Detection of p53 gene mutations by single strand conformational polymorphism (SSCP) in human acute myeloid leukemia-derived cell lines
We have identified new mutations in the p53 gene in 3/11 growth factor-independent and in 2/8 growth factor-dependent human acute myeloid leukemia (AML)-derived cell lines by single-strand conformational polymorphism (SSCP) and sequencing analysis. MEG-01 had a triplet deletion at codon 304; F-36P,...
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| Veröffentlicht in: | Leukemia research 2002-02, Vol.26 (2), p.207-214 |
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| creator | Fleckenstein, Diana S Uphoff, Cord C Drexler, Hans G Quentmeier, Hilmar |
| description | We have identified new mutations in the p53 gene in 3/11 growth factor-independent and in 2/8 growth factor-dependent human acute myeloid leukemia (AML)-derived cell lines by single-strand conformational polymorphism (SSCP) and sequencing analysis. MEG-01 had a triplet deletion at codon 304; F-36P, NB-4 and MV4-11 showed point mutations at codon 344. F-36P had a second point mutation at codon 270 and NB-4 additionally at codon 319. M-MOK had a nucleotide substitution at codon 191. The frequency of p53 mutations in the cytokine-independent cell lines was comparable to that in the cytokine-dependent lines. These results suggest that loss of Wild type (wt) p53 is not the decisive event causing tumor cells to proliferate in vitro without externally added growth factors. |
| doi_str_mv | 10.1016/S0145-2126(01)00107-2 |
| format | Article |
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MEG-01 had a triplet deletion at codon 304; F-36P, NB-4 and MV4-11 showed point mutations at codon 344. F-36P had a second point mutation at codon 270 and NB-4 additionally at codon 319. M-MOK had a nucleotide substitution at codon 191. The frequency of p53 mutations in the cytokine-independent cell lines was comparable to that in the cytokine-dependent lines. These results suggest that loss of Wild type (wt) p53 is not the decisive event causing tumor cells to proliferate in vitro without externally added growth factors.</description><identifier>ISSN: 0145-2126</identifier><identifier>EISSN: 1873-5835</identifier><identifier>DOI: 10.1016/S0145-2126(01)00107-2</identifier><identifier>PMID: 11755471</identifier><identifier>CODEN: LEREDD</identifier><language>eng</language><publisher>Oxford: Elsevier Ltd</publisher><subject>Acute Disease ; Biological and medical sciences ; Blotting, Western ; Cell Division - drug effects ; Codon - genetics ; DNA Mutational Analysis ; DNA, Neoplasm - genetics ; Genes, p53 ; Granulocyte Colony-Stimulating Factor - pharmacology ; Granulocyte-Macrophage Colony-Stimulating Factor - pharmacology ; Hematologic and hematopoietic diseases ; Humans ; Interleukin-3 - pharmacology ; Leukemia, Myeloid - genetics ; Leukemia, Myeloid - pathology ; Leukemias. Malignant lymphomas. Malignant reticulosis. Myelofibrosis ; Medical sciences ; p53 Mutation detection ; Point Mutation ; Polymorphism, Single-Stranded Conformational ; Reverse Transcriptase Polymerase Chain Reaction ; RNA, Messenger - biosynthesis ; RNA, Messenger - genetics ; RNA, Neoplasm - biosynthesis ; RNA, Neoplasm - genetics ; Sequence Deletion ; Sequencing analysis ; Single strand conformational polymorphism ; Tumor Cells, Cultured - chemistry ; Tumor Cells, Cultured - drug effects ; Tumor Suppressor Protein p53 - physiology</subject><ispartof>Leukemia research, 2002-02, Vol.26 (2), p.207-214</ispartof><rights>2002 Elsevier Science Ltd</rights><rights>2002 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c422t-f2e039446c9d67c21a640920b0610bcdfd7ebfec36464fb38681621cbed3b8843</citedby><cites>FETCH-LOGICAL-c422t-f2e039446c9d67c21a640920b0610bcdfd7ebfec36464fb38681621cbed3b8843</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/S0145-2126(01)00107-2$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,780,784,3550,27924,27925,45995</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=13439337$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/11755471$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Fleckenstein, Diana S</creatorcontrib><creatorcontrib>Uphoff, Cord C</creatorcontrib><creatorcontrib>Drexler, Hans G</creatorcontrib><creatorcontrib>Quentmeier, Hilmar</creatorcontrib><title>Detection of p53 gene mutations by single strand conformational polymorphism (SSCP) in human acute myeloid leukemia-derived cell lines</title><title>Leukemia research</title><addtitle>Leuk Res</addtitle><description>We have identified new mutations in the p53 gene in 3/11 growth factor-independent and in 2/8 growth factor-dependent human acute myeloid leukemia (AML)-derived cell lines by single-strand conformational polymorphism (SSCP) and sequencing analysis. MEG-01 had a triplet deletion at codon 304; F-36P, NB-4 and MV4-11 showed point mutations at codon 344. F-36P had a second point mutation at codon 270 and NB-4 additionally at codon 319. M-MOK had a nucleotide substitution at codon 191. The frequency of p53 mutations in the cytokine-independent cell lines was comparable to that in the cytokine-dependent lines. These results suggest that loss of Wild type (wt) p53 is not the decisive event causing tumor cells to proliferate in vitro without externally added growth factors.</description><subject>Acute Disease</subject><subject>Biological and medical sciences</subject><subject>Blotting, Western</subject><subject>Cell Division - drug effects</subject><subject>Codon - genetics</subject><subject>DNA Mutational Analysis</subject><subject>DNA, Neoplasm - genetics</subject><subject>Genes, p53</subject><subject>Granulocyte Colony-Stimulating Factor - pharmacology</subject><subject>Granulocyte-Macrophage Colony-Stimulating Factor - pharmacology</subject><subject>Hematologic and hematopoietic diseases</subject><subject>Humans</subject><subject>Interleukin-3 - pharmacology</subject><subject>Leukemia, Myeloid - genetics</subject><subject>Leukemia, Myeloid - pathology</subject><subject>Leukemias. Malignant lymphomas. Malignant reticulosis. Myelofibrosis</subject><subject>Medical sciences</subject><subject>p53 Mutation detection</subject><subject>Point Mutation</subject><subject>Polymorphism, Single-Stranded Conformational</subject><subject>Reverse Transcriptase Polymerase Chain Reaction</subject><subject>RNA, Messenger - biosynthesis</subject><subject>RNA, Messenger - genetics</subject><subject>RNA, Neoplasm - biosynthesis</subject><subject>RNA, Neoplasm - genetics</subject><subject>Sequence Deletion</subject><subject>Sequencing analysis</subject><subject>Single strand conformational polymorphism</subject><subject>Tumor Cells, Cultured - chemistry</subject><subject>Tumor Cells, Cultured - drug effects</subject><subject>Tumor Suppressor Protein p53 - physiology</subject><issn>0145-2126</issn><issn>1873-5835</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2002</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkctu1DAUhi0EokPhEUDegNpFwPckK4SGq1QJpIG15dgnrcGxUzupNC_Ac5PMjOiy8sKS_Z1zfp0PoZeUvKWEqnc7QoWsGGXqgtBLQiipK_YIbWhT80o2XD5Gm__IGXpWym9CiGxp-xSdUVpLKWq6QX8_wgR28ini1ONRcnwNEfAwT2Z9LLjb4-LjdQBcpmyiwzbFPuXh8G0CHlPYDymPN74M-GK32_64xD7im3kwERs7T0uzPYTkHQ4w_4HBm8pB9newtIIQcPARynP0pDehwIvTfY5-ff70c_u1uvr-5dv2w1VlBWNT1TMgvBVC2dap2jJqlCAtIx1RlHTW9a6GrgfLlVCi73ijGqoYtR043jWN4OfozbHvmNPtDGXSgy9rDBMhzUXXlEspm_ZBkDZsPfUCyiNocyolQ6_H7AeT95oSvZrSB1N61aAJ1QdTmi11r04D5m4Ad191UrMAr0-AKdaEflm-9eWe44K3nK8B3h85WPZ25yHrYj1EC87nxax2yT8Q5R-Y57DX</recordid><startdate>20020201</startdate><enddate>20020201</enddate><creator>Fleckenstein, Diana S</creator><creator>Uphoff, Cord C</creator><creator>Drexler, Hans G</creator><creator>Quentmeier, Hilmar</creator><general>Elsevier Ltd</general><general>Elsevier Science</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7TO</scope><scope>H94</scope><scope>7X8</scope></search><sort><creationdate>20020201</creationdate><title>Detection of p53 gene mutations by single strand conformational polymorphism (SSCP) in human acute myeloid leukemia-derived cell lines</title><author>Fleckenstein, Diana S ; Uphoff, Cord C ; Drexler, Hans G ; Quentmeier, Hilmar</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c422t-f2e039446c9d67c21a640920b0610bcdfd7ebfec36464fb38681621cbed3b8843</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2002</creationdate><topic>Acute Disease</topic><topic>Biological and medical sciences</topic><topic>Blotting, Western</topic><topic>Cell Division - drug effects</topic><topic>Codon - genetics</topic><topic>DNA Mutational Analysis</topic><topic>DNA, Neoplasm - genetics</topic><topic>Genes, p53</topic><topic>Granulocyte Colony-Stimulating Factor - pharmacology</topic><topic>Granulocyte-Macrophage Colony-Stimulating Factor - pharmacology</topic><topic>Hematologic and hematopoietic diseases</topic><topic>Humans</topic><topic>Interleukin-3 - pharmacology</topic><topic>Leukemia, Myeloid - genetics</topic><topic>Leukemia, Myeloid - pathology</topic><topic>Leukemias. Malignant lymphomas. Malignant reticulosis. Myelofibrosis</topic><topic>Medical sciences</topic><topic>p53 Mutation detection</topic><topic>Point Mutation</topic><topic>Polymorphism, Single-Stranded Conformational</topic><topic>Reverse Transcriptase Polymerase Chain Reaction</topic><topic>RNA, Messenger - biosynthesis</topic><topic>RNA, Messenger - genetics</topic><topic>RNA, Neoplasm - biosynthesis</topic><topic>RNA, Neoplasm - genetics</topic><topic>Sequence Deletion</topic><topic>Sequencing analysis</topic><topic>Single strand conformational polymorphism</topic><topic>Tumor Cells, Cultured - chemistry</topic><topic>Tumor Cells, Cultured - drug effects</topic><topic>Tumor Suppressor Protein p53 - physiology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Fleckenstein, Diana S</creatorcontrib><creatorcontrib>Uphoff, Cord C</creatorcontrib><creatorcontrib>Drexler, Hans G</creatorcontrib><creatorcontrib>Quentmeier, Hilmar</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Leukemia research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Fleckenstein, Diana S</au><au>Uphoff, Cord C</au><au>Drexler, Hans G</au><au>Quentmeier, Hilmar</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Detection of p53 gene mutations by single strand conformational polymorphism (SSCP) in human acute myeloid leukemia-derived cell lines</atitle><jtitle>Leukemia research</jtitle><addtitle>Leuk Res</addtitle><date>2002-02-01</date><risdate>2002</risdate><volume>26</volume><issue>2</issue><spage>207</spage><epage>214</epage><pages>207-214</pages><issn>0145-2126</issn><eissn>1873-5835</eissn><coden>LEREDD</coden><abstract>We have identified new mutations in the p53 gene in 3/11 growth factor-independent and in 2/8 growth factor-dependent human acute myeloid leukemia (AML)-derived cell lines by single-strand conformational polymorphism (SSCP) and sequencing analysis. MEG-01 had a triplet deletion at codon 304; F-36P, NB-4 and MV4-11 showed point mutations at codon 344. F-36P had a second point mutation at codon 270 and NB-4 additionally at codon 319. M-MOK had a nucleotide substitution at codon 191. The frequency of p53 mutations in the cytokine-independent cell lines was comparable to that in the cytokine-dependent lines. These results suggest that loss of Wild type (wt) p53 is not the decisive event causing tumor cells to proliferate in vitro without externally added growth factors.</abstract><cop>Oxford</cop><pub>Elsevier Ltd</pub><pmid>11755471</pmid><doi>10.1016/S0145-2126(01)00107-2</doi><tpages>8</tpages></addata></record> |
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| subjects | Acute Disease Biological and medical sciences Blotting, Western Cell Division - drug effects Codon - genetics DNA Mutational Analysis DNA, Neoplasm - genetics Genes, p53 Granulocyte Colony-Stimulating Factor - pharmacology Granulocyte-Macrophage Colony-Stimulating Factor - pharmacology Hematologic and hematopoietic diseases Humans Interleukin-3 - pharmacology Leukemia, Myeloid - genetics Leukemia, Myeloid - pathology Leukemias. Malignant lymphomas. Malignant reticulosis. Myelofibrosis Medical sciences p53 Mutation detection Point Mutation Polymorphism, Single-Stranded Conformational Reverse Transcriptase Polymerase Chain Reaction RNA, Messenger - biosynthesis RNA, Messenger - genetics RNA, Neoplasm - biosynthesis RNA, Neoplasm - genetics Sequence Deletion Sequencing analysis Single strand conformational polymorphism Tumor Cells, Cultured - chemistry Tumor Cells, Cultured - drug effects Tumor Suppressor Protein p53 - physiology |
| title | Detection of p53 gene mutations by single strand conformational polymorphism (SSCP) in human acute myeloid leukemia-derived cell lines |
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