Karyotypic progression in human tumors
Identifieur interne : 000B35 ( Istex/Corpus ); précédent : 000B34; suivant : 000B36Karyotypic progression in human tumors
Auteurs : Sandra R. WolmanSource :
- Cancer and Metastasis Reviews [ 0167-7659 ] ; 1983-09-01.
English descriptors
- KwdEn :
- Teeft :
- Aberration, Abnormal, Abnormality, Acad, Acute nonlymphocytic leukemia, Adenoma, Aneuploid, Aneuploidy, Anll, Benign, Bladder, Bowel, Breakage, Cancer genet cytogenet, Carcinogenesis, Carcinoma, Cell lines, Chromosomal, Chromosomal aberration, Chromosomal aberrations, Chromosomal specificity, Chromosome, Chromosome aberrations, Chromosome abnormalities, Chromosome changes, Chromosome number, Clinical progression, Clonal, Clone, Cold spring harbor laboratory, Cytogenet, Cytogenetic, Cytometry, Deletion, Diploid, Effusion, Fibroblast, Flow cytometry, Gene, Gene amplification, Genet, Genetic instability, Hematologic, Heterogeneity, Histologic, Hsrs, Human cancer, Human tumors, Hyperploid, Karyotype, Karyotypic, Karyotypic progression, Lesion, Leukemia, Leukemic, Leukemic cells, Lymphocyte, Lymphoma, Malignancy, Malignant, Malignant transformation, Malignant tumors, Many tumors, Marker chromosomes, Metaphase, Metastasis, Metastatic, Metastatic disease, Monosomy, Mutation, Myeloproliferative, Natl, Natl cancer inst, Neoplasm, Neuroblastoma, Nonlymphocytic, Nonrandom, Nowell, Oncogene, Other aspects, Ovarian, Phenotype, Ploidy, Polyploidy, Preleukemic, Primary tumor, Primary tumors, Proc, Proc natl acad, Prognostic, Prognostic value, Progression, Rearrangement, Recombinant, Recurrence, Retinoblastoma, Sandberg, Sequential, Solid tumors, Structural aberrations, Syndrome, Tetraploid, Tetraploidy, Translocation, Trisomy, Tumor, Tumor behavior, Tumor cell populations, Tumor cells, Tumor development, Tumor progression, Wolman.
Abstract
Summary: Karyotypic progression may be viewed in at least two ways. One approach seeks evidence for increasing and progressive deviation from the normal chromosome pattern in tumors. The clearest examples, found in some leukemias, are those in which successive karyotypic changes are superimposed on an already aberrant cell population. Evidence of chromosomal progression within solid tumors is far less frequent, possibly because the tumors themselves are at a relatively late stage in their evolution. An alternative approach, therefore, attempts to correlate the extent of karyotypic deviation with other aspects of tumor progression. Recent data, based on classical cytogenetic analyses and flow cytometry, are presented to determine relationships between karyotype and specific origin and morphology of tumors. The predominant theme which emerges, not surprisingly, is that the more deviant chromosome patterns are associated with other measures of increased biologic malignancy. What is surprising is the degree to which these properties are expressed in primary tumors and the relative lack of evidence for further karyotypic evolution with recurrence or metastasis. Examples of genetic instability, evolution through polyploidy, gene amplification, and selection for specific chromosomal rearrangement are found in populations of premalignant and malignant human cells. There is increasing recognition of the importance of tumor-specific chromosome aberrations in the stepwise progression from the normal to the fully neoplastic cell.
Url:
DOI: 10.1007/BF00048481
Links to Exploration step
ISTEX:A9D0058C9812EAA30DF90CB279051FCAFB742FA7Le document en format XML
<record><TEI wicri:istexFullTextTei="biblStruct"><teiHeader><fileDesc><titleStmt><title xml:lang="en">Karyotypic progression in human tumors</title><author><name sortKey="Wolman, Sandra R" sort="Wolman, Sandra R" uniqKey="Wolman S" first="Sandra R." last="Wolman">Sandra R. Wolman</name><affiliation><mods:affiliation>Department of Pathology, New York University, School of Medicine, New York, USA</mods:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">ISTEX</idno><idno type="RBID">ISTEX:A9D0058C9812EAA30DF90CB279051FCAFB742FA7</idno><date when="1983" year="1983">1983</date><idno type="doi">10.1007/BF00048481</idno><idno type="url">https://api.istex.fr/document/A9D0058C9812EAA30DF90CB279051FCAFB742FA7/fulltext/pdf</idno><idno type="wicri:Area/Istex/Corpus">000B35</idno><idno type="wicri:explorRef" wicri:stream="Istex" wicri:step="Corpus" wicri:corpus="ISTEX">000B35</idno></publicationStmt><sourceDesc><biblStruct><analytic><title level="a" type="main" xml:lang="en">Karyotypic progression in human tumors</title><author><name sortKey="Wolman, Sandra R" sort="Wolman, Sandra R" uniqKey="Wolman S" first="Sandra R." last="Wolman">Sandra R. Wolman</name><affiliation><mods:affiliation>Department of Pathology, New York University, School of Medicine, New York, USA</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j">Cancer and Metastasis Reviews</title><title level="j" type="abbrev">Cancer Metast Rev</title><idno type="ISSN">0167-7659</idno><idno type="eISSN">1573-7233</idno><imprint><publisher>Martinus Nijhoff, The Hague/Kluwer Academic Publishers</publisher><pubPlace>Dordrecht</pubPlace><date type="published" when="1983-09-01">1983-09-01</date><biblScope unit="volume">2</biblScope><biblScope unit="issue">3</biblScope><biblScope unit="page" from="257">257</biblScope><biblScope unit="page" to="293">293</biblScope></imprint><idno type="ISSN">0167-7659</idno></series></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0167-7659</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>amplification</term><term>chromosome</term><term>instability</term><term>progression</term><term>rearrangement</term><term>specificity</term></keywords><keywords scheme="Teeft" xml:lang="en"><term>Aberration</term><term>Abnormal</term><term>Abnormality</term><term>Acad</term><term>Acute nonlymphocytic leukemia</term><term>Adenoma</term><term>Aneuploid</term><term>Aneuploidy</term><term>Anll</term><term>Benign</term><term>Bladder</term><term>Bowel</term><term>Breakage</term><term>Cancer genet cytogenet</term><term>Carcinogenesis</term><term>Carcinoma</term><term>Cell lines</term><term>Chromosomal</term><term>Chromosomal aberration</term><term>Chromosomal aberrations</term><term>Chromosomal specificity</term><term>Chromosome</term><term>Chromosome aberrations</term><term>Chromosome abnormalities</term><term>Chromosome changes</term><term>Chromosome number</term><term>Clinical progression</term><term>Clonal</term><term>Clone</term><term>Cold spring harbor laboratory</term><term>Cytogenet</term><term>Cytogenetic</term><term>Cytometry</term><term>Deletion</term><term>Diploid</term><term>Effusion</term><term>Fibroblast</term><term>Flow cytometry</term><term>Gene</term><term>Gene amplification</term><term>Genet</term><term>Genetic instability</term><term>Hematologic</term><term>Heterogeneity</term><term>Histologic</term><term>Hsrs</term><term>Human cancer</term><term>Human tumors</term><term>Hyperploid</term><term>Karyotype</term><term>Karyotypic</term><term>Karyotypic progression</term><term>Lesion</term><term>Leukemia</term><term>Leukemic</term><term>Leukemic cells</term><term>Lymphocyte</term><term>Lymphoma</term><term>Malignancy</term><term>Malignant</term><term>Malignant transformation</term><term>Malignant tumors</term><term>Many tumors</term><term>Marker chromosomes</term><term>Metaphase</term><term>Metastasis</term><term>Metastatic</term><term>Metastatic disease</term><term>Monosomy</term><term>Mutation</term><term>Myeloproliferative</term><term>Natl</term><term>Natl cancer inst</term><term>Neoplasm</term><term>Neuroblastoma</term><term>Nonlymphocytic</term><term>Nonrandom</term><term>Nowell</term><term>Oncogene</term><term>Other aspects</term><term>Ovarian</term><term>Phenotype</term><term>Ploidy</term><term>Polyploidy</term><term>Preleukemic</term><term>Primary tumor</term><term>Primary tumors</term><term>Proc</term><term>Proc natl acad</term><term>Prognostic</term><term>Prognostic value</term><term>Progression</term><term>Rearrangement</term><term>Recombinant</term><term>Recurrence</term><term>Retinoblastoma</term><term>Sandberg</term><term>Sequential</term><term>Solid tumors</term><term>Structural aberrations</term><term>Syndrome</term><term>Tetraploid</term><term>Tetraploidy</term><term>Translocation</term><term>Trisomy</term><term>Tumor</term><term>Tumor behavior</term><term>Tumor cell populations</term><term>Tumor cells</term><term>Tumor development</term><term>Tumor progression</term><term>Wolman</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Summary: Karyotypic progression may be viewed in at least two ways. One approach seeks evidence for increasing and progressive deviation from the normal chromosome pattern in tumors. The clearest examples, found in some leukemias, are those in which successive karyotypic changes are superimposed on an already aberrant cell population. Evidence of chromosomal progression within solid tumors is far less frequent, possibly because the tumors themselves are at a relatively late stage in their evolution. An alternative approach, therefore, attempts to correlate the extent of karyotypic deviation with other aspects of tumor progression. Recent data, based on classical cytogenetic analyses and flow cytometry, are presented to determine relationships between karyotype and specific origin and morphology of tumors. The predominant theme which emerges, not surprisingly, is that the more deviant chromosome patterns are associated with other measures of increased biologic malignancy. What is surprising is the degree to which these properties are expressed in primary tumors and the relative lack of evidence for further karyotypic evolution with recurrence or metastasis. Examples of genetic instability, evolution through polyploidy, gene amplification, and selection for specific chromosomal rearrangement are found in populations of premalignant and malignant human cells. There is increasing recognition of the importance of tumor-specific chromosome aberrations in the stepwise progression from the normal to the fully neoplastic cell.</div></front></TEI><istex><corpusName>springer-journals</corpusName><keywords><teeft><json:string>chromosome</json:string><json:string>chromosomal</json:string><json:string>karyotypic</json:string><json:string>diploid</json:string><json:string>abnormality</json:string><json:string>translocation</json:string><json:string>metastasis</json:string><json:string>malignant</json:string><json:string>karyotype</json:string><json:string>rearrangement</json:string><json:string>genet</json:string><json:string>cytogenetic</json:string><json:string>deletion</json:string><json:string>cytogenet</json:string><json:string>aneuploid</json:string><json:string>karyotypic progression</json:string><json:string>cancer genet cytogenet</json:string><json:string>metaphase</json:string><json:string>ploidy</json:string><json:string>tumor 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mice</json:string><json:string>cytogenetic abnormalities</json:string><json:string>cell carcinoma</json:string><json:string>numerical aberrations</json:string><json:string>balanced translocation</json:string><json:string>normal karyotype</json:string><json:string>renal tumors</json:string><json:string>small fraction</json:string><json:string>modal number</json:string><json:string>salivary gland</json:string><json:string>double minutes</json:string><json:string>cultured cells</json:string><json:string>chromosomal rearrangement</json:string><json:string>small proportion</json:string><json:string>anal quant cytol</json:string><json:string>aneuploid tumors</json:string><json:string>diploid tumors</json:string><json:string>renal cancer</json:string><json:string>chromosome studies</json:string><json:string>small deletions</json:string><json:string>ovarian cancer</json:string><json:string>ovarian cancers</json:string><json:string>cell line</json:string><json:string>chromosomal 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blood lymphocytes</json:string><json:string>strict sense</json:string><json:string>reciprocal exchange</json:string><json:string>genetic predisposition</json:string><json:string>karyotypic abnormality</json:string><json:string>second group</json:string><json:string>certain kinds</json:string><json:string>primary diagnosis</json:string><json:string>antitumor therapy</json:string><json:string>tumor predisposition</json:string><json:string>metal carcinogenesis</json:string><json:string>myelogenous leukemia</json:string><json:string>several cases</json:string><json:string>myeloid leukemias</json:string><json:string>karyotypic aberration</json:string><json:string>positive correlation</json:string><json:string>effective trisomy</json:string><json:string>chromosome alterations</json:string><json:string>survival times</json:string><json:string>survival time</json:string><json:string>chromosomal findings</json:string><json:string>such studies</json:string><json:string>oncogene 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level</json:string><json:string>ploidy levels</json:string><json:string>breast carcinoma</json:string><json:string>individual cases</json:string><json:string>marker formation</json:string><json:string>cytogenetic evidence</json:string><json:string>lung cancer</json:string><json:string>large bowel</json:string><json:string>particular interest</json:string><json:string>constitutional predisposition</json:string><json:string>villous adenoma</json:string><json:string>chromosomal mode</json:string><json:string>structural rearrangement</json:string><json:string>clinical behavior</json:string><json:string>diploid cells</json:string><json:string>tumor tissue</json:string><json:string>other tissues</json:string><json:string>abnormal values</json:string><json:string>other markers</json:string><json:string>hypotetraploid mode</json:string><json:string>urinary bladder</json:string><json:string>great need</json:string><json:string>direct tumor preparations</json:string><json:string>other laboratories</json:string><json:string>cytogenetic specificity</json:string><json:string>bladder tumors</json:string><json:string>bladder washings</json:string><json:string>many instances</json:string><json:string>relative lack</json:string><json:string>effusion fluids</json:string><json:string>karyotypic alterations</json:string><json:string>small number</json:string><json:string>metaphase analysis</json:string><json:string>gene product</json:string><json:string>chromosomal studies</json:string><json:string>gene activity</json:string><json:string>other tumors</json:string><json:string>light chain expression</json:string><json:string>small numbers</json:string><json:string>individual genes</json:string><json:string>predominant pattern</json:string><json:string>individual cells</json:string><json:string>chemical carcinogens</json:string><json:string>human tumor cells</json:string><json:string>chromosomal rearrangements</json:string><json:string>cytophotometric studies</json:string><json:string>malignant phenotype</json:string><json:string>recent review</json:string><json:string>same patient</json:string><json:string>large numbers</json:string><json:string>true diploidy</json:string><json:string>genetic susceptibility</json:string><json:string>many genes</json:string><json:string>staining regions</json:string><json:string>patient survival</json:string><json:string>stromal cells</json:string><json:string>particular chromosomes</json:string><json:string>individual nuclei</json:string><json:string>plenum press</json:string><json:string>chromosome instability</json:string><json:string>testicular tumors</json:string><json:string>further aberration</json:string><json:string>many studies</json:string><json:string>diploid values</json:string><json:string>poor prognosis</json:string><json:string>familial polyposis coli</json:string><json:string>entire series</json:string><json:string>karyotypic aberrations</json:string><json:string>lesser extent</json:string><json:string>hereditary retinoblastoma</json:string><json:string>personal communication</json:string><json:string>bowel cancer</json:string><json:string>simian sarcoma virus</json:string><json:string>human immunoglobulin</json:string><json:string>double minute chromosomes</json:string><json:string>extra sets</json:string></teeft></keywords><author><json:item><name>Sandra R. Wolman</name><affiliations><json:string>Department of Pathology, New York University, School of Medicine, New York, USA</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>chromosome</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>progression</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>instability</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>rearrangement</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>amplification</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>specificity</value></json:item></subject><articleId><json:string>BF00048481</json:string><json:string>Art4</json:string></articleId><arkIstex>ark:/67375/1BB-P8XB5QZ2-5</arkIstex><language><json:string>eng</json:string></language><originalGenre><json:string>OriginalPaper</json:string></originalGenre><abstract>Summary: Karyotypic progression may be viewed in at least two ways. One approach seeks evidence for increasing and progressive deviation from the normal chromosome pattern in tumors. The clearest examples, found in some leukemias, are those in which successive karyotypic changes are superimposed on an already aberrant cell population. Evidence of chromosomal progression within solid tumors is far less frequent, possibly because the tumors themselves are at a relatively late stage in their evolution. An alternative approach, therefore, attempts to correlate the extent of karyotypic deviation with other aspects of tumor progression. Recent data, based on classical cytogenetic analyses and flow cytometry, are presented to determine relationships between karyotype and specific origin and morphology of tumors. The predominant theme which emerges, not surprisingly, is that the more deviant chromosome patterns are associated with other measures of increased biologic malignancy. What is surprising is the degree to which these properties are expressed in primary tumors and the relative lack of evidence for further karyotypic evolution with recurrence or metastasis. Examples of genetic instability, evolution through polyploidy, gene amplification, and selection for specific chromosomal rearrangement are found in populations of premalignant and malignant human cells. There is increasing recognition of the importance of tumor-specific chromosome aberrations in the stepwise progression from the normal to the fully neoplastic cell.</abstract><qualityIndicators><score>9.592</score><pdfWordCount>20570</pdfWordCount><pdfCharCount>129691</pdfCharCount><pdfVersion>1.3</pdfVersion><pdfPageCount>37</pdfPageCount><pdfPageSize>555 x 735 pts</pdfPageSize><refBibsNative>false</refBibsNative><abstractWordCount>216</abstractWordCount><abstractCharCount>1543</abstractCharCount><keywordCount>6</keywordCount></qualityIndicators><title>Karyotypic progression in human tumors</title><pmid><json:string>6231097</json:string></pmid><genre><json:string>research-article</json:string></genre><host><title>Cancer and Metastasis Reviews</title><language><json:string>unknown</json:string></language><publicationDate>1983</publicationDate><copyrightDate>1983</copyrightDate><issn><json:string>0167-7659</json:string></issn><eissn><json:string>1573-7233</json:string></eissn><journalId><json:string>10555</json:string></journalId><volume>2</volume><issue>3</issue><pages><first>257</first><last>293</last></pages><genre><json:string>journal</json:string></genre><subject><json:item><value>Cancer Research</value></json:item><json:item><value>Oncology</value></json:item></subject></host><namedEntities><unitex><date></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:/67375/1BB-P8XB5QZ2-5</json:string></ark><categories><wos><json:string>1 - science</json:string><json:string>2 - oncology</json:string></wos><scienceMetrix><json:string>1 - health sciences</json:string><json:string>2 - clinical medicine</json:string><json:string>3 - oncology & carcinogenesis</json:string></scienceMetrix><scopus><json:string>1 - Life Sciences</json:string><json:string>2 - Biochemistry, Genetics and Molecular Biology</json:string><json:string>3 - Cancer Research</json:string><json:string>1 - Health Sciences</json:string><json:string>2 - Medicine</json:string><json:string>3 - Oncology</json:string></scopus><inist><json:string>1 - sciences appliquees, technologies et medecines</json:string><json:string>2 - sciences biologiques et medicales</json:string><json:string>3 - sciences medicales</json:string></inist></categories><publicationDate>1983</publicationDate><copyrightDate>1983</copyrightDate><doi><json:string>10.1007/BF00048481</json:string></doi><id>A9D0058C9812EAA30DF90CB279051FCAFB742FA7</id><score>1</score><fulltext><json:item><extension>pdf</extension><original>true</original><mimetype>application/pdf</mimetype><uri>https://api.istex.fr/document/A9D0058C9812EAA30DF90CB279051FCAFB742FA7/fulltext/pdf</uri></json:item><json:item><extension>zip</extension><original>false</original><mimetype>application/zip</mimetype><uri>https://api.istex.fr/document/A9D0058C9812EAA30DF90CB279051FCAFB742FA7/fulltext/zip</uri></json:item><istex:fulltextTEI uri="https://api.istex.fr/document/A9D0058C9812EAA30DF90CB279051FCAFB742FA7/fulltext/tei"><teiHeader><fileDesc><titleStmt><title level="a" type="main" xml:lang="en">Karyotypic progression in human tumors</title><respStmt><resp>Références bibliographiques récupérées via GROBID</resp><name resp="ISTEX-API">ISTEX-API (INIST-CNRS)</name></respStmt></titleStmt><publicationStmt><authority>ISTEX</authority><publisher scheme="https://publisher-list.data.istex.fr">Martinus Nijhoff, The Hague/Kluwer Academic Publishers</publisher><pubPlace>Dordrecht</pubPlace><availability><licence><p>Martinus Nijhoff Publishers, 1983</p></licence><p scheme="https://loaded-corpus.data.istex.fr/ark:/67375/XBH-3XSW68JL-F">springer</p></availability><date>1983</date></publicationStmt><notesStmt><note type="research-article" scheme="https://content-type.data.istex.fr/ark:/67375/XTP-1JC4F85T-7">research-article</note><note type="journal" scheme="https://publication-type.data.istex.fr/ark:/67375/JMC-0GLKJH51-B">journal</note></notesStmt><sourceDesc><biblStruct type="inbook"><analytic><title level="a" type="main" xml:lang="en">Karyotypic progression in human tumors</title><author xml:id="author-0000" corresp="yes"><persName><forename type="first">Sandra</forename><surname>Wolman</surname></persName><affiliation>Department of Pathology, New York University, School of Medicine, New York, USA</affiliation></author><idno type="istex">A9D0058C9812EAA30DF90CB279051FCAFB742FA7</idno><idno type="ark">ark:/67375/1BB-P8XB5QZ2-5</idno><idno type="DOI">10.1007/BF00048481</idno><idno type="article-id">BF00048481</idno><idno type="article-id">Art4</idno></analytic><monogr><title level="j">Cancer and Metastasis Reviews</title><title level="j" type="abbrev">Cancer Metast Rev</title><idno type="pISSN">0167-7659</idno><idno type="eISSN">1573-7233</idno><idno type="journal-ID">true</idno><idno type="issue-article-count">6</idno><idno type="volume-issue-count">4</idno><imprint><publisher>Martinus Nijhoff, The Hague/Kluwer Academic Publishers</publisher><pubPlace>Dordrecht</pubPlace><date type="published" when="1983-09-01"></date><biblScope unit="volume">2</biblScope><biblScope unit="issue">3</biblScope><biblScope unit="page" from="257">257</biblScope><biblScope unit="page" to="293">293</biblScope></imprint></monogr></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>1983</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>Summary: Karyotypic progression may be viewed in at least two ways. One approach seeks evidence for increasing and progressive deviation from the normal chromosome pattern in tumors. The clearest examples, found in some leukemias, are those in which successive karyotypic changes are superimposed on an already aberrant cell population. Evidence of chromosomal progression within solid tumors is far less frequent, possibly because the tumors themselves are at a relatively late stage in their evolution. An alternative approach, therefore, attempts to correlate the extent of karyotypic deviation with other aspects of tumor progression. Recent data, based on classical cytogenetic analyses and flow cytometry, are presented to determine relationships between karyotype and specific origin and morphology of tumors. The predominant theme which emerges, not surprisingly, is that the more deviant chromosome patterns are associated with other measures of increased biologic malignancy. What is surprising is the degree to which these properties are expressed in primary tumors and the relative lack of evidence for further karyotypic evolution with recurrence or metastasis. Examples of genetic instability, evolution through polyploidy, gene amplification, and selection for specific chromosomal rearrangement are found in populations of premalignant and malignant human cells. There is increasing recognition of the importance of tumor-specific chromosome aberrations in the stepwise progression from the normal to the fully neoplastic cell.</p></abstract><textClass xml:lang="en"><keywords scheme="keyword"><list><head>Keywords</head><item><term>chromosome</term></item><item><term>progression</term></item><item><term>instability</term></item><item><term>rearrangement</term></item><item><term>amplification</term></item><item><term>specificity</term></item></list></keywords></textClass><textClass><keywords scheme="Journal Subject"><list><head>Medicine & Public Health</head><item><term>Cancer Research</term></item><item><term>Oncology</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="1983-09-01">Published</change><change xml:id="refBibs-istex" who="#ISTEX-API" when="2017-12-1">References added</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><extension>txt</extension><original>false</original><mimetype>text/plain</mimetype><uri>https://api.istex.fr/document/A9D0058C9812EAA30DF90CB279051FCAFB742FA7/fulltext/txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="corpus springer-journals not found" wicri:toSee="no header"><istex:xmlDeclaration>version="1.0" encoding="UTF-8"</istex:xmlDeclaration><istex:docType PUBLIC="-//Springer-Verlag//DTD A++ V2.4//EN" URI="http://devel.springer.de/A++/V2.4/DTD/A++V2.4.dtd" name="istex:docType"></istex:docType><istex:document><Publisher><PublisherInfo><PublisherName>Martinus Nijhoff, The Hague/Kluwer Academic Publishers</PublisherName><PublisherLocation>Dordrecht</PublisherLocation></PublisherInfo><Journal><JournalInfo JournalProductType="ArchiveJournal" NumberingStyle="Unnumbered"><JournalID>10555</JournalID><JournalPrintISSN>0167-7659</JournalPrintISSN><JournalElectronicISSN>1573-7233</JournalElectronicISSN><JournalTitle>Cancer and Metastasis Reviews</JournalTitle><JournalAbbreviatedTitle>Cancer Metast Rev</JournalAbbreviatedTitle><JournalSubjectGroup><JournalSubject Type="Primary">Medicine & Public Health</JournalSubject><JournalSubject Type="Secondary">Cancer Research</JournalSubject><JournalSubject Type="Secondary">Oncology</JournalSubject></JournalSubjectGroup></JournalInfo><Volume><VolumeInfo VolumeType="Regular" TocLevels="0"><VolumeIDStart>2</VolumeIDStart><VolumeIDEnd>2</VolumeIDEnd><VolumeIssueCount>4</VolumeIssueCount></VolumeInfo><Issue IssueType="Regular"><IssueInfo TocLevels="0"><IssueIDStart>3</IssueIDStart><IssueIDEnd>3</IssueIDEnd><IssueArticleCount>6</IssueArticleCount><IssueHistory><CoverDate><DateString>1983</DateString><Year>1983</Year><Month>9</Month></CoverDate></IssueHistory><IssueCopyright><CopyrightHolderName>Martinus Nijhoff Publishers</CopyrightHolderName><CopyrightYear>1983</CopyrightYear></IssueCopyright></IssueInfo><Article ID="Art4"><ArticleInfo Language="En" ArticleType="OriginalPaper" NumberingStyle="Unnumbered" TocLevels="0" ContainsESM="No"><ArticleID>BF00048481</ArticleID><ArticleDOI>10.1007/BF00048481</ArticleDOI><ArticleSequenceNumber>4</ArticleSequenceNumber><ArticleTitle Language="En">Karyotypic progression in human tumors</ArticleTitle><ArticleFirstPage>257</ArticleFirstPage><ArticleLastPage>293</ArticleLastPage><ArticleHistory><RegistrationDate><Year>2004</Year><Month>5</Month><Day>4</Day></RegistrationDate></ArticleHistory><ArticleCopyright><CopyrightHolderName>Martinus Nijhoff Publishers</CopyrightHolderName><CopyrightYear>1983</CopyrightYear></ArticleCopyright><ArticleGrants Type="Regular"><MetadataGrant Grant="OpenAccess"></MetadataGrant><AbstractGrant Grant="OpenAccess"></AbstractGrant><BodyPDFGrant Grant="Restricted"></BodyPDFGrant><BodyHTMLGrant Grant="Restricted"></BodyHTMLGrant><BibliographyGrant Grant="Restricted"></BibliographyGrant><ESMGrant Grant="Restricted"></ESMGrant></ArticleGrants><ArticleContext><JournalID>10555</JournalID><VolumeIDStart>2</VolumeIDStart><VolumeIDEnd>2</VolumeIDEnd><IssueIDStart>3</IssueIDStart><IssueIDEnd>3</IssueIDEnd></ArticleContext></ArticleInfo><ArticleHeader><AuthorGroup><Author AffiliationIDS="Aff1" CorrespondingAffiliationID="Aff2"><AuthorName DisplayOrder="Western"><GivenName>Sandra</GivenName><GivenName>R.</GivenName><FamilyName>Wolman</FamilyName></AuthorName></Author><Affiliation ID="Aff1"><OrgDivision>Department of Pathology</OrgDivision><OrgName>New York University, School of Medicine</OrgName><OrgAddress><City>New York</City><Country>USA</Country></OrgAddress></Affiliation><Affiliation ID="Aff2"><OrgDivision>Department of Pathology</OrgDivision><OrgName>NYU School of Medicine</OrgName><OrgAddress><Street>550 First Avenue</Street><Postcode>10016</Postcode><City>New York</City><State>NY</State><Country>USA</Country></OrgAddress></Affiliation></AuthorGroup><Abstract ID="Abs1" Language="En"><Heading>Summary</Heading><Para>Karyotypic progression may be viewed in at least two ways. One approach seeks evidence for increasing and progressive deviation from the normal chromosome pattern in tumors. The clearest examples, found in some leukemias, are those in which successive karyotypic changes are superimposed on an already aberrant cell population. Evidence of chromosomal progression within solid tumors is far less frequent, possibly because the tumors themselves are at a relatively late stage in their evolution. An alternative approach, therefore, attempts to correlate the extent of karyotypic deviation with other aspects of tumor progression. Recent data, based on classical cytogenetic analyses and flow cytometry, are presented to determine relationships between karyotype and specific origin and morphology of tumors. The predominant theme which emerges, not surprisingly, is that the more deviant chromosome patterns are associated with other measures of increased biologic malignancy. What is surprising is the degree to which these properties are expressed in primary tumors and the relative lack of evidence for further karyotypic evolution with recurrence or metastasis.</Para><Para>Examples of genetic instability, evolution through polyploidy, gene amplification, and selection for specific chromosomal rearrangement are found in populations of premalignant and malignant human cells. There is increasing recognition of the importance of tumor-specific chromosome aberrations in the stepwise progression from the normal to the fully neoplastic cell.</Para></Abstract><KeywordGroup Language="En"><Heading>Keywords</Heading><Keyword>chromosome</Keyword><Keyword>progression</Keyword><Keyword>instability</Keyword><Keyword>rearrangement</Keyword><Keyword>amplification</Keyword><Keyword>specificity</Keyword></KeywordGroup></ArticleHeader><NoBody></NoBody></Article></Issue></Volume></Journal></Publisher></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Karyotypic progression in human tumors</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Karyotypic progression in human tumors</title></titleInfo><name type="personal" displayLabel="corresp"><namePart type="given">Sandra</namePart><namePart type="given">R.</namePart><namePart type="family">Wolman</namePart><affiliation>Department of Pathology, New York University, School of Medicine, New York, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="research-article" displayLabel="OriginalPaper" 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>Martinus Nijhoff, The Hague/Kluwer Academic Publishers</publisher><place><placeTerm type="text">Dordrecht</placeTerm></place><dateIssued encoding="w3cdtf">1983-09-01</dateIssued><dateIssued encoding="w3cdtf">1983</dateIssued><copyrightDate encoding="w3cdtf">1983</copyrightDate></originInfo><language><languageTerm type="code" authority="rfc3066">en</languageTerm><languageTerm type="code" authority="iso639-2b">eng</languageTerm></language><abstract lang="en">Summary: Karyotypic progression may be viewed in at least two ways. One approach seeks evidence for increasing and progressive deviation from the normal chromosome pattern in tumors. The clearest examples, found in some leukemias, are those in which successive karyotypic changes are superimposed on an already aberrant cell population. Evidence of chromosomal progression within solid tumors is far less frequent, possibly because the tumors themselves are at a relatively late stage in their evolution. An alternative approach, therefore, attempts to correlate the extent of karyotypic deviation with other aspects of tumor progression. Recent data, based on classical cytogenetic analyses and flow cytometry, are presented to determine relationships between karyotype and specific origin and morphology of tumors. The predominant theme which emerges, not surprisingly, is that the more deviant chromosome patterns are associated with other measures of increased biologic malignancy. What is surprising is the degree to which these properties are expressed in primary tumors and the relative lack of evidence for further karyotypic evolution with recurrence or metastasis. Examples of genetic instability, evolution through polyploidy, gene amplification, and selection for specific chromosomal rearrangement are found in populations of premalignant and malignant human cells. There is increasing recognition of the importance of tumor-specific chromosome aberrations in the stepwise progression from the normal to the fully neoplastic cell.</abstract><subject lang="en"><genre>Keywords</genre><topic>chromosome</topic><topic>progression</topic><topic>instability</topic><topic>rearrangement</topic><topic>amplification</topic><topic>specificity</topic></subject><relatedItem type="host"><titleInfo><title>Cancer and Metastasis Reviews</title></titleInfo><titleInfo type="abbreviated"><title>Cancer Metast Rev</title></titleInfo><genre type="journal" displayLabel="Archive Journal" authority="ISTEX" valueURI="https://publication-type.data.istex.fr/ark:/67375/JMC-0GLKJH51-B">journal</genre><originInfo><publisher>Springer</publisher><dateIssued encoding="w3cdtf">1983-09-01</dateIssued><copyrightDate encoding="w3cdtf">1983</copyrightDate></originInfo><subject><genre>Medicine & Public Health</genre><topic>Cancer Research</topic><topic>Oncology</topic></subject><identifier type="ISSN">0167-7659</identifier><identifier type="eISSN">1573-7233</identifier><identifier type="JournalID">10555</identifier><identifier type="IssueArticleCount">6</identifier><identifier type="VolumeIssueCount">4</identifier><part><date>1983</date><detail type="volume"><number>2</number><caption>vol.</caption></detail><detail type="issue"><number>3</number><caption>no.</caption></detail><extent unit="pages"><start>257</start><end>293</end></extent></part><recordInfo><recordOrigin>Martinus Nijhoff Publishers, 1983</recordOrigin></recordInfo></relatedItem><identifier type="istex">A9D0058C9812EAA30DF90CB279051FCAFB742FA7</identifier><identifier type="ark">ark:/67375/1BB-P8XB5QZ2-5</identifier><identifier type="DOI">10.1007/BF00048481</identifier><identifier type="ArticleID">BF00048481</identifier><identifier type="ArticleID">Art4</identifier><accessCondition type="use and reproduction" contentType="copyright">Martinus Nijhoff Publishers, 1983</accessCondition><recordInfo><recordContentSource authority="ISTEX" authorityURI="https://loaded-corpus.data.istex.fr" valueURI="https://loaded-corpus.data.istex.fr/ark:/67375/XBH-3XSW68JL-F">springer</recordContentSource><recordOrigin>Martinus Nijhoff Publishers, 1983</recordOrigin></recordInfo></mods><json:item><extension>json</extension><original>false</original><mimetype>application/json</mimetype><uri>https://api.istex.fr/document/A9D0058C9812EAA30DF90CB279051FCAFB742FA7/metadata/json</uri></json:item></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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