proliferation. Cancer cells selectively consumed exogenous serine, which was converted to intracellular glycine and one-carbon units for building nucleotides. Restriction of exogenous glycine or depletion of the glycine cleavage system did not impede proliferation. In the absence of serine, uptake of exogenous glycine was unable to support nucleotide synthesis. Indeed, higher concentrations of glycine inhibited proliferation. Under these conditions, glycine was converted to serine, a reaction that would deplete the one-carbon pool. Providing one-carbon units by adding formate rescued nucleotide synthesis and growth of glycine-fed cells. We conclude that nucleotide synthesis and cancer cell proliferation are supported by serine—rather than glycine—consumption. [Copyright &y& Elsevier]

Published
2014
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239. Mutant p53 in Cancer: New Functions and Therapeutic Opportunities.

Author

Muller, Patricia?A.J. and Vousden, Karen?H.

Subjects
*GENETIC mutation, *P53 protein, *CANCER genetics, *METASTASIS, *TUMOR suppressor proteins, *EXPERIMENTAL therapeutics, *CANCER invasiveness
Abstract

Many different types of cancer show a high incidence of TP53 mutations, leading to the expression of mutant p53 proteins. There is growing evidence that these mutant p53s have both lost wild-type p53 tumor suppressor activity and gained functions that help to contribute to malignant progression. Understanding the functions of mutant p53 will help in the development of new therapeutic approaches that may be useful in a broad range of cancer types. [ABSTRACT FROM AUTHOR]

Published
2014
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