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E G Van Meir - One of the best experts on this subject based on the ideXlab platform.
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frequent co alterations of tp53 p16 cdkn2a p14arf pten tumor suppressor genes in human Glioma Cell lines
Brain Pathology, 1999Co-Authors: Nobuaki Ishii, Mitsuhiro Tada, Annieclaire Diserens, Daniel Maier, Adrian Merlo, Yutaka Sawamura, E G Van MeirAbstract:In this study we established the simultaneous status of TP53, p16, p14ARF and PTEN tumor suppressor genes in 34 randomly chosen human Glioma Cell lines. Nine Cell lines (26.4%) harbored mutations or deletions in all four tumor suppressor genes and 22 Cell lines (64%) had alterations in at least three. Mutations/deletions were found at the following frequencies: TP53 (76.5%), p14ARF (64.7%), p16 (64.7%), PTEN (73.5%). Thus, there was a high incidence of alterations in the Cellular pathways involving the p53 transcription factor (94.1%), the retinoblastoma protein (64.7%) and the PTEN phosphatase (73.5%) and 91% of Cell lines carried mutations in two or more pathways. This provides the first clear genetic evidence that these tumor suppressors participate in biological pathways which are functioning separately/independently in Glioma Cells. The status of the gene alterations did not correlate with tumorigenicity in immunocompromized mice or any clinical parameters. Although the mutation rate was higher in Glioma Cell lines than that reported for Glioma tissues, the alterations were molecularly representative of those found in adult de novo glioblastoma. This study highlights the importance of developing therapeutic approaches applicable to tumors with a broad range of genetic alterations and also provides an invaluable panel of Glioma Cell lines to make this possible.
Nobuaki Ishii - One of the best experts on this subject based on the ideXlab platform.
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frequent co alterations of tp53 p16 cdkn2a p14arf pten tumor suppressor genes in human Glioma Cell lines
Brain Pathology, 1999Co-Authors: Nobuaki Ishii, Mitsuhiro Tada, Annieclaire Diserens, Daniel Maier, Adrian Merlo, Yutaka Sawamura, E G Van MeirAbstract:In this study we established the simultaneous status of TP53, p16, p14ARF and PTEN tumor suppressor genes in 34 randomly chosen human Glioma Cell lines. Nine Cell lines (26.4%) harbored mutations or deletions in all four tumor suppressor genes and 22 Cell lines (64%) had alterations in at least three. Mutations/deletions were found at the following frequencies: TP53 (76.5%), p14ARF (64.7%), p16 (64.7%), PTEN (73.5%). Thus, there was a high incidence of alterations in the Cellular pathways involving the p53 transcription factor (94.1%), the retinoblastoma protein (64.7%) and the PTEN phosphatase (73.5%) and 91% of Cell lines carried mutations in two or more pathways. This provides the first clear genetic evidence that these tumor suppressors participate in biological pathways which are functioning separately/independently in Glioma Cells. The status of the gene alterations did not correlate with tumorigenicity in immunocompromized mice or any clinical parameters. Although the mutation rate was higher in Glioma Cell lines than that reported for Glioma tissues, the alterations were molecularly representative of those found in adult de novo glioblastoma. This study highlights the importance of developing therapeutic approaches applicable to tumors with a broad range of genetic alterations and also provides an invaluable panel of Glioma Cell lines to make this possible.
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frequent co alterations of tp53 p16 cdkn2a p14arf pten tumor suppressor genes in human Glioma Cell lines
Brain Pathology, 1999Co-Authors: Nobuaki Ishii, Mitsuhiro Tada, Annieclaire Diserens, Daniel Maier, Adrian Merlo, Yutaka Sawamura, E G Van MeirAbstract:In this study we established the simultaneous status of TP53, p16, p14ARF and PTEN tumor suppressor genes in 34 randomly chosen human Glioma Cell lines. Nine Cell lines (26.4%) harbored mutations or deletions in all four tumor suppressor genes and 22 Cell lines (64%) had alterations in at least three. Mutations/deletions were found at the following frequencies: TP53 (76.5%), p14ARF (64.7%), p16 (64.7%), PTEN (73.5%). Thus, there was a high incidence of alterations in the Cellular pathways involving the p53 transcription factor (94.1%), the retinoblastoma protein (64.7%) and the PTEN phosphatase (73.5%) and 91% of Cell lines carried mutations in two or more pathways. This provides the first clear genetic evidence that these tumor suppressors participate in biological pathways which are functioning separately/independently in Glioma Cells. The status of the gene alterations did not correlate with tumorigenicity in immunocompromized mice or any clinical parameters. Although the mutation rate was higher in Glioma Cell lines than that reported for Glioma tissues, the alterations were molecularly representative of those found in adult de novo glioblastoma. This study highlights the importance of developing therapeutic approaches applicable to tumors with a broad range of genetic alterations and also provides an invaluable panel of Glioma Cell lines to make this possible.
Mitsuhiro Tada - One of the best experts on this subject based on the ideXlab platform.
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Mechanism of hyperploid Cell formation induced by microtubule inhibiting drug in Glioma Cell lines
Oncogene, 2001Co-Authors: Hiromasa Tsuiki, Masayuki Nitta, Mitsuhiro Tada, Masaki Inagaki, Yukitaka Ushio, Hideyuki SayaAbstract:Mechanism of hyperploid Cell formation induced by microtubule inhibiting drug in Glioma Cell lines
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frequent co alterations of tp53 p16 cdkn2a p14arf pten tumor suppressor genes in human Glioma Cell lines
Brain Pathology, 1999Co-Authors: Nobuaki Ishii, Mitsuhiro Tada, Annieclaire Diserens, Daniel Maier, Adrian Merlo, Yutaka Sawamura, E G Van MeirAbstract:In this study we established the simultaneous status of TP53, p16, p14ARF and PTEN tumor suppressor genes in 34 randomly chosen human Glioma Cell lines. Nine Cell lines (26.4%) harbored mutations or deletions in all four tumor suppressor genes and 22 Cell lines (64%) had alterations in at least three. Mutations/deletions were found at the following frequencies: TP53 (76.5%), p14ARF (64.7%), p16 (64.7%), PTEN (73.5%). Thus, there was a high incidence of alterations in the Cellular pathways involving the p53 transcription factor (94.1%), the retinoblastoma protein (64.7%) and the PTEN phosphatase (73.5%) and 91% of Cell lines carried mutations in two or more pathways. This provides the first clear genetic evidence that these tumor suppressors participate in biological pathways which are functioning separately/independently in Glioma Cells. The status of the gene alterations did not correlate with tumorigenicity in immunocompromized mice or any clinical parameters. Although the mutation rate was higher in Glioma Cell lines than that reported for Glioma tissues, the alterations were molecularly representative of those found in adult de novo glioblastoma. This study highlights the importance of developing therapeutic approaches applicable to tumors with a broad range of genetic alterations and also provides an invaluable panel of Glioma Cell lines to make this possible.
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frequent co alterations of tp53 p16 cdkn2a p14arf pten tumor suppressor genes in human Glioma Cell lines
Brain Pathology, 1999Co-Authors: Nobuaki Ishii, Mitsuhiro Tada, Annieclaire Diserens, Daniel Maier, Adrian Merlo, Yutaka Sawamura, E G Van MeirAbstract:In this study we established the simultaneous status of TP53, p16, p14ARF and PTEN tumor suppressor genes in 34 randomly chosen human Glioma Cell lines. Nine Cell lines (26.4%) harbored mutations or deletions in all four tumor suppressor genes and 22 Cell lines (64%) had alterations in at least three. Mutations/deletions were found at the following frequencies: TP53 (76.5%), p14ARF (64.7%), p16 (64.7%), PTEN (73.5%). Thus, there was a high incidence of alterations in the Cellular pathways involving the p53 transcription factor (94.1%), the retinoblastoma protein (64.7%) and the PTEN phosphatase (73.5%) and 91% of Cell lines carried mutations in two or more pathways. This provides the first clear genetic evidence that these tumor suppressors participate in biological pathways which are functioning separately/independently in Glioma Cells. The status of the gene alterations did not correlate with tumorigenicity in immunocompromized mice or any clinical parameters. Although the mutation rate was higher in Glioma Cell lines than that reported for Glioma tissues, the alterations were molecularly representative of those found in adult de novo glioblastoma. This study highlights the importance of developing therapeutic approaches applicable to tumors with a broad range of genetic alterations and also provides an invaluable panel of Glioma Cell lines to make this possible.
Annieclaire Diserens - One of the best experts on this subject based on the ideXlab platform.
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dna fingerprinting of Glioma Cell lines and considerations on similarity measurements
Neuro-oncology, 2012Co-Authors: Pierre Bady, Annieclaire Diserens, Vincent Castella, Stefanie Kalt, Karl Heinimann, Mariefrance Hamou, Mauro Delorenzi, Monika E HegiAbstract:Glioma Cell lines are an important tool for research in basic and translational neuro-oncology. Documentation of their genetic identity has become a requirement for scientific journals and grant applications to exclude cross-contamination and misidentification that lead to misinterpretation of results. Here, we report the standard 16 marker short tandem repeat (STR) DNA fingerprints for a panel of 39 widely used Glioma Cell lines as reference. Comparison of the fingerprints among themselves and with the large DSMZ database comprising 9 marker STRs for 2278 Cell lines uncovered 3 misidentified Cell lines and confirmed previously known cross-contaminations. Furthermore, 2 Glioma Cell lines exhibited identity scores of 0.8, which is proposed as the cutoff for detecting cross-contamination. Additional characteristics, comprising lack of a B-raf mutation in one line and a similarity score of 1 with the original tumor tissue in the other, excluded a cross-contamination. Subsequent simulation procedures suggested that, when using DNA fingerprints comprising only 9 STR markers, the commonly used similarity score of 0.8 is not sufficiently stringent to unambiguously differentiate the origin. DNA fingerprints are confounded by frequent genetic alterations in cancer Cell lines, particularly loss of heterozygosity, that reduce the informativeness of STR markers and, thereby, the overall power for distinction. The similarity score depends on the number of markers measured; thus, more markers or additional Cell line characteristics, such as information on specific mutations, may be necessary to clarify the origin.
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frequent co alterations of tp53 p16 cdkn2a p14arf pten tumor suppressor genes in human Glioma Cell lines
Brain Pathology, 1999Co-Authors: Nobuaki Ishii, Mitsuhiro Tada, Annieclaire Diserens, Daniel Maier, Adrian Merlo, Yutaka Sawamura, E G Van MeirAbstract:In this study we established the simultaneous status of TP53, p16, p14ARF and PTEN tumor suppressor genes in 34 randomly chosen human Glioma Cell lines. Nine Cell lines (26.4%) harbored mutations or deletions in all four tumor suppressor genes and 22 Cell lines (64%) had alterations in at least three. Mutations/deletions were found at the following frequencies: TP53 (76.5%), p14ARF (64.7%), p16 (64.7%), PTEN (73.5%). Thus, there was a high incidence of alterations in the Cellular pathways involving the p53 transcription factor (94.1%), the retinoblastoma protein (64.7%) and the PTEN phosphatase (73.5%) and 91% of Cell lines carried mutations in two or more pathways. This provides the first clear genetic evidence that these tumor suppressors participate in biological pathways which are functioning separately/independently in Glioma Cells. The status of the gene alterations did not correlate with tumorigenicity in immunocompromized mice or any clinical parameters. Although the mutation rate was higher in Glioma Cell lines than that reported for Glioma tissues, the alterations were molecularly representative of those found in adult de novo glioblastoma. This study highlights the importance of developing therapeutic approaches applicable to tumors with a broad range of genetic alterations and also provides an invaluable panel of Glioma Cell lines to make this possible.
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frequent co alterations of tp53 p16 cdkn2a p14arf pten tumor suppressor genes in human Glioma Cell lines
Brain Pathology, 1999Co-Authors: Nobuaki Ishii, Mitsuhiro Tada, Annieclaire Diserens, Daniel Maier, Adrian Merlo, Yutaka Sawamura, E G Van MeirAbstract:In this study we established the simultaneous status of TP53, p16, p14ARF and PTEN tumor suppressor genes in 34 randomly chosen human Glioma Cell lines. Nine Cell lines (26.4%) harbored mutations or deletions in all four tumor suppressor genes and 22 Cell lines (64%) had alterations in at least three. Mutations/deletions were found at the following frequencies: TP53 (76.5%), p14ARF (64.7%), p16 (64.7%), PTEN (73.5%). Thus, there was a high incidence of alterations in the Cellular pathways involving the p53 transcription factor (94.1%), the retinoblastoma protein (64.7%) and the PTEN phosphatase (73.5%) and 91% of Cell lines carried mutations in two or more pathways. This provides the first clear genetic evidence that these tumor suppressors participate in biological pathways which are functioning separately/independently in Glioma Cells. The status of the gene alterations did not correlate with tumorigenicity in immunocompromized mice or any clinical parameters. Although the mutation rate was higher in Glioma Cell lines than that reported for Glioma tissues, the alterations were molecularly representative of those found in adult de novo glioblastoma. This study highlights the importance of developing therapeutic approaches applicable to tumors with a broad range of genetic alterations and also provides an invaluable panel of Glioma Cell lines to make this possible.
E G Van Meir - One of the best experts on this subject based on the ideXlab platform.
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frequent co alterations of tp53 p16 cdkn2a p14arf pten tumor suppressor genes in human Glioma Cell lines
Brain Pathology, 1999Co-Authors: Nobuaki Ishii, Mitsuhiro Tada, Annieclaire Diserens, Daniel Maier, Adrian Merlo, Yutaka Sawamura, E G Van MeirAbstract:In this study we established the simultaneous status of TP53, p16, p14ARF and PTEN tumor suppressor genes in 34 randomly chosen human Glioma Cell lines. Nine Cell lines (26.4%) harbored mutations or deletions in all four tumor suppressor genes and 22 Cell lines (64%) had alterations in at least three. Mutations/deletions were found at the following frequencies: TP53 (76.5%), p14ARF (64.7%), p16 (64.7%), PTEN (73.5%). Thus, there was a high incidence of alterations in the Cellular pathways involving the p53 transcription factor (94.1%), the retinoblastoma protein (64.7%) and the PTEN phosphatase (73.5%) and 91% of Cell lines carried mutations in two or more pathways. This provides the first clear genetic evidence that these tumor suppressors participate in biological pathways which are functioning separately/independently in Glioma Cells. The status of the gene alterations did not correlate with tumorigenicity in immunocompromized mice or any clinical parameters. Although the mutation rate was higher in Glioma Cell lines than that reported for Glioma tissues, the alterations were molecularly representative of those found in adult de novo glioblastoma. This study highlights the importance of developing therapeutic approaches applicable to tumors with a broad range of genetic alterations and also provides an invaluable panel of Glioma Cell lines to make this possible.