Development of interferon-α resistant subline from human chronic myelogenous leukemia cell line KT-1
Interferon-alpha (IFN-alpha) is one of the most effective therapeutic agents for a number of hematological malignancies, including chronic myelogenous leukemia (CML). Nevertheless, its efficacy is limited because of the development of resistance to IFN-alpha therapy. Previously, we established the n...
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| Veröffentlicht in: | Internal medicine (Tokyo, 1992) 1992), 2001-07, Vol.40 (7), p.607-612 |
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| container_title | Internal medicine (Tokyo, 1992) |
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| creator | YAMAUCHI, Hayato SAKAI, Ikuya NARUMI, Hirosi TAKEUCHI, Kazuto SOGA, Shinji FUJITA, Shigeru |
| description | Interferon-alpha (IFN-alpha) is one of the most effective therapeutic agents for a number of hematological malignancies, including chronic myelogenous leukemia (CML). Nevertheless, its efficacy is limited because of the development of resistance to IFN-alpha therapy. Previously, we established the novel human CML cell line KT-1, which is sensitive to the antiproliferative effects of IFN-alpha. Here, we report the establishment of an IFN-alpha-resistant subline, KT-1/A3R alpha 1000, by culturing KT-1/A3 cells (IFN-alpha-sensitive subline of KT-1) with increasing concentrations of IFN-alpha, in order to analyze the mechanism of acquisition of IFN-alpha resistance in CML cells after IFN-alpha therapy.
We developed an IFN-alpha-resistant tumor cell variant, KT-1/A3R alpha 1000, from the KT-1/A3 cell line by culturing cells with increasing concentrations of IFN-alpha. This subline was examined for its ability to proliferate and its resistance to apoptosis in high concentrations of IFN-alpha. The induction of the ISGF3 complex in response to IFN-alpha alpha in KT-1/A3R alpha 1000 was compared with that in the parental cell.
The levels of interferon-stimulated gene factor 3 components (STAT1, STAT2, and p48) proteins and STAT2 tyrosine phosphorylation induced after IFN-alpha treatment were unchanged, but formation of the ISGF3 complex was remarkably reduced in KT-1/A3R alpha 1000 cells compared to parental cells.
The KT-1/A3R alpha 1000 subline is a useful model for studying the mechanism of IFN-alpha resistance after IFN-alpha therapy. |
| doi_str_mv | 10.2169/internalmedicine.40.607 |
| format | Article |
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We developed an IFN-alpha-resistant tumor cell variant, KT-1/A3R alpha 1000, from the KT-1/A3 cell line by culturing cells with increasing concentrations of IFN-alpha. This subline was examined for its ability to proliferate and its resistance to apoptosis in high concentrations of IFN-alpha. The induction of the ISGF3 complex in response to IFN-alpha alpha in KT-1/A3R alpha 1000 was compared with that in the parental cell.
The levels of interferon-stimulated gene factor 3 components (STAT1, STAT2, and p48) proteins and STAT2 tyrosine phosphorylation induced after IFN-alpha treatment were unchanged, but formation of the ISGF3 complex was remarkably reduced in KT-1/A3R alpha 1000 cells compared to parental cells.
The KT-1/A3R alpha 1000 subline is a useful model for studying the mechanism of IFN-alpha resistance after IFN-alpha therapy.</description><identifier>ISSN: 0918-2918</identifier><identifier>EISSN: 1349-7235</identifier><identifier>DOI: 10.2169/internalmedicine.40.607</identifier><identifier>PMID: 11506301</identifier><language>eng</language><publisher>Tokyo: Japanese Society of Internal Medicine</publisher><subject>Antineoplastic agents ; Antineoplastic Agents - therapeutic use ; Apoptosis - drug effects ; Biological and medical sciences ; Cell Line, Transformed - drug effects ; Chemotherapy ; Drug Resistance, Neoplasm - genetics ; Electrophoresis, Polyacrylamide Gel ; Humans ; Interferon-alpha - therapeutic use ; Leukemia, Myelogenous, Chronic, BCR-ABL Positive - drug therapy ; Leukemia, Myelogenous, Chronic, BCR-ABL Positive - metabolism ; Medical sciences ; Pharmacology. Drug treatments ; Phosphorylation ; Tyrosine - metabolism</subject><ispartof>Internal medicine (Tokyo, 1992), 2001-07, Vol.40 (7), p.607-612</ispartof><rights>2002 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c535t-3e99b57a955636ae98fa506811c7768e320203a3717dd03ca481147b09c91883</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,777,781,27905,27906</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=14144545$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/11506301$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>YAMAUCHI, Hayato</creatorcontrib><creatorcontrib>SAKAI, Ikuya</creatorcontrib><creatorcontrib>NARUMI, Hirosi</creatorcontrib><creatorcontrib>TAKEUCHI, Kazuto</creatorcontrib><creatorcontrib>SOGA, Shinji</creatorcontrib><creatorcontrib>FUJITA, Shigeru</creatorcontrib><title>Development of interferon-α resistant subline from human chronic myelogenous leukemia cell line KT-1</title><title>Internal medicine (Tokyo, 1992)</title><addtitle>Intern Med</addtitle><description>Interferon-alpha (IFN-alpha) is one of the most effective therapeutic agents for a number of hematological malignancies, including chronic myelogenous leukemia (CML). Nevertheless, its efficacy is limited because of the development of resistance to IFN-alpha therapy. Previously, we established the novel human CML cell line KT-1, which is sensitive to the antiproliferative effects of IFN-alpha. Here, we report the establishment of an IFN-alpha-resistant subline, KT-1/A3R alpha 1000, by culturing KT-1/A3 cells (IFN-alpha-sensitive subline of KT-1) with increasing concentrations of IFN-alpha, in order to analyze the mechanism of acquisition of IFN-alpha resistance in CML cells after IFN-alpha therapy.
We developed an IFN-alpha-resistant tumor cell variant, KT-1/A3R alpha 1000, from the KT-1/A3 cell line by culturing cells with increasing concentrations of IFN-alpha. This subline was examined for its ability to proliferate and its resistance to apoptosis in high concentrations of IFN-alpha. The induction of the ISGF3 complex in response to IFN-alpha alpha in KT-1/A3R alpha 1000 was compared with that in the parental cell.
The levels of interferon-stimulated gene factor 3 components (STAT1, STAT2, and p48) proteins and STAT2 tyrosine phosphorylation induced after IFN-alpha treatment were unchanged, but formation of the ISGF3 complex was remarkably reduced in KT-1/A3R alpha 1000 cells compared to parental cells.
The KT-1/A3R alpha 1000 subline is a useful model for studying the mechanism of IFN-alpha resistance after IFN-alpha therapy.</description><subject>Antineoplastic agents</subject><subject>Antineoplastic Agents - therapeutic use</subject><subject>Apoptosis - drug effects</subject><subject>Biological and medical sciences</subject><subject>Cell Line, Transformed - drug effects</subject><subject>Chemotherapy</subject><subject>Drug Resistance, Neoplasm - genetics</subject><subject>Electrophoresis, Polyacrylamide Gel</subject><subject>Humans</subject><subject>Interferon-alpha - therapeutic use</subject><subject>Leukemia, Myelogenous, Chronic, BCR-ABL Positive - drug therapy</subject><subject>Leukemia, Myelogenous, Chronic, BCR-ABL Positive - metabolism</subject><subject>Medical sciences</subject><subject>Pharmacology. Drug treatments</subject><subject>Phosphorylation</subject><subject>Tyrosine - metabolism</subject><issn>0918-2918</issn><issn>1349-7235</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2001</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpdkE1OwzAQhS0EoqVwBfAGdil2bMfxEpVfUYlN95HjTqghcYqdIPVYXIQz4baRKrGxF_O9N28eQleUTFOaqVvrOvBO1w0srbEOppxMMyKP0JgyrhKZMnGMxkTRPEnjM0JnIXwQwnKp0lM0olSQjBE6RnAP31C36wZch9sK74wr8K1Lfn-wh2BDp-Mo9GUd9-DKtw1e9Y122KwiZQ1uNtHgHVzbB1xD_wmN1dhAXeOd4nWR0HN0Uuk6wMXwT9Di8WExe07mb08vs7t5YgQTXcJAqVJIrYTIWKZB5ZWOQXNKjZRZDiwlKWGaSSqXS8KM5nHEZUmUiUfmbIJu9rZr3371ELqisWGbRDuI6QpJiUoFkxGUe9D4NgQPVbH2ttF-U1BSbAsu_hdccFLEgqPycljRl3F20A2NRuB6AHQwuq68dsaGA8cp54IL9gcqXoob</recordid><startdate>20010701</startdate><enddate>20010701</enddate><creator>YAMAUCHI, Hayato</creator><creator>SAKAI, Ikuya</creator><creator>NARUMI, Hirosi</creator><creator>TAKEUCHI, Kazuto</creator><creator>SOGA, Shinji</creator><creator>FUJITA, Shigeru</creator><general>Japanese Society of Internal Medicine</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>7X8</scope></search><sort><creationdate>20010701</creationdate><title>Development of interferon-α resistant subline from human chronic myelogenous leukemia cell line KT-1</title><author>YAMAUCHI, Hayato ; SAKAI, Ikuya ; NARUMI, Hirosi ; TAKEUCHI, Kazuto ; SOGA, Shinji ; FUJITA, Shigeru</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c535t-3e99b57a955636ae98fa506811c7768e320203a3717dd03ca481147b09c91883</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2001</creationdate><topic>Antineoplastic agents</topic><topic>Antineoplastic Agents - therapeutic use</topic><topic>Apoptosis - drug effects</topic><topic>Biological and medical sciences</topic><topic>Cell Line, Transformed - drug effects</topic><topic>Chemotherapy</topic><topic>Drug Resistance, Neoplasm - genetics</topic><topic>Electrophoresis, Polyacrylamide Gel</topic><topic>Humans</topic><topic>Interferon-alpha - therapeutic use</topic><topic>Leukemia, Myelogenous, Chronic, BCR-ABL Positive - drug therapy</topic><topic>Leukemia, Myelogenous, Chronic, BCR-ABL Positive - metabolism</topic><topic>Medical sciences</topic><topic>Pharmacology. Drug treatments</topic><topic>Phosphorylation</topic><topic>Tyrosine - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>YAMAUCHI, Hayato</creatorcontrib><creatorcontrib>SAKAI, Ikuya</creatorcontrib><creatorcontrib>NARUMI, Hirosi</creatorcontrib><creatorcontrib>TAKEUCHI, Kazuto</creatorcontrib><creatorcontrib>SOGA, Shinji</creatorcontrib><creatorcontrib>FUJITA, Shigeru</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>MEDLINE - Academic</collection><jtitle>Internal medicine (Tokyo, 1992)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>YAMAUCHI, Hayato</au><au>SAKAI, Ikuya</au><au>NARUMI, Hirosi</au><au>TAKEUCHI, Kazuto</au><au>SOGA, Shinji</au><au>FUJITA, Shigeru</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Development of interferon-α resistant subline from human chronic myelogenous leukemia cell line KT-1</atitle><jtitle>Internal medicine (Tokyo, 1992)</jtitle><addtitle>Intern Med</addtitle><date>2001-07-01</date><risdate>2001</risdate><volume>40</volume><issue>7</issue><spage>607</spage><epage>612</epage><pages>607-612</pages><issn>0918-2918</issn><eissn>1349-7235</eissn><abstract>Interferon-alpha (IFN-alpha) is one of the most effective therapeutic agents for a number of hematological malignancies, including chronic myelogenous leukemia (CML). Nevertheless, its efficacy is limited because of the development of resistance to IFN-alpha therapy. Previously, we established the novel human CML cell line KT-1, which is sensitive to the antiproliferative effects of IFN-alpha. Here, we report the establishment of an IFN-alpha-resistant subline, KT-1/A3R alpha 1000, by culturing KT-1/A3 cells (IFN-alpha-sensitive subline of KT-1) with increasing concentrations of IFN-alpha, in order to analyze the mechanism of acquisition of IFN-alpha resistance in CML cells after IFN-alpha therapy.
We developed an IFN-alpha-resistant tumor cell variant, KT-1/A3R alpha 1000, from the KT-1/A3 cell line by culturing cells with increasing concentrations of IFN-alpha. This subline was examined for its ability to proliferate and its resistance to apoptosis in high concentrations of IFN-alpha. The induction of the ISGF3 complex in response to IFN-alpha alpha in KT-1/A3R alpha 1000 was compared with that in the parental cell.
The levels of interferon-stimulated gene factor 3 components (STAT1, STAT2, and p48) proteins and STAT2 tyrosine phosphorylation induced after IFN-alpha treatment were unchanged, but formation of the ISGF3 complex was remarkably reduced in KT-1/A3R alpha 1000 cells compared to parental cells.
The KT-1/A3R alpha 1000 subline is a useful model for studying the mechanism of IFN-alpha resistance after IFN-alpha therapy.</abstract><cop>Tokyo</cop><pub>Japanese Society of Internal Medicine</pub><pmid>11506301</pmid><doi>10.2169/internalmedicine.40.607</doi><tpages>6</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Antineoplastic agents Antineoplastic Agents - therapeutic use Apoptosis - drug effects Biological and medical sciences Cell Line, Transformed - drug effects Chemotherapy Drug Resistance, Neoplasm - genetics Electrophoresis, Polyacrylamide Gel Humans Interferon-alpha - therapeutic use Leukemia, Myelogenous, Chronic, BCR-ABL Positive - drug therapy Leukemia, Myelogenous, Chronic, BCR-ABL Positive - metabolism Medical sciences Pharmacology. Drug treatments Phosphorylation Tyrosine - metabolism |
| title | Development of interferon-α resistant subline from human chronic myelogenous leukemia cell line KT-1 |
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