PubMed:14678959 JSONTXT

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    PubMed_Structured_Abstracts

    {"project":"PubMed_Structured_Abstracts","denotations":[{"id":"T1","span":{"begin":164,"end":311},"obj":"OBJECTIVE"},{"id":"T2","span":{"begin":333,"end":642},"obj":"METHODS"},{"id":"T3","span":{"begin":652,"end":1599},"obj":"RESULTS"},{"id":"T4","span":{"begin":1613,"end":1850},"obj":"CONCLUSIONS"}],"text":"Glutathione S-transferase pi amplification is associated with cisplatin resistance in head and neck squamous cell carcinoma cell lines and primary tumors.\nPURPOSE: The purpose is to evaluate the association of glutathione S-transferase pi (GST-pi) amplification and cisplatin resistance in head and neck cancer.\nEXPERIMENTAL DESIGN: An analysis of chromosomal abnormalities in 10 head and neck cancer cell lines by comparative genomic hybridization was performed. GST-pi amplification and expression were evaluated in head and neck cell lines and paraffin-embedded tissue by fluorescence in situ hybridization (FISH) and immunohistochemistry.\nRESULTS: Changes in the DNA copy number were seen in all 10 cell lines by comparative genomic hybridization. The most frequent chromosomal alterations were: gain at 3q; loss at 3p; gain at 8q; loss of 18q; gain at 20q; loss at 8p; and gain of 11q11-q13. Using FISH, 9 of 10 cell lines showed increased GST-pi copy number. GST-pi amplification was detected in 7 of 10 cell lines. Five were relatively cisplatin resistant, and 2 were relatively cisplatin sensitive (mean IC(50), 11.2 and 2.75 microM). Two relatively cisplatin-sensitive cell lines showed GST-pi gain and another relatively cisplatin-sensitive cell line had predominantly two copies of the gene. In 10 tumor specimens, 4 had two copies of GST-pi. All 4 had a complete response to neoadjuvant chemotherapy, 3 of whom are alive \u003e50 months from treatment compared with 2 patients showing GST-pi amplification. Neither responded to chemotherapy, and both died of disease \u003c9 months from diagnosis.\nCONCLUSIONS: Using FISH, GST-pi amplification is a common event in head and neck squamous cell carcinoma and may be associated with cisplatin resistance and poor clinical outcomes in head and neck cancer patients treated with cisplatin-based therapy."}

    PubmedHPO

    {"project":"PubmedHPO","denotations":[{"id":"T1","span":{"begin":304,"end":310},"obj":"HP_0002664"}],"text":"Glutathione S-transferase pi amplification is associated with cisplatin resistance in head and neck squamous cell carcinoma cell lines and primary tumors.\nPURPOSE: The purpose is to evaluate the association of glutathione S-transferase pi (GST-pi) amplification and cisplatin resistance in head and neck cancer.\nEXPERIMENTAL DESIGN: An analysis of chromosomal abnormalities in 10 head and neck cancer cell lines by comparative genomic hybridization was performed. GST-pi amplification and expression were evaluated in head and neck cell lines and paraffin-embedded tissue by fluorescence in situ hybridization (FISH) and immunohistochemistry.\nRESULTS: Changes in the DNA copy number were seen in all 10 cell lines by comparative genomic hybridization. The most frequent chromosomal alterations were: gain at 3q; loss at 3p; gain at 8q; loss of 18q; gain at 20q; loss at 8p; and gain of 11q11-q13. Using FISH, 9 of 10 cell lines showed increased GST-pi copy number. GST-pi amplification was detected in 7 of 10 cell lines. Five were relatively cisplatin resistant, and 2 were relatively cisplatin sensitive (mean IC(50), 11.2 and 2.75 microM). Two relatively cisplatin-sensitive cell lines showed GST-pi gain and another relatively cisplatin-sensitive cell line had predominantly two copies of the gene. In 10 tumor specimens, 4 had two copies of GST-pi. All 4 had a complete response to neoadjuvant chemotherapy, 3 of whom are alive \u003e50 months from treatment compared with 2 patients showing GST-pi amplification. Neither responded to chemotherapy, and both died of disease \u003c9 months from diagnosis.\nCONCLUSIONS: Using FISH, GST-pi amplification is a common event in head and neck squamous cell carcinoma and may be associated with cisplatin resistance and poor clinical outcomes in head and neck cancer patients treated with cisplatin-based therapy."}

    DisGeNET5_gene_disease

    {"project":"DisGeNET5_gene_disease","denotations":[{"id":"14678959-0#0#25#gene27306","span":{"begin":0,"end":25},"obj":"gene27306"},{"id":"14678959-0#86#123#diseaseC1168401","span":{"begin":86,"end":123},"obj":"diseaseC1168401"},{"id":"14678959-1#46#71#gene27306","span":{"begin":210,"end":235},"obj":"gene27306"},{"id":"14678959-1#126#146#diseaseC0278996","span":{"begin":290,"end":310},"obj":"diseaseC0278996"},{"id":"14678959-13#12#15#gene373156","span":{"begin":1625,"end":1628},"obj":"gene373156"},{"id":"14678959-13#12#15#gene133482","span":{"begin":1625,"end":1628},"obj":"gene133482"},{"id":"14678959-13#12#15#gene373156","span":{"begin":1625,"end":1628},"obj":"gene373156"},{"id":"14678959-13#12#15#gene133482","span":{"begin":1625,"end":1628},"obj":"gene133482"},{"id":"14678959-13#54#91#diseaseC1168401","span":{"begin":1667,"end":1704},"obj":"diseaseC1168401"},{"id":"14678959-13#170#190#diseaseC0278996","span":{"begin":1783,"end":1803},"obj":"diseaseC0278996"}],"relations":[{"id":"0#25#gene2730686#123#diseaseC1168401","pred":"associated_with","subj":"14678959-0#0#25#gene27306","obj":"14678959-0#86#123#diseaseC1168401"},{"id":"46#71#gene27306126#146#diseaseC0278996","pred":"associated_with","subj":"14678959-1#46#71#gene27306","obj":"14678959-1#126#146#diseaseC0278996"},{"id":"12#15#gene37315654#91#diseaseC1168401","pred":"associated_with","subj":"14678959-13#12#15#gene373156","obj":"14678959-13#54#91#diseaseC1168401"},{"id":"12#15#gene373156170#190#diseaseC0278996","pred":"associated_with","subj":"14678959-13#12#15#gene373156","obj":"14678959-13#170#190#diseaseC0278996"},{"id":"12#15#gene13348254#91#diseaseC1168401","pred":"associated_with","subj":"14678959-13#12#15#gene133482","obj":"14678959-13#54#91#diseaseC1168401"},{"id":"12#15#gene133482170#190#diseaseC0278996","pred":"associated_with","subj":"14678959-13#12#15#gene133482","obj":"14678959-13#170#190#diseaseC0278996"},{"id":"12#15#gene37315654#91#diseaseC1168401","pred":"associated_with","subj":"14678959-13#12#15#gene373156","obj":"14678959-13#54#91#diseaseC1168401"},{"id":"12#15#gene373156170#190#diseaseC0278996","pred":"associated_with","subj":"14678959-13#12#15#gene373156","obj":"14678959-13#170#190#diseaseC0278996"},{"id":"12#15#gene13348254#91#diseaseC1168401","pred":"associated_with","subj":"14678959-13#12#15#gene133482","obj":"14678959-13#54#91#diseaseC1168401"},{"id":"12#15#gene133482170#190#diseaseC0278996","pred":"associated_with","subj":"14678959-13#12#15#gene133482","obj":"14678959-13#170#190#diseaseC0278996"}],"text":"Glutathione S-transferase pi amplification is associated with cisplatin resistance in head and neck squamous cell carcinoma cell lines and primary tumors.\nPURPOSE: The purpose is to evaluate the association of glutathione S-transferase pi (GST-pi) amplification and cisplatin resistance in head and neck cancer.\nEXPERIMENTAL DESIGN: An analysis of chromosomal abnormalities in 10 head and neck cancer cell lines by comparative genomic hybridization was performed. GST-pi amplification and expression were evaluated in head and neck cell lines and paraffin-embedded tissue by fluorescence in situ hybridization (FISH) and immunohistochemistry.\nRESULTS: Changes in the DNA copy number were seen in all 10 cell lines by comparative genomic hybridization. The most frequent chromosomal alterations were: gain at 3q; loss at 3p; gain at 8q; loss of 18q; gain at 20q; loss at 8p; and gain of 11q11-q13. Using FISH, 9 of 10 cell lines showed increased GST-pi copy number. GST-pi amplification was detected in 7 of 10 cell lines. Five were relatively cisplatin resistant, and 2 were relatively cisplatin sensitive (mean IC(50), 11.2 and 2.75 microM). Two relatively cisplatin-sensitive cell lines showed GST-pi gain and another relatively cisplatin-sensitive cell line had predominantly two copies of the gene. In 10 tumor specimens, 4 had two copies of GST-pi. All 4 had a complete response to neoadjuvant chemotherapy, 3 of whom are alive \u003e50 months from treatment compared with 2 patients showing GST-pi amplification. Neither responded to chemotherapy, and both died of disease \u003c9 months from diagnosis.\nCONCLUSIONS: Using FISH, GST-pi amplification is a common event in head and neck squamous cell carcinoma and may be associated with cisplatin resistance and poor clinical outcomes in head and neck cancer patients treated with cisplatin-based therapy."}

    DisGeNET

    {"project":"DisGeNET","denotations":[{"id":"T0","span":{"begin":0,"end":25},"obj":"gene:27306"},{"id":"T1","span":{"begin":86,"end":123},"obj":"disease:C1168401"},{"id":"T2","span":{"begin":240,"end":243},"obj":"gene:373156"},{"id":"T3","span":{"begin":290,"end":310},"obj":"disease:C0278996"},{"id":"T4","span":{"begin":210,"end":235},"obj":"gene:27306"},{"id":"T5","span":{"begin":290,"end":310},"obj":"disease:C0278996"},{"id":"T6","span":{"begin":240,"end":243},"obj":"gene:133482"},{"id":"T7","span":{"begin":290,"end":310},"obj":"disease:C0278996"}],"relations":[{"id":"R1","pred":"associated_with","subj":"T0","obj":"T1"},{"id":"R2","pred":"associated_with","subj":"T2","obj":"T3"},{"id":"R3","pred":"associated_with","subj":"T4","obj":"T5"},{"id":"R4","pred":"associated_with","subj":"T6","obj":"T7"}],"namespaces":[{"prefix":"gene","uri":"http://www.ncbi.nlm.nih.gov/gene/"},{"prefix":"disease","uri":"http://purl.bioontology.org/ontology/MEDLINEPLUS/"}],"text":"Glutathione S-transferase pi amplification is associated with cisplatin resistance in head and neck squamous cell carcinoma cell lines and primary tumors.\nPURPOSE: The purpose is to evaluate the association of glutathione S-transferase pi (GST-pi) amplification and cisplatin resistance in head and neck cancer.\nEXPERIMENTAL DESIGN: An analysis of chromosomal abnormalities in 10 head and neck cancer cell lines by comparative genomic hybridization was performed. GST-pi amplification and expression were evaluated in head and neck cell lines and paraffin-embedded tissue by fluorescence in situ hybridization (FISH) and immunohistochemistry.\nRESULTS: Changes in the DNA copy number were seen in all 10 cell lines by comparative genomic hybridization. The most frequent chromosomal alterations were: gain at 3q; loss at 3p; gain at 8q; loss of 18q; gain at 20q; loss at 8p; and gain of 11q11-q13. Using FISH, 9 of 10 cell lines showed increased GST-pi copy number. GST-pi amplification was detected in 7 of 10 cell lines. Five were relatively cisplatin resistant, and 2 were relatively cisplatin sensitive (mean IC(50), 11.2 and 2.75 microM). Two relatively cisplatin-sensitive cell lines showed GST-pi gain and another relatively cisplatin-sensitive cell line had predominantly two copies of the gene. In 10 tumor specimens, 4 had two copies of GST-pi. All 4 had a complete response to neoadjuvant chemotherapy, 3 of whom are alive \u003e50 months from treatment compared with 2 patients showing GST-pi amplification. Neither responded to chemotherapy, and both died of disease \u003c9 months from diagnosis.\nCONCLUSIONS: Using FISH, GST-pi amplification is a common event in head and neck squamous cell carcinoma and may be associated with cisplatin resistance and poor clinical outcomes in head and neck cancer patients treated with cisplatin-based therapy."}