Loading…
Nonrandom chromosomal changes in transitional cell carcinoma of the bladder
Nine cases of transitional cell carcinoma (eight from the urinary bladder and one from the ureter; six noninvasive and three invasive) were subjected to detailed cytogenetic analysis with a G-banding method. The synchronization of primary cultures with methotrexate for high-resolution banding was pe...
Saved in:
| Published in: | Cancer research (Chicago, Ill.) Ill.), 1984-03, Vol.44 (3), p.1257-1264 |
|---|---|
| Main Authors: | , , , , |
| Format: | Article |
| Language: | English |
| Subjects: | |
| Online Access: | Get full text |
| Tags: |
Add Tag
No Tags, Be the first to tag this record!
|
| cited_by | |
|---|---|
| cites | |
| container_end_page | 1264 |
| container_issue | 3 |
| container_start_page | 1257 |
| container_title | Cancer research (Chicago, Ill.) |
| container_volume | 44 |
| creator | GIBAS, Z PROUT, G. R. JR CONNOLLY, J. G PONTES, J. E SANDBERG, A. A |
| description | Nine cases of transitional cell carcinoma (eight from the urinary bladder and one from the ureter; six noninvasive and three invasive) were subjected to detailed cytogenetic analysis with a G-banding method. The synchronization of primary cultures with methotrexate for high-resolution banding was performed in five cases. In the remaining four cases, the chromosomes were obtained from short-term cultures after prolonged (16 hr) exposure to Colcemid. Two cases were near-tetraploid, one was hypotriploid, and six were near-diploid (three hyperdiploid and three hypodiploid). All but one case showed various structural abnormalities in the karyotype. The chromosomal changes ranged from the presence of only two abnormal chromosomes (markers) to complex karyotypes with as many as 15 markers. In most tumors, the origin of the marker chromosomes could be readily deciphered. The nonrandom chromosomal aberrations included: (a) an isochrosome of the short arm of chromosome 5 (three cases); (b) monosomy of chromosome 9 found in four cases (this was the sole abnormality in one case); (c) involvement of chromosome 8 as an isochromosome of the long arm (two cases) or loss of the short arm due to deletion (one case) or translocation (one case); and (d) interstitial deletion of chromosome 13 (three cases). Our results indicate that the formation of i(5p) and monosomy 9 may be the primary karyotypic changes in two subgroups of transitional cell carcinoma. Involvement of chromosomes 8 and 13, on the other hand, seems to be a result of secondary karyotypic evolution. Two invasive tumors showed the presence of secondary clones, with additional structural chromosome aberrations superimposed on those already existing in the main cell population. In both cases, the additional aberrations involved the short arm of chromosome 11, resulting in loss of genetic material from the short arm. The short arm of chromosome 11, is the putative site of an oncogene which has been isolated from human bladder carcinoma cell lines. Deletion of the 11p was also seen in one case of noninvasive transitional cell carcinoma localized in the ureter; the material from 11p was probably translocated to chromosome 13. These findings suggest that the loss of genetic material from the short arm of chromosome 11 is a secondary event in the karyotypic evolution of transitional cell carcinoma, probably related to the invasive behavior of the tumor. |
| format | article |
| fullrecord | <record><control><sourceid>proquest_pubme</sourceid><recordid>TN_cdi_proquest_miscellaneous_80926299</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>80926299</sourcerecordid><originalsourceid>FETCH-LOGICAL-h299t-f6b1ef4e8ba807b51ad9b27f6166bad2244b0186584e56d229fc024a2b8f49563</originalsourceid><addsrcrecordid>eNqFkE1PwzAMhiMEGmPwE5B6QNwqJWk-j2gChpjgAufKaRMW1CYj6Q78ezJRceVi-_X7yLZ8gpaEN6qWjPFTtMQYq5ozSc_RRc6fRXKC-QIthNCUYblEzy8xJAh9HKtul-IYcxxhKDWED5srH6qp2NlPPoZj3w4lQOp8KFwVXTXtbGUG6HubLtGZgyHbqzmv0PvD_dt6U29fH5_Wd9t6R7WeaicMsY5ZZUBhaTiBXhsqnSBCGOgpZcxgogRXzHJRtHYdpgyoUY5pLpoVuv2du0_x62Dz1I4-Hy-DYOMhtwprKsqqf0HSaEw5lgW8nsGDGW3f7pMfIX2385uKfzP7kDsYXHlJ5_MfppTkuGmaHyyacQ0</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>13902507</pqid></control><display><type>article</type><title>Nonrandom chromosomal changes in transitional cell carcinoma of the bladder</title><source>Free E-Journal (出版社公開部分のみ）</source><creator>GIBAS, Z ; PROUT, G. R. JR ; CONNOLLY, J. G ; PONTES, J. E ; SANDBERG, A. A</creator><creatorcontrib>GIBAS, Z ; PROUT, G. R. JR ; CONNOLLY, J. G ; PONTES, J. E ; SANDBERG, A. A</creatorcontrib><description>Nine cases of transitional cell carcinoma (eight from the urinary bladder and one from the ureter; six noninvasive and three invasive) were subjected to detailed cytogenetic analysis with a G-banding method. The synchronization of primary cultures with methotrexate for high-resolution banding was performed in five cases. In the remaining four cases, the chromosomes were obtained from short-term cultures after prolonged (16 hr) exposure to Colcemid. Two cases were near-tetraploid, one was hypotriploid, and six were near-diploid (three hyperdiploid and three hypodiploid). All but one case showed various structural abnormalities in the karyotype. The chromosomal changes ranged from the presence of only two abnormal chromosomes (markers) to complex karyotypes with as many as 15 markers. In most tumors, the origin of the marker chromosomes could be readily deciphered. The nonrandom chromosomal aberrations included: (a) an isochrosome of the short arm of chromosome 5 (three cases); (b) monosomy of chromosome 9 found in four cases (this was the sole abnormality in one case); (c) involvement of chromosome 8 as an isochromosome of the long arm (two cases) or loss of the short arm due to deletion (one case) or translocation (one case); and (d) interstitial deletion of chromosome 13 (three cases). Our results indicate that the formation of i(5p) and monosomy 9 may be the primary karyotypic changes in two subgroups of transitional cell carcinoma. Involvement of chromosomes 8 and 13, on the other hand, seems to be a result of secondary karyotypic evolution. Two invasive tumors showed the presence of secondary clones, with additional structural chromosome aberrations superimposed on those already existing in the main cell population. In both cases, the additional aberrations involved the short arm of chromosome 11, resulting in loss of genetic material from the short arm. The short arm of chromosome 11, is the putative site of an oncogene which has been isolated from human bladder carcinoma cell lines. Deletion of the 11p was also seen in one case of noninvasive transitional cell carcinoma localized in the ureter; the material from 11p was probably translocated to chromosome 13. These findings suggest that the loss of genetic material from the short arm of chromosome 11 is a secondary event in the karyotypic evolution of transitional cell carcinoma, probably related to the invasive behavior of the tumor.</description><identifier>ISSN: 0008-5472</identifier><identifier>EISSN: 1538-7445</identifier><identifier>PMID: 6692407</identifier><identifier>CODEN: CNREA8</identifier><language>eng</language><publisher>Philadelphia, PA: American Association for Cancer Research</publisher><subject>Aged ; Biological and medical sciences ; Carcinoma, Transitional Cell - genetics ; Carcinoma, Transitional Cell - pathology ; Cells, Cultured ; Chromosome Aberrations ; Chromosome Disorders ; Clone Cells ; Female ; Humans ; Karyotyping ; Male ; Medical sciences ; Metaphase ; Middle Aged ; Nephrology. Urinary tract diseases ; Ploidies ; Translocation, Genetic ; Tumors of the urinary system ; Urinary Bladder Neoplasms - genetics ; Urinary Bladder Neoplasms - pathology ; Urinary tract. Prostate gland</subject><ispartof>Cancer research (Chicago, Ill.), 1984-03, Vol.44 (3), p.1257-1264</ispartof><rights>1985 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>315,786,790</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=8875033$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/6692407$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>GIBAS, Z</creatorcontrib><creatorcontrib>PROUT, G. R. JR</creatorcontrib><creatorcontrib>CONNOLLY, J. G</creatorcontrib><creatorcontrib>PONTES, J. E</creatorcontrib><creatorcontrib>SANDBERG, A. A</creatorcontrib><title>Nonrandom chromosomal changes in transitional cell carcinoma of the bladder</title><title>Cancer research (Chicago, Ill.)</title><addtitle>Cancer Res</addtitle><description>Nine cases of transitional cell carcinoma (eight from the urinary bladder and one from the ureter; six noninvasive and three invasive) were subjected to detailed cytogenetic analysis with a G-banding method. The synchronization of primary cultures with methotrexate for high-resolution banding was performed in five cases. In the remaining four cases, the chromosomes were obtained from short-term cultures after prolonged (16 hr) exposure to Colcemid. Two cases were near-tetraploid, one was hypotriploid, and six were near-diploid (three hyperdiploid and three hypodiploid). All but one case showed various structural abnormalities in the karyotype. The chromosomal changes ranged from the presence of only two abnormal chromosomes (markers) to complex karyotypes with as many as 15 markers. In most tumors, the origin of the marker chromosomes could be readily deciphered. The nonrandom chromosomal aberrations included: (a) an isochrosome of the short arm of chromosome 5 (three cases); (b) monosomy of chromosome 9 found in four cases (this was the sole abnormality in one case); (c) involvement of chromosome 8 as an isochromosome of the long arm (two cases) or loss of the short arm due to deletion (one case) or translocation (one case); and (d) interstitial deletion of chromosome 13 (three cases). Our results indicate that the formation of i(5p) and monosomy 9 may be the primary karyotypic changes in two subgroups of transitional cell carcinoma. Involvement of chromosomes 8 and 13, on the other hand, seems to be a result of secondary karyotypic evolution. Two invasive tumors showed the presence of secondary clones, with additional structural chromosome aberrations superimposed on those already existing in the main cell population. In both cases, the additional aberrations involved the short arm of chromosome 11, resulting in loss of genetic material from the short arm. The short arm of chromosome 11, is the putative site of an oncogene which has been isolated from human bladder carcinoma cell lines. Deletion of the 11p was also seen in one case of noninvasive transitional cell carcinoma localized in the ureter; the material from 11p was probably translocated to chromosome 13. These findings suggest that the loss of genetic material from the short arm of chromosome 11 is a secondary event in the karyotypic evolution of transitional cell carcinoma, probably related to the invasive behavior of the tumor.</description><subject>Aged</subject><subject>Biological and medical sciences</subject><subject>Carcinoma, Transitional Cell - genetics</subject><subject>Carcinoma, Transitional Cell - pathology</subject><subject>Cells, Cultured</subject><subject>Chromosome Aberrations</subject><subject>Chromosome Disorders</subject><subject>Clone Cells</subject><subject>Female</subject><subject>Humans</subject><subject>Karyotyping</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Metaphase</subject><subject>Middle Aged</subject><subject>Nephrology. Urinary tract diseases</subject><subject>Ploidies</subject><subject>Translocation, Genetic</subject><subject>Tumors of the urinary system</subject><subject>Urinary Bladder Neoplasms - genetics</subject><subject>Urinary Bladder Neoplasms - pathology</subject><subject>Urinary tract. Prostate gland</subject><issn>0008-5472</issn><issn>1538-7445</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1984</creationdate><recordtype>article</recordtype><recordid>eNqFkE1PwzAMhiMEGmPwE5B6QNwqJWk-j2gChpjgAufKaRMW1CYj6Q78ezJRceVi-_X7yLZ8gpaEN6qWjPFTtMQYq5ozSc_RRc6fRXKC-QIthNCUYblEzy8xJAh9HKtul-IYcxxhKDWED5srH6qp2NlPPoZj3w4lQOp8KFwVXTXtbGUG6HubLtGZgyHbqzmv0PvD_dt6U29fH5_Wd9t6R7WeaicMsY5ZZUBhaTiBXhsqnSBCGOgpZcxgogRXzHJRtHYdpgyoUY5pLpoVuv2du0_x62Dz1I4-Hy-DYOMhtwprKsqqf0HSaEw5lgW8nsGDGW3f7pMfIX2385uKfzP7kDsYXHlJ5_MfppTkuGmaHyyacQ0</recordid><startdate>19840301</startdate><enddate>19840301</enddate><creator>GIBAS, Z</creator><creator>PROUT, G. R. JR</creator><creator>CONNOLLY, J. G</creator><creator>PONTES, J. E</creator><creator>SANDBERG, A. A</creator><general>American Association for Cancer Research</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>8FD</scope><scope>FR3</scope><scope>P64</scope><scope>RC3</scope><scope>7X8</scope></search><sort><creationdate>19840301</creationdate><title>Nonrandom chromosomal changes in transitional cell carcinoma of the bladder</title><author>GIBAS, Z ; PROUT, G. R. JR ; CONNOLLY, J. G ; PONTES, J. E ; SANDBERG, A. A</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-h299t-f6b1ef4e8ba807b51ad9b27f6166bad2244b0186584e56d229fc024a2b8f49563</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1984</creationdate><topic>Aged</topic><topic>Biological and medical sciences</topic><topic>Carcinoma, Transitional Cell - genetics</topic><topic>Carcinoma, Transitional Cell - pathology</topic><topic>Cells, Cultured</topic><topic>Chromosome Aberrations</topic><topic>Chromosome Disorders</topic><topic>Clone Cells</topic><topic>Female</topic><topic>Humans</topic><topic>Karyotyping</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Metaphase</topic><topic>Middle Aged</topic><topic>Nephrology. Urinary tract diseases</topic><topic>Ploidies</topic><topic>Translocation, Genetic</topic><topic>Tumors of the urinary system</topic><topic>Urinary Bladder Neoplasms - genetics</topic><topic>Urinary Bladder Neoplasms - pathology</topic><topic>Urinary tract. Prostate gland</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>GIBAS, Z</creatorcontrib><creatorcontrib>PROUT, G. R. JR</creatorcontrib><creatorcontrib>CONNOLLY, J. G</creatorcontrib><creatorcontrib>PONTES, J. E</creatorcontrib><creatorcontrib>SANDBERG, A. A</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>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Cancer research (Chicago, Ill.)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>GIBAS, Z</au><au>PROUT, G. R. JR</au><au>CONNOLLY, J. G</au><au>PONTES, J. E</au><au>SANDBERG, A. A</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Nonrandom chromosomal changes in transitional cell carcinoma of the bladder</atitle><jtitle>Cancer research (Chicago, Ill.)</jtitle><addtitle>Cancer Res</addtitle><date>1984-03-01</date><risdate>1984</risdate><volume>44</volume><issue>3</issue><spage>1257</spage><epage>1264</epage><pages>1257-1264</pages><issn>0008-5472</issn><eissn>1538-7445</eissn><coden>CNREA8</coden><notes>ObjectType-Article-2</notes><notes>SourceType-Scholarly Journals-1</notes><notes>ObjectType-Feature-1</notes><notes>content type line 23</notes><notes>ObjectType-Article-1</notes><notes>ObjectType-Feature-2</notes><abstract>Nine cases of transitional cell carcinoma (eight from the urinary bladder and one from the ureter; six noninvasive and three invasive) were subjected to detailed cytogenetic analysis with a G-banding method. The synchronization of primary cultures with methotrexate for high-resolution banding was performed in five cases. In the remaining four cases, the chromosomes were obtained from short-term cultures after prolonged (16 hr) exposure to Colcemid. Two cases were near-tetraploid, one was hypotriploid, and six were near-diploid (three hyperdiploid and three hypodiploid). All but one case showed various structural abnormalities in the karyotype. The chromosomal changes ranged from the presence of only two abnormal chromosomes (markers) to complex karyotypes with as many as 15 markers. In most tumors, the origin of the marker chromosomes could be readily deciphered. The nonrandom chromosomal aberrations included: (a) an isochrosome of the short arm of chromosome 5 (three cases); (b) monosomy of chromosome 9 found in four cases (this was the sole abnormality in one case); (c) involvement of chromosome 8 as an isochromosome of the long arm (two cases) or loss of the short arm due to deletion (one case) or translocation (one case); and (d) interstitial deletion of chromosome 13 (three cases). Our results indicate that the formation of i(5p) and monosomy 9 may be the primary karyotypic changes in two subgroups of transitional cell carcinoma. Involvement of chromosomes 8 and 13, on the other hand, seems to be a result of secondary karyotypic evolution. Two invasive tumors showed the presence of secondary clones, with additional structural chromosome aberrations superimposed on those already existing in the main cell population. In both cases, the additional aberrations involved the short arm of chromosome 11, resulting in loss of genetic material from the short arm. The short arm of chromosome 11, is the putative site of an oncogene which has been isolated from human bladder carcinoma cell lines. Deletion of the 11p was also seen in one case of noninvasive transitional cell carcinoma localized in the ureter; the material from 11p was probably translocated to chromosome 13. These findings suggest that the loss of genetic material from the short arm of chromosome 11 is a secondary event in the karyotypic evolution of transitional cell carcinoma, probably related to the invasive behavior of the tumor.</abstract><cop>Philadelphia, PA</cop><pub>American Association for Cancer Research</pub><pmid>6692407</pmid><tpages>8</tpages></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0008-5472 |
| ispartof | Cancer research (Chicago, Ill.), 1984-03, Vol.44 (3), p.1257-1264 |
| issn | 0008-5472 1538-7445 |
| language | eng |
| recordid | cdi_proquest_miscellaneous_80926299 |
| source | Free E-Journal (出版社公開部分のみ） |
| subjects | Aged Biological and medical sciences Carcinoma, Transitional Cell - genetics Carcinoma, Transitional Cell - pathology Cells, Cultured Chromosome Aberrations Chromosome Disorders Clone Cells Female Humans Karyotyping Male Medical sciences Metaphase Middle Aged Nephrology. Urinary tract diseases Ploidies Translocation, Genetic Tumors of the urinary system Urinary Bladder Neoplasms - genetics Urinary Bladder Neoplasms - pathology Urinary tract. Prostate gland |
| title | Nonrandom chromosomal changes in transitional cell carcinoma of the bladder |
| url | http://sfxeu10.hosted.exlibrisgroup.com/loughborough?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2024-09-22T04%3A54%3A46IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_pubme&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Nonrandom%20chromosomal%20changes%20in%20transitional%20cell%20carcinoma%20of%20the%20bladder&rft.jtitle=Cancer%20research%20(Chicago,%20Ill.)&rft.au=GIBAS,%20Z&rft.date=1984-03-01&rft.volume=44&rft.issue=3&rft.spage=1257&rft.epage=1264&rft.pages=1257-1264&rft.issn=0008-5472&rft.eissn=1538-7445&rft.coden=CNREA8&rft_id=info:doi/&rft_dat=%3Cproquest_pubme%3E80926299%3C/proquest_pubme%3E%3Cgrp_id%3Ecdi_FETCH-LOGICAL-h299t-f6b1ef4e8ba807b51ad9b27f6166bad2244b0186584e56d229fc024a2b8f49563%3C/grp_id%3E%3Coa%3E%3C/oa%3E%3Curl%3E%3C/url%3E&rft_id=info:oai/&rft_pqid=13902507&rft_id=info:pmid/6692407&rfr_iscdi=true |