Antisense Therapy Specific to Mutated K-ras Gene in Hamster Pancreatic Cancer Model. Can it Inhibit the Growth of 5-FU and MMC-resistant Metastatic and Remetastatic Cell Lines?
K-ras point mutation at codon 12 has a relationship greater than 90% with pancreatic cancer. Cancer therapy should also include the treatment of metastatic disease because it is known that the properties of metastatic cells may vary considerably from those of the primary tumor. Aim: To clarify if th...
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| Veröffentlicht in: | In vivo (Athens) 2004-03, Vol.18 (2), p.113-117 |
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| creator | Morioka, Cíntia Yoko Saito, Seiji Machado, Marcel Cerqueira Cesar Ohzawa, Kouji Kubrusly, Márcia Saldanha Cunha, José Eduardo Monteiro Watanabe, Akiharu |
| description | K-ras point mutation at codon 12 has a relationship greater than 90% with pancreatic cancer. Cancer therapy should also include
the treatment of metastatic disease because it is known that the properties of metastatic cells may vary considerably from
those of the primary tumor. Aim: To clarify if the same drugs, which can inhibit the tumor growth in the parental cell line,
can inhibit the pancreatic metastatic and remetastatic cell lines at the same concentrations and to compare the inhibition
with antisense oligonucleotides mismatched to K-ras gene, in Syrian golden hamsters. Materials and Methods: HaP-T1, a BHP-induced
hamster pancreatic cancer cell line, MS-PaS-1 (a metastatic cell line established from âreturn tripâ metastases from the liver
to the pancreas) and MS-PaS-2 named as a âremetastatic cell lineâ, i.e., metastases from MS-PaS-1, were used. MTT and MTT-agarose
assays were performed, using 5-Fluorouracil (5-FU), Mitomycin C (MMC) and antisense oligonucleotide specific to K-ras oncogene.
Results: The inhibitory concentration (IC 50 ) of 5-FU, which inhibited HaP-T1, had to be increased by 50-fold to inhibit MS-PaS-1 and 100-fold to inhibit MS-PaS-2. MMC
had to be increased by 10-fold to inhibit MS-PaS-1 and 50-fold to inhibit MS-PaS-2. However, IC 50 was the same when antisense oligonucleotide was tried in these 3 cell lines. Conclusion: Antisense oligonucleotide-targeted
K-ras gene may be a good choice for therapy because it could inhibit the growth in metastatic and remetastatic cells as well
as in primary tumor cells. |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_pubme</sourceid><recordid>TN_cdi_proquest_miscellaneous_71874581</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>71874581</sourcerecordid><originalsourceid>FETCH-LOGICAL-h168t-b0dc0da1b6f2037b36e275ebfa14565d1d09f623b3afe3362a3c02f54c338dd13</originalsourceid><addsrcrecordid>eNpFkN1KxDAQhYsouv68gsyFeFdJmk3bvRIp7ipuUfwB78q0mdpIm65JVvGtfESzqHg1Z858HGZmK5rwbMbjTE5n29GEJTKPc8mf96J9514ZSzPGkt1oj0vOBRPZJPq6MF47Mo7gsSOLq094WFGjW92AH6Fce_Sk4Ca26GBBhkAbuMLBebJwh6axhD6wRZDBKUdF_dmmA-3h2nS6DtV3BAs7fvgOxhZkPH8CNArKsogtOe08Gg8leQxqE7YZ3tPwbxTU97DUhtz5YbTTYu_o6LceRE_zy8fiKl7eLq6Li2Xc8TT3cc1UwxTyOm2TcGgtUkoySXWLfCpTqbhiszZNRC2wJSHSBEXDklZOGyFypbg4iE5_cld2fFuT89WgXRP2QEPj2lUZz7OpzDfg8S-4rgdS1crqAe1n9ffjAJz8AJ1-6T60pcoN2PcBF5V-53mVVIEU373zhpE</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>71874581</pqid></control><display><type>article</type><title>Antisense Therapy Specific to Mutated K-ras Gene in Hamster Pancreatic Cancer Model. Can it Inhibit the Growth of 5-FU and MMC-resistant Metastatic and Remetastatic Cell Lines?</title><source>MEDLINE</source><source>EZB-FREE-00999 freely available EZB journals</source><creator>Morioka, Cíntia Yoko ; Saito, Seiji ; Machado, Marcel Cerqueira Cesar ; Ohzawa, Kouji ; Kubrusly, Márcia Saldanha ; Cunha, José Eduardo Monteiro ; Watanabe, Akiharu</creator><creatorcontrib>Morioka, Cíntia Yoko ; Saito, Seiji ; Machado, Marcel Cerqueira Cesar ; Ohzawa, Kouji ; Kubrusly, Márcia Saldanha ; Cunha, José Eduardo Monteiro ; Watanabe, Akiharu</creatorcontrib><description>K-ras point mutation at codon 12 has a relationship greater than 90% with pancreatic cancer. Cancer therapy should also include
the treatment of metastatic disease because it is known that the properties of metastatic cells may vary considerably from
those of the primary tumor. Aim: To clarify if the same drugs, which can inhibit the tumor growth in the parental cell line,
can inhibit the pancreatic metastatic and remetastatic cell lines at the same concentrations and to compare the inhibition
with antisense oligonucleotides mismatched to K-ras gene, in Syrian golden hamsters. Materials and Methods: HaP-T1, a BHP-induced
hamster pancreatic cancer cell line, MS-PaS-1 (a metastatic cell line established from âreturn tripâ metastases from the liver
to the pancreas) and MS-PaS-2 named as a âremetastatic cell lineâ, i.e., metastases from MS-PaS-1, were used. MTT and MTT-agarose
assays were performed, using 5-Fluorouracil (5-FU), Mitomycin C (MMC) and antisense oligonucleotide specific to K-ras oncogene.
Results: The inhibitory concentration (IC 50 ) of 5-FU, which inhibited HaP-T1, had to be increased by 50-fold to inhibit MS-PaS-1 and 100-fold to inhibit MS-PaS-2. MMC
had to be increased by 10-fold to inhibit MS-PaS-1 and 50-fold to inhibit MS-PaS-2. However, IC 50 was the same when antisense oligonucleotide was tried in these 3 cell lines. Conclusion: Antisense oligonucleotide-targeted
K-ras gene may be a good choice for therapy because it could inhibit the growth in metastatic and remetastatic cells as well
as in primary tumor cells.</description><identifier>ISSN: 0258-851X</identifier><identifier>EISSN: 1791-7549</identifier><identifier>PMID: 15113037</identifier><language>eng</language><publisher>Greece: International Institute of Anticancer Research</publisher><subject>Animals ; Antineoplastic Agents - pharmacology ; Cell Line, Tumor - drug effects ; Cell Transplantation ; Cricetinae ; Disease Models, Animal ; DNA, Neoplasm - genetics ; Drug Screening Assays, Antitumor ; Fluorouracil - pharmacology ; Genes, ras ; Liver Neoplasms, Experimental - drug therapy ; Liver Neoplasms, Experimental - pathology ; Male ; Mesocricetus ; Mitomycin - pharmacology ; Mutation ; Neoplasm Metastasis - drug therapy ; Neoplasm Metastasis - genetics ; Neoplasm Metastasis - pathology ; Neoplasm Transplantation ; Oligonucleotides, Antisense - pharmacology ; Oligonucleotides, Antisense - therapeutic use ; Pancreatic Neoplasms - drug therapy ; Pancreatic Neoplasms - genetics ; Pancreatic Neoplasms - secondary</subject><ispartof>In vivo (Athens), 2004-03, Vol.18 (2), p.113-117</ispartof><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/15113037$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Morioka, Cíntia Yoko</creatorcontrib><creatorcontrib>Saito, Seiji</creatorcontrib><creatorcontrib>Machado, Marcel Cerqueira Cesar</creatorcontrib><creatorcontrib>Ohzawa, Kouji</creatorcontrib><creatorcontrib>Kubrusly, Márcia Saldanha</creatorcontrib><creatorcontrib>Cunha, José Eduardo Monteiro</creatorcontrib><creatorcontrib>Watanabe, Akiharu</creatorcontrib><title>Antisense Therapy Specific to Mutated K-ras Gene in Hamster Pancreatic Cancer Model. Can it Inhibit the Growth of 5-FU and MMC-resistant Metastatic and Remetastatic Cell Lines?</title><title>In vivo (Athens)</title><addtitle>In Vivo</addtitle><description>K-ras point mutation at codon 12 has a relationship greater than 90% with pancreatic cancer. Cancer therapy should also include
the treatment of metastatic disease because it is known that the properties of metastatic cells may vary considerably from
those of the primary tumor. Aim: To clarify if the same drugs, which can inhibit the tumor growth in the parental cell line,
can inhibit the pancreatic metastatic and remetastatic cell lines at the same concentrations and to compare the inhibition
with antisense oligonucleotides mismatched to K-ras gene, in Syrian golden hamsters. Materials and Methods: HaP-T1, a BHP-induced
hamster pancreatic cancer cell line, MS-PaS-1 (a metastatic cell line established from âreturn tripâ metastases from the liver
to the pancreas) and MS-PaS-2 named as a âremetastatic cell lineâ, i.e., metastases from MS-PaS-1, were used. MTT and MTT-agarose
assays were performed, using 5-Fluorouracil (5-FU), Mitomycin C (MMC) and antisense oligonucleotide specific to K-ras oncogene.
Results: The inhibitory concentration (IC 50 ) of 5-FU, which inhibited HaP-T1, had to be increased by 50-fold to inhibit MS-PaS-1 and 100-fold to inhibit MS-PaS-2. MMC
had to be increased by 10-fold to inhibit MS-PaS-1 and 50-fold to inhibit MS-PaS-2. However, IC 50 was the same when antisense oligonucleotide was tried in these 3 cell lines. Conclusion: Antisense oligonucleotide-targeted
K-ras gene may be a good choice for therapy because it could inhibit the growth in metastatic and remetastatic cells as well
as in primary tumor cells.</description><subject>Animals</subject><subject>Antineoplastic Agents - pharmacology</subject><subject>Cell Line, Tumor - drug effects</subject><subject>Cell Transplantation</subject><subject>Cricetinae</subject><subject>Disease Models, Animal</subject><subject>DNA, Neoplasm - genetics</subject><subject>Drug Screening Assays, Antitumor</subject><subject>Fluorouracil - pharmacology</subject><subject>Genes, ras</subject><subject>Liver Neoplasms, Experimental - drug therapy</subject><subject>Liver Neoplasms, Experimental - pathology</subject><subject>Male</subject><subject>Mesocricetus</subject><subject>Mitomycin - pharmacology</subject><subject>Mutation</subject><subject>Neoplasm Metastasis - drug therapy</subject><subject>Neoplasm Metastasis - genetics</subject><subject>Neoplasm Metastasis - pathology</subject><subject>Neoplasm Transplantation</subject><subject>Oligonucleotides, Antisense - pharmacology</subject><subject>Oligonucleotides, Antisense - therapeutic use</subject><subject>Pancreatic Neoplasms - drug therapy</subject><subject>Pancreatic Neoplasms - genetics</subject><subject>Pancreatic Neoplasms - secondary</subject><issn>0258-851X</issn><issn>1791-7549</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2004</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpFkN1KxDAQhYsouv68gsyFeFdJmk3bvRIp7ipuUfwB78q0mdpIm65JVvGtfESzqHg1Z858HGZmK5rwbMbjTE5n29GEJTKPc8mf96J9514ZSzPGkt1oj0vOBRPZJPq6MF47Mo7gsSOLq094WFGjW92AH6Fce_Sk4Ca26GBBhkAbuMLBebJwh6axhD6wRZDBKUdF_dmmA-3h2nS6DtV3BAs7fvgOxhZkPH8CNArKsogtOe08Gg8leQxqE7YZ3tPwbxTU97DUhtz5YbTTYu_o6LceRE_zy8fiKl7eLq6Li2Xc8TT3cc1UwxTyOm2TcGgtUkoySXWLfCpTqbhiszZNRC2wJSHSBEXDklZOGyFypbg4iE5_cld2fFuT89WgXRP2QEPj2lUZz7OpzDfg8S-4rgdS1crqAe1n9ffjAJz8AJ1-6T60pcoN2PcBF5V-53mVVIEU373zhpE</recordid><startdate>20040301</startdate><enddate>20040301</enddate><creator>Morioka, Cíntia Yoko</creator><creator>Saito, Seiji</creator><creator>Machado, Marcel Cerqueira Cesar</creator><creator>Ohzawa, Kouji</creator><creator>Kubrusly, Márcia Saldanha</creator><creator>Cunha, José Eduardo Monteiro</creator><creator>Watanabe, Akiharu</creator><general>International Institute of Anticancer Research</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>7X8</scope></search><sort><creationdate>20040301</creationdate><title>Antisense Therapy Specific to Mutated K-ras Gene in Hamster Pancreatic Cancer Model. Can it Inhibit the Growth of 5-FU and MMC-resistant Metastatic and Remetastatic Cell Lines?</title><author>Morioka, Cíntia Yoko ; Saito, Seiji ; Machado, Marcel Cerqueira Cesar ; Ohzawa, Kouji ; Kubrusly, Márcia Saldanha ; Cunha, José Eduardo Monteiro ; Watanabe, Akiharu</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-h168t-b0dc0da1b6f2037b36e275ebfa14565d1d09f623b3afe3362a3c02f54c338dd13</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2004</creationdate><topic>Animals</topic><topic>Antineoplastic Agents - pharmacology</topic><topic>Cell Line, Tumor - drug effects</topic><topic>Cell Transplantation</topic><topic>Cricetinae</topic><topic>Disease Models, Animal</topic><topic>DNA, Neoplasm - genetics</topic><topic>Drug Screening Assays, Antitumor</topic><topic>Fluorouracil - pharmacology</topic><topic>Genes, ras</topic><topic>Liver Neoplasms, Experimental - drug therapy</topic><topic>Liver Neoplasms, Experimental - pathology</topic><topic>Male</topic><topic>Mesocricetus</topic><topic>Mitomycin - pharmacology</topic><topic>Mutation</topic><topic>Neoplasm Metastasis - drug therapy</topic><topic>Neoplasm Metastasis - genetics</topic><topic>Neoplasm Metastasis - pathology</topic><topic>Neoplasm Transplantation</topic><topic>Oligonucleotides, Antisense - pharmacology</topic><topic>Oligonucleotides, Antisense - therapeutic use</topic><topic>Pancreatic Neoplasms - drug therapy</topic><topic>Pancreatic Neoplasms - genetics</topic><topic>Pancreatic Neoplasms - secondary</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Morioka, Cíntia Yoko</creatorcontrib><creatorcontrib>Saito, Seiji</creatorcontrib><creatorcontrib>Machado, Marcel Cerqueira Cesar</creatorcontrib><creatorcontrib>Ohzawa, Kouji</creatorcontrib><creatorcontrib>Kubrusly, Márcia Saldanha</creatorcontrib><creatorcontrib>Cunha, José Eduardo Monteiro</creatorcontrib><creatorcontrib>Watanabe, Akiharu</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>MEDLINE - Academic</collection><jtitle>In vivo (Athens)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Morioka, Cíntia Yoko</au><au>Saito, Seiji</au><au>Machado, Marcel Cerqueira Cesar</au><au>Ohzawa, Kouji</au><au>Kubrusly, Márcia Saldanha</au><au>Cunha, José Eduardo Monteiro</au><au>Watanabe, Akiharu</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Antisense Therapy Specific to Mutated K-ras Gene in Hamster Pancreatic Cancer Model. Can it Inhibit the Growth of 5-FU and MMC-resistant Metastatic and Remetastatic Cell Lines?</atitle><jtitle>In vivo (Athens)</jtitle><addtitle>In Vivo</addtitle><date>2004-03-01</date><risdate>2004</risdate><volume>18</volume><issue>2</issue><spage>113</spage><epage>117</epage><pages>113-117</pages><issn>0258-851X</issn><eissn>1791-7549</eissn><abstract>K-ras point mutation at codon 12 has a relationship greater than 90% with pancreatic cancer. Cancer therapy should also include
the treatment of metastatic disease because it is known that the properties of metastatic cells may vary considerably from
those of the primary tumor. Aim: To clarify if the same drugs, which can inhibit the tumor growth in the parental cell line,
can inhibit the pancreatic metastatic and remetastatic cell lines at the same concentrations and to compare the inhibition
with antisense oligonucleotides mismatched to K-ras gene, in Syrian golden hamsters. Materials and Methods: HaP-T1, a BHP-induced
hamster pancreatic cancer cell line, MS-PaS-1 (a metastatic cell line established from âreturn tripâ metastases from the liver
to the pancreas) and MS-PaS-2 named as a âremetastatic cell lineâ, i.e., metastases from MS-PaS-1, were used. MTT and MTT-agarose
assays were performed, using 5-Fluorouracil (5-FU), Mitomycin C (MMC) and antisense oligonucleotide specific to K-ras oncogene.
Results: The inhibitory concentration (IC 50 ) of 5-FU, which inhibited HaP-T1, had to be increased by 50-fold to inhibit MS-PaS-1 and 100-fold to inhibit MS-PaS-2. MMC
had to be increased by 10-fold to inhibit MS-PaS-1 and 50-fold to inhibit MS-PaS-2. However, IC 50 was the same when antisense oligonucleotide was tried in these 3 cell lines. Conclusion: Antisense oligonucleotide-targeted
K-ras gene may be a good choice for therapy because it could inhibit the growth in metastatic and remetastatic cells as well
as in primary tumor cells.</abstract><cop>Greece</cop><pub>International Institute of Anticancer Research</pub><pmid>15113037</pmid><tpages>5</tpages></addata></record> |
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| source | MEDLINE; EZB-FREE-00999 freely available EZB journals |
| subjects | Animals Antineoplastic Agents - pharmacology Cell Line, Tumor - drug effects Cell Transplantation Cricetinae Disease Models, Animal DNA, Neoplasm - genetics Drug Screening Assays, Antitumor Fluorouracil - pharmacology Genes, ras Liver Neoplasms, Experimental - drug therapy Liver Neoplasms, Experimental - pathology Male Mesocricetus Mitomycin - pharmacology Mutation Neoplasm Metastasis - drug therapy Neoplasm Metastasis - genetics Neoplasm Metastasis - pathology Neoplasm Transplantation Oligonucleotides, Antisense - pharmacology Oligonucleotides, Antisense - therapeutic use Pancreatic Neoplasms - drug therapy Pancreatic Neoplasms - genetics Pancreatic Neoplasms - secondary |
| title | Antisense Therapy Specific to Mutated K-ras Gene in Hamster Pancreatic Cancer Model. Can it Inhibit the Growth of 5-FU and MMC-resistant Metastatic and Remetastatic Cell Lines? |
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