Possible significance of Ph, Zinc and BCR-ABL chimaerism in the pathogenesis of chronic myeloid leukaemia
Identifieur interne : 002673 ( Istex/Corpus ); précédent : 002672; suivant : 002674Possible significance of Ph, Zinc and BCR-ABL chimaerism in the pathogenesis of chronic myeloid leukaemia
Auteurs : I. M. JibrinSource :
- Medical Hypotheses [ 0306-9877 ] ; 1995.
English descriptors
- Teeft :
- Abnormal, Acrodermatitis enteropathy, Adaptive mechanism, Alkaline phosphatase, Blastic crisis, Blastic transformation, Catalytic function, Cell division, Cell membranes, Cellular proliferation, Chimaeric gene, Chromosome, Chromosome studies, Chronic myeloid leukaemia, Cytogenetic changes, Deficient tissues, Gene chimaerism, Intermediate changes, Isoferritin inhibition, Leukaemia, Leukaemic, Leukaemic cells, Major breakpoint cluster region, Major form, Medical hypotheses, Neutrophil, Normal subjects, Oxford press, Oxford textbook, Pathogenesis, Philadelphia chromosome, Phosphatase, Point mutation, Polymerase, Possible significance, Protein synthesis, Radiation injury, Receptor protein, Regulator unit, Ribonuclease activity, Structural gene, Structural stability.
Abstract
Abstract: Available evidence suggests a double-pathway two-staged genetic alteration in the pathogenesis of Chronic Myeloid Leukaemia (CML). The regular Ph' defect results in BCR-ABL gene chimaerism on the one hand and suppressed synthesis of the protein responsible for Zn absorption on the ether. The resulting Zn deficiency leads, through its metalloenzymes, to a low NAP activity and depressed DNA & RNA polymerase activities: the latter necessitates an adaptive mechanism to sustain cell division despite low zinc. This adaptation is in the form of another gene alteration; a point mutation in the BCR-ABL chimaeric gene, now an oncogene, whose onco-proteins are zinc-independent and stimulate cell division more efficiently (though abnormally also) than the polymerases while defying the usual mechanisms regulating DNA synthesis and cell division. Thus it seems possible that assisted transcellular zinc transport could prevent development of CML in Ph'-positive individuals and the enhanced (abnormal) cellular proliferation might be specifically inhibited.
Url:
DOI: 10.1016/0306-9877(95)90185-X
Links to Exploration step
ISTEX:30530F776267C10DFAB75CDA63D69B9D5E73D33CLe document en format XML
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Jibrin</name><affiliation><mods:affiliation>Nitel Health Centre, Nitel Training School, Cappa - Oshodi, Lagos, Nigeria</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j">Medical Hypotheses</title><title level="j" type="abbrev">YMEHY</title><idno type="ISSN">0306-9877</idno><imprint><publisher>ELSEVIER</publisher><date type="published" when="1995">1995</date><biblScope unit="volume">44</biblScope><biblScope unit="issue">4</biblScope><biblScope unit="page" from="301">301</biblScope><biblScope unit="page" to="305">305</biblScope></imprint><idno type="ISSN">0306-9877</idno></series></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0306-9877</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="Teeft" xml:lang="en"><term>Abnormal</term><term>Acrodermatitis enteropathy</term><term>Adaptive mechanism</term><term>Alkaline phosphatase</term><term>Blastic crisis</term><term>Blastic transformation</term><term>Catalytic function</term><term>Cell division</term><term>Cell membranes</term><term>Cellular proliferation</term><term>Chimaeric gene</term><term>Chromosome</term><term>Chromosome studies</term><term>Chronic myeloid leukaemia</term><term>Cytogenetic changes</term><term>Deficient tissues</term><term>Gene chimaerism</term><term>Intermediate changes</term><term>Isoferritin inhibition</term><term>Leukaemia</term><term>Leukaemic</term><term>Leukaemic cells</term><term>Major breakpoint cluster region</term><term>Major form</term><term>Medical hypotheses</term><term>Neutrophil</term><term>Normal subjects</term><term>Oxford press</term><term>Oxford textbook</term><term>Pathogenesis</term><term>Philadelphia chromosome</term><term>Phosphatase</term><term>Point mutation</term><term>Polymerase</term><term>Possible significance</term><term>Protein synthesis</term><term>Radiation injury</term><term>Receptor protein</term><term>Regulator unit</term><term>Ribonuclease activity</term><term>Structural gene</term><term>Structural stability</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Abstract: Available evidence suggests a double-pathway two-staged genetic alteration in the pathogenesis of Chronic Myeloid Leukaemia (CML). The regular Ph' defect results in BCR-ABL gene chimaerism on the one hand and suppressed synthesis of the protein responsible for Zn absorption on the ether. The resulting Zn deficiency leads, through its metalloenzymes, to a low NAP activity and depressed DNA & RNA polymerase activities: the latter necessitates an adaptive mechanism to sustain cell division despite low zinc. This adaptation is in the form of another gene alteration; a point mutation in the BCR-ABL chimaeric gene, now an oncogene, whose onco-proteins are zinc-independent and stimulate cell division more efficiently (though abnormally also) than the polymerases while defying the usual mechanisms regulating DNA synthesis and cell division. Thus it seems possible that assisted transcellular zinc transport could prevent development of CML in Ph'-positive individuals and the enhanced (abnormal) cellular proliferation might be specifically inhibited.</div></front></TEI><istex><corpusName>elsevier</corpusName><keywords><teeft><json:string>chromosome</json:string><json:string>cell division</json:string><json:string>phosphatase</json:string><json:string>leukaemic</json:string><json:string>neutrophil</json:string><json:string>polymerase</json:string><json:string>leukaemia</json:string><json:string>alkaline phosphatase</json:string><json:string>leukaemic cells</json:string><json:string>pathogenesis</json:string><json:string>chimaeric gene</json:string><json:string>chronic myeloid leukaemia</json:string><json:string>possible significance</json:string><json:string>structural gene</json:string><json:string>catalytic function</json:string><json:string>structural stability</json:string><json:string>ribonuclease activity</json:string><json:string>receptor protein</json:string><json:string>intermediate changes</json:string><json:string>gene chimaerism</json:string><json:string>point mutation</json:string><json:string>medical hypotheses</json:string><json:string>oxford textbook</json:string><json:string>blastic transformation</json:string><json:string>cellular proliferation</json:string><json:string>regulator unit</json:string><json:string>adaptive mechanism</json:string><json:string>philadelphia chromosome</json:string><json:string>major breakpoint cluster region</json:string><json:string>major form</json:string><json:string>protein synthesis</json:string><json:string>deficient tissues</json:string><json:string>normal subjects</json:string><json:string>acrodermatitis enteropathy</json:string><json:string>cell membranes</json:string><json:string>radiation injury</json:string><json:string>isoferritin inhibition</json:string><json:string>blastic crisis</json:string><json:string>cytogenetic changes</json:string><json:string>chromosome studies</json:string><json:string>oxford press</json:string><json:string>abnormal</json:string></teeft></keywords><author><json:item><name>I.M. 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This adaptation is in the form of another gene alteration; a point mutation in the BCR-ABL chimaeric gene, now an oncogene, whose onco-proteins are zinc-independent and stimulate cell division more efficiently (though abnormally also) than the polymerases while defying the usual mechanisms regulating DNA synthesis and cell division. Thus it seems possible that assisted transcellular zinc transport could prevent development of CML in Ph'-positive individuals and the enhanced (abnormal) cellular proliferation might be specifically inhibited.</abstract><qualityIndicators><score>6.679</score><pdfWordCount>2867</pdfWordCount><pdfCharCount>17008</pdfCharCount><pdfVersion>1.3</pdfVersion><pdfPageCount>5</pdfPageCount><pdfPageSize>540 x 720 pts</pdfPageSize><refBibsNative>true</refBibsNative><abstractWordCount>151</abstractWordCount><abstractCharCount>1065</abstractCharCount><keywordCount>0</keywordCount></qualityIndicators><title>Possible significance of Ph, Zinc and BCR-ABL chimaerism in the pathogenesis of chronic myeloid leukaemia</title><pmid><json:string>7666834</json:string></pmid><pii><json:string>0306-9877(95)90185-X</json:string></pii><genre><json:string>research-article</json:string></genre><serie><title>A Short Textbook of Haematology</title><language><json:string>unknown</json:string></language><pages><first>357</first></pages></serie><host><title>Medical Hypotheses</title><language><json:string>unknown</json:string></language><publicationDate>1995</publicationDate><issn><json:string>0306-9877</json:string></issn><pii><json:string>S0306-9877(00)X0308-8</json:string></pii><volume>44</volume><issue>4</issue><pages><first>301</first><last>305</last></pages><genre><json:string>journal</json:string></genre></host><namedEntities><unitex><date><json:string>1993</json:string><json:string>1960</json:string></date><geogName></geogName><orgName></orgName><orgName_funder></orgName_funder><orgName_provider></orgName_provider><persName></persName><placeName></placeName><ref_url></ref_url><ref_bibl></ref_bibl><bibl></bibl></unitex></namedEntities><ark><json:string>ark:/67375/6H6-MC7419SL-S</json:string></ark><categories><wos><json:string>1 - 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Oshodi, Lagos, Nigeria</affiliation></author><idno type="istex">30530F776267C10DFAB75CDA63D69B9D5E73D33C</idno><idno type="ark">ark:/67375/6H6-MC7419SL-S</idno><idno type="DOI">10.1016/0306-9877(95)90185-X</idno><idno type="PII">0306-9877(95)90185-X</idno></analytic><monogr><title level="j">Medical Hypotheses</title><title level="j" type="abbrev">YMEHY</title><idno type="pISSN">0306-9877</idno><idno type="PII">S0306-9877(00)X0308-8</idno><imprint><publisher>ELSEVIER</publisher><date type="published" when="1995"></date><biblScope unit="volume">44</biblScope><biblScope unit="issue">4</biblScope><biblScope unit="page" from="301">301</biblScope><biblScope unit="page" to="305">305</biblScope></imprint></monogr></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>1993</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>Abstract: Available evidence suggests a double-pathway two-staged genetic alteration in the pathogenesis of Chronic Myeloid Leukaemia (CML). The regular Ph' defect results in BCR-ABL gene chimaerism on the one hand and suppressed synthesis of the protein responsible for Zn absorption on the ether. The resulting Zn deficiency leads, through its metalloenzymes, to a low NAP activity and depressed DNA & RNA polymerase activities: the latter necessitates an adaptive mechanism to sustain cell division despite low zinc. This adaptation is in the form of another gene alteration; a point mutation in the BCR-ABL chimaeric gene, now an oncogene, whose onco-proteins are zinc-independent and stimulate cell division more efficiently (though abnormally also) than the polymerases while defying the usual mechanisms regulating DNA synthesis and cell division. Thus it seems possible that assisted transcellular zinc transport could prevent development of CML in Ph'-positive individuals and the enhanced (abnormal) cellular proliferation might be specifically inhibited.</p></abstract></profileDesc><revisionDesc><change when="1995">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><extension>txt</extension><original>false</original><mimetype>text/plain</mimetype><uri>https://api.istex.fr/ark:/67375/6H6-MC7419SL-S/fulltext.txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="Elsevier, elements deleted: tail"><istex:xmlDeclaration>version="1.0" encoding="utf-8"</istex:xmlDeclaration><istex:docType PUBLIC="-//ES//DTD journal article DTD version 4.5.2//EN//XML" URI="art452.dtd" name="istex:docType"></istex:docType><istex:document><converted-article version="4.5.2" docsubtype="fla"><item-info><jid>YMEHY</jid><aid>9590185X</aid><ce:pii>0306-9877(95)90185-X</ce:pii><ce:doi>10.1016/0306-9877(95)90185-X</ce:doi><ce:copyright type="unknown" year="1993"></ce:copyright></item-info><head><ce:title>Possible significance of Ph, Zinc and BCR-ABL chimaerism in the pathogenesis of chronic myeloid leukaemia</ce:title><ce:author-group><ce:author><ce:given-name>I.M.</ce:given-name><ce:surname>Jibrin</ce:surname></ce:author><ce:affiliation><ce:textfn>Nitel Health Centre, Nitel Training School, Cappa - Oshodi, Lagos, Nigeria</ce:textfn></ce:affiliation></ce:author-group><ce:date-received day="15" month="6" year="1994"></ce:date-received><ce:date-accepted day="24" month="8" year="1994"></ce:date-accepted><ce:abstract><ce:section-title>Abstract</ce:section-title><ce:abstract-sec><ce:simple-para>Available evidence suggests a double-pathway two-staged genetic alteration in the pathogenesis of Chronic Myeloid Leukaemia (CML). The regular Ph' defect results in BCR-ABL gene chimaerism on the one hand and suppressed synthesis of the protein responsible for Zn absorption on the ether. The resulting Zn deficiency leads, through its metalloenzymes, to a low NAP activity and depressed DNA & RNA polymerase activities: the latter necessitates an adaptive mechanism to sustain cell division despite low zinc. This adaptation is in the form of another gene alteration; a point mutation in the BCR-ABL chimaeric gene, now an oncogene, whose onco-proteins are zinc-independent and stimulate cell division more efficiently (though abnormally also) than the polymerases while defying the usual mechanisms regulating DNA synthesis and cell division. Thus it seems possible that assisted transcellular zinc transport could prevent development of CML in Ph'-positive individuals and the enhanced (abnormal) cellular proliferation might be specifically inhibited.</ce:simple-para></ce:abstract-sec></ce:abstract></head></converted-article></istex:document></istex:metadataXml><mods version="3.6"><titleInfo><title>Possible significance of Ph, Zinc and BCR-ABL chimaerism in the pathogenesis of chronic myeloid leukaemia</title></titleInfo><titleInfo type="alternative" contentType="CDATA"><title>Possible significance of Ph, Zinc and BCR-ABL chimaerism in the pathogenesis of chronic myeloid leukaemia</title></titleInfo><name type="personal"><namePart type="given">I.M.</namePart><namePart type="family">Jibrin</namePart><affiliation>Nitel Health Centre, Nitel Training School, Cappa - Oshodi, Lagos, Nigeria</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="research-article" displayLabel="Full-length article" authority="ISTEX" authorityURI="https://content-type.data.istex.fr" valueURI="https://content-type.data.istex.fr/ark:/67375/XTP-1JC4F85T-7">research-article</genre><originInfo><publisher>ELSEVIER</publisher><dateIssued encoding="w3cdtf">1995</dateIssued><copyrightDate encoding="w3cdtf">1993</copyrightDate></originInfo><language><languageTerm type="code" authority="iso639-2b">eng</languageTerm><languageTerm type="code" authority="rfc3066">en</languageTerm></language><abstract lang="en">Abstract: Available evidence suggests a double-pathway two-staged genetic alteration in the pathogenesis of Chronic Myeloid Leukaemia (CML). The regular Ph' defect results in BCR-ABL gene chimaerism on the one hand and suppressed synthesis of the protein responsible for Zn absorption on the ether. The resulting Zn deficiency leads, through its metalloenzymes, to a low NAP activity and depressed DNA & RNA polymerase activities: the latter necessitates an adaptive mechanism to sustain cell division despite low zinc. This adaptation is in the form of another gene alteration; a point mutation in the BCR-ABL chimaeric gene, now an oncogene, whose onco-proteins are zinc-independent and stimulate cell division more efficiently (though abnormally also) than the polymerases while defying the usual mechanisms regulating DNA synthesis and cell division. Thus it seems possible that assisted transcellular zinc transport could prevent development of CML in Ph'-positive individuals and the enhanced (abnormal) cellular proliferation might be specifically inhibited.</abstract><relatedItem type="host"><titleInfo><title>Medical Hypotheses</title></titleInfo><titleInfo type="abbreviated"><title>YMEHY</title></titleInfo><genre type="journal" authority="ISTEX" authorityURI="https://publication-type.data.istex.fr" valueURI="https://publication-type.data.istex.fr/ark:/67375/JMC-0GLKJH51-B">journal</genre><originInfo><publisher>ELSEVIER</publisher><dateIssued encoding="w3cdtf">1995</dateIssued></originInfo><identifier type="ISSN">0306-9877</identifier><identifier type="PII">S0306-9877(00)X0308-8</identifier><part><date>1995</date><detail type="volume"><number>44</number><caption>vol.</caption></detail><detail type="issue"><number>4</number><caption>no.</caption></detail><extent unit="issue-pages"><start>229</start><end>306</end></extent><extent unit="pages"><start>301</start><end>305</end></extent></part></relatedItem><identifier type="istex">30530F776267C10DFAB75CDA63D69B9D5E73D33C</identifier><identifier type="ark">ark:/67375/6H6-MC7419SL-S</identifier><identifier type="DOI">10.1016/0306-9877(95)90185-X</identifier><identifier type="PII">0306-9877(95)90185-X</identifier><recordInfo><recordContentSource authority="ISTEX" authorityURI="https://loaded-corpus.data.istex.fr" valueURI="https://loaded-corpus.data.istex.fr/ark:/67375/XBH-HKKZVM7B-M">elsevier</recordContentSource></recordInfo></mods><json:item><extension>json</extension><original>false</original><mimetype>application/json</mimetype><uri>https://api.istex.fr/ark:/67375/6H6-MC7419SL-S/record.json</uri></json:item></metadata></istex></record>Pour manipuler ce document sous Unix (Dilib)
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