Search

Your search keyword '"Slebos, Robert J.C."' showing total 10 results
Start Over Author "Slebos, Robert J.C."
10 results on '"Slebos, Robert J.C."'

1. Integrated Proteomic and Glycoproteomic Characterization of Human High-Grade Serous Ovarian Carcinoma

Author

Pandey, Akhilesh, Paulovich, Amanda, Hoofnagle, Andrew, Zhang, Bing, Mani, D.R., Liebler, Daniel C., Ransohoff, David F., Fenyo, David, Tabb, David L., Levine, Douglas A., Kuhn, Eric, White, Forest M., Whiteley, Gordon A., Zhu, Heng, Shih, Ie-Ming, Bavarva, Jasmin, McDermott, Jason E., Whiteaker, Jeffrey, Ketchum, Karen A., Clauser, Karl R., Ruggles, Kelly, Elburn, Kimberly, Ding, Li, Hannick, Linda, Zimmerman, Lisa J., Watson, Mark, Thiagarajan, Mathangi, Ellis, Matthew J.C., Oberti, Mauricio, Mesri, Mehdi, Sanders, Melinda E., Borucki, Melissa, Gillette, Michael A., Snyder, Michael, Edwards, Nathan J., Vatanian, Negin, Rudnick, Paul A., McGarvey, Peter B., Mertins, Philip, Townsend, R. Reid, Thangudu, Ratna R., Smith, Richard D., Rivers, Robert C., Slebos, Robert J.C., Payne, Samuel H., Davies, Sherri R., Cai, Shuang, Stein, Stephen E., Carr, Steven A., Skates, Steven J., Madhavan, Subha, Liu, Tao, Chen, Xian, Zhao, Yingming, Wang, Yue, Shi, Zhiao, Hu, Yingwei, Pan, Jianbo, Shah, Punit, Ao, Minghui, Thomas, Stefani N., Liu, Yang, Chen, Lijun, Schnaubelt, Michael, Clark, David J., Rodriguez, Henry, Boja, Emily S., Hiltke, Tara, Kinsinger, Christopher R., Rodland, Karin D., Li, Qing Kay, Qian, Jiang, Zhang, Zhen, Chan, Daniel W., and Zhang, Hui

Published
2020
Full Text
View/download PDF

2. Integrated Proteomic and Glycoproteomic Characterization of Human High-Grade Serous Ovarian Carcinoma

Author

Hu, Yingwei, primary, Pan, Jianbo, additional, Shah, Punit, additional, Ao, Minghui, additional, Thomas, Stefani N., additional, Liu, Yang, additional, Chen, Lijun, additional, Schnaubelt, Michael, additional, Clark, David J., additional, Rodriguez, Henry, additional, Boja, Emily S., additional, Hiltke, Tara, additional, Kinsinger, Christopher R., additional, Rodland, Karin D., additional, Li, Qing Kay, additional, Qian, Jiang, additional, Zhang, Zhen, additional, Chan, Daniel W., additional, Zhang, Hui, additional, Pandey, Akhilesh, additional, Paulovich, Amanda, additional, Hoofnagle, Andrew, additional, Zhang, Bing, additional, Mani, D.R., additional, Liebler, Daniel C., additional, Ransohoff, David F., additional, Fenyo, David, additional, Tabb, David L., additional, Levine, Douglas A., additional, Kuhn, Eric, additional, White, Forest M., additional, Whiteley, Gordon A., additional, Zhu, Heng, additional, Shih, Ie-Ming, additional, Bavarva, Jasmin, additional, McDermott, Jason E., additional, Whiteaker, Jeffrey, additional, Ketchum, Karen A., additional, Clauser, Karl R., additional, Ruggles, Kelly, additional, Elburn, Kimberly, additional, Ding, Li, additional, Hannick, Linda, additional, Zimmerman, Lisa J., additional, Watson, Mark, additional, Thiagarajan, Mathangi, additional, Ellis, Matthew J.C., additional, Oberti, Mauricio, additional, Mesri, Mehdi, additional, Sanders, Melinda E., additional, Borucki, Melissa, additional, Gillette, Michael A., additional, Snyder, Michael, additional, Edwards, Nathan J., additional, Vatanian, Negin, additional, Rudnick, Paul A., additional, McGarvey, Peter B., additional, Mertins, Philip, additional, Townsend, R. Reid, additional, Thangudu, Ratna R., additional, Smith, Richard D., additional, Rivers, Robert C., additional, Slebos, Robert J.C., additional, Payne, Samuel H., additional, Davies, Sherri R., additional, Cai, Shuang, additional, Stein, Stephen E., additional, Carr, Steven A., additional, Skates, Steven J., additional, Madhavan, Subha, additional, Liu, Tao, additional, Chen, Xian, additional, Zhao, Yingming, additional, Wang, Yue, additional, and Shi, Zhiao, additional

Published
2020
Full Text
View/download PDF

3. K-ras oncogene activation as a prognostic marker in adenocarcinoma of the lung

Author

Slebos, Robert J.C., Kibbelaar, Robert E., Dalesio, Otilia, Kooistra, Anko, Stam, Jacob, Meijer, Chris J.L.M., Wagenaar, Sjoerd S., Vanderschueren, Ronald G.J.R.A., van Zandwijk, Nico, Mooi, Wolter J., Bos, Johannes L., and Rodenhuis, Sjoerd

Subjects
Oncogenes -- Abnormalities, Ras genes -- Physiological aspects, Adenocarcinoma -- Causes of, Adenocarcinoma -- Prognosis, DNA damage -- Physiological aspects, Cancer -- Genetic aspects
Abstract

Oncogenes are genes in human cells which, when activated, may be related to the development of cancer. Understanding of the malignant transformation of cells has been greatly advanced in recent years by the recognition that the cancer-causing genes found in some viruses have counterparts in normal cells. A number of such oncogenes have been described, and it is believed that at least in some cases the transformation of a normal cell into a malignant cell results from a mutation in one of these oncogenes. One such family of oncogenes is the ras gene. There are three main subgroups, H-ras, K-ras, and N-ras, all of which encode a protein with a molecular weight of 21 kilodaltons. Tissues removed from 69 patients with adenocarcinoma of the lung were tested for the activation of one site in the ras oncogene by a specific mutation at one location (codon 12). A mutation at this site has been previously found in approximately one third of lung adenocarcinomas. By amplifying the quantity of DNA available, specific DNA segments that included the K-ras oncogene site could be measured from 69 adenocarcinoma patients. Nineteen of these patients were found to have tumors that had a single mutation in the K-ras oncogene. The presence of this mutation was a highly unfavorable sign. Twelve of the 19 died during the follow-up period, compared with 16 out of 50 patients who did not have a mutation of the K-ras oncogene. Patients without the mutation also had a longer period when they were free of disease following their original surgery. The results show that the presence of a mutation to the K-ras oncogene, despite radical surgery and only small original tumors, is associated with a very poor prognosis. (Consumer Summary produced by Reliance Medical Information, Inc.)

Published
1990

4. The ras oncogenes in human lung cancer

Author

Rodenhuis, Sjoerd and Slebos, Robert J.C.

Subjects
Lung cancer -- Causes of, Lung cancer -- Development and progression, Lung cancer -- Genetic aspects, Ras genes -- Physiological aspects, Tumors -- Genetic aspects, Oncogenes -- Physiological aspects, Health
Abstract

Genes that have the potential for causing cancer are called oncogenes. The proteins produced by oncogenes have the ability to alter or transform the growth pattern of normal cells so that they grow abnormally. Oncogenes come from proto-oncogenes. Proto-oncogenes are normal genes that produce proteins that are important in regulating cell growth and gene expression. A proto-oncogene can be activated and can acquire the ability to transform a normal cell into a cancer cell through several different genetic alterations. These possible alterations include gene amplification (altered gene replication resulting in an increase in the number of copies of a particular gene), chromosomal translocation (the transfer of a gene to a different chromosome, where it does not belong), and point mutation (a change in a single amino acid that alters the protein). The common mechanism of activation for the ras family of oncogenes involves a point mutation. Three ras genes associated with human cancer have been identified; they are Harvey-ras (H-ras), Kirsten-ras (K-ras) and N-ras. These ras proteins become capable of transforming a normal cell into a cancer cell when a single amino acid, located at a critical spot in the protein, is replaced by a different amino acid. The altered ras protein interacts with and permanently activates a cell membrane protein that stimulates cell growth. When this happens, the cells are no longer able to regulate their growth pattern and begin to from a tumor. In animal studies, K-ras mutations have been associated with lung adenocarcinoma. K-ras was activated by point mutations caused by benzo(a)pyrene (a component of cigarette smoke). Also, K-ras mutations have been identified in human lung adenocarcinomas. The association of specific ras proteins with specific types of cancer, such as K-ras with lung adenocarcinoma, will provide a means for the classification of malignant diseases. (Consumer Summary produced by Reliance Medical Information, Inc.)

Published
1990

8. K-rasOncogene Activation as a Prognostic Marker in Adenocarcinoma of the Lung

Author

Slebos, Robert J.C., primary, Kibbelaar, Robert E., additional, Dalesio, Otilia, additional, Kooistra, Anko, additional, Stam, Jacob, additional, Meijer, Chris J.L.M., additional, Wagenaar, Sjoerd S., additional, Vanderschueren, Ronald G.J.R.A., additional, van Zandwijk, Nico, additional, Mooi, Wolter J., additional, Bos, Johannes L., additional, and Rodenhuis, Sjoerd, additional

Published
1990
Full Text
View/download PDF

9. A Rapid and Simple Procedure for the Routine Detection of rasPoint Mutations in FormalinFixed ParaffinEmbedded Tissues

Author

Slebos, Robert J.C., Boerrigter, Lucie, Evers, Siegina G., Wisman, Peter, Mooi, Wolter J., and Rodenhuis, Sjoerd

Abstract

The use of the polymerase chain reaction (PCR) to detect specific DNA sequences in small amounts of tissues or cells has become a widespread tool in the field of molecular biology. With the better understanding of the clinical significance of oncogene activations in human tumors, the application of PCR in a routine setting is rapidly gaining importance. We have developed a rapid and simple procedure for the detection of mutated rasoncogenes in routinely fixed, paraffin-embedded tissue samples. DNA is isolated from three 10 μm tissue sections by incubation with a nonionic detergent and proteinase K, and can be directly used for amplification by PCR. The amplified DNA fragments are then dot-blotted onto nylon membranes and are hybridized to radioactively labeled oligodeoxynucleotides, specific for each of the mutated rassequences. After a selective washing procedure, only fully matched oligodeoxynucleotides remain bound to the membrane, thus revealing the nature of the sequences that were present in the starting material. With this method, the detection of point mutations in rasgenes can be performed in a routine setting, and the results of the analyses can be available in as few as 3–4 days.

Published
1992

Catalog

Books, media, physical & digital resources
See catalog results