TEL is one of the targets for deletion on 12p in many cases of childhood B-lineage acute lymphoblastic leukemia
Abnormalities of the short arm of chromosome 12 including loss of heterozygosity (LOH) and TEL/AML-1 fusion resulting from a t(12;21)(p13;q22) translocation are frequently observed in childhood acute lymphoblastic leukemia (ALL). We investigated 21 DNA samples of childhood ALL which had LOH at 12p13...
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| Veröffentlicht in: | Leukemia 1997-08, Vol.11 (8), p.1220-1223 |
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| creator | TAKEUCHI, S SERIU, T BARTRAM, C. R GOLUB, T. R REITER, A MIYOSHI, I GILLILAND, D. G KOEFFLER, H. P |
| description | Abnormalities of the short arm of chromosome 12 including loss of heterozygosity (LOH) and TEL/AML-1 fusion resulting from a t(12;21)(p13;q22) translocation are frequently observed in childhood acute lymphoblastic leukemia (ALL). We investigated 21 DNA samples of childhood ALL which had LOH at 12p13. Rearrangement of TEL was observed in eight cases and another case showed a homozygous deletion of TEL. Two informative samples with TEL rearrangement had a deletion localized to the 5' region of this gene. The deletion in these two cases includes the helix-loop-helix (HLH) domain. This is consistent with the hypothesis that the normal tel can heterodimerize with the TEL/AML-1 gene product and inhibit the transforming capacity of the chimeric protein. Presumably, loss of the HLH of the normal remaining TEL allele abrogates this tumor suppressor-like function. The case with homozygous deletion of TEL is also consistent with this gene having qualities of a tumor suppressor. One unusual case had T-ALL rather than B-lineage ALL and the leukemic cells had rearrangement of TEL, but they did not have an alteration of the remaining TEL allele suggesting that the etiology of this disease may be different. This analysis further emphasizes the importance of loss of the normal TEL allele in childhood precursor B-lineage ALL. |
| doi_str_mv | 10.1038/sj.leu.2400743 |
| format | Article |
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R ; GOLUB, T. R ; REITER, A ; MIYOSHI, I ; GILLILAND, D. G ; KOEFFLER, H. P</creator><creatorcontrib>TAKEUCHI, S ; SERIU, T ; BARTRAM, C. R ; GOLUB, T. R ; REITER, A ; MIYOSHI, I ; GILLILAND, D. G ; KOEFFLER, H. P</creatorcontrib><description>Abnormalities of the short arm of chromosome 12 including loss of heterozygosity (LOH) and TEL/AML-1 fusion resulting from a t(12;21)(p13;q22) translocation are frequently observed in childhood acute lymphoblastic leukemia (ALL). We investigated 21 DNA samples of childhood ALL which had LOH at 12p13. Rearrangement of TEL was observed in eight cases and another case showed a homozygous deletion of TEL. Two informative samples with TEL rearrangement had a deletion localized to the 5' region of this gene. The deletion in these two cases includes the helix-loop-helix (HLH) domain. This is consistent with the hypothesis that the normal tel can heterodimerize with the TEL/AML-1 gene product and inhibit the transforming capacity of the chimeric protein. Presumably, loss of the HLH of the normal remaining TEL allele abrogates this tumor suppressor-like function. The case with homozygous deletion of TEL is also consistent with this gene having qualities of a tumor suppressor. One unusual case had T-ALL rather than B-lineage ALL and the leukemic cells had rearrangement of TEL, but they did not have an alteration of the remaining TEL allele suggesting that the etiology of this disease may be different. This analysis further emphasizes the importance of loss of the normal TEL allele in childhood precursor B-lineage ALL.</description><identifier>ISSN: 0887-6924</identifier><identifier>EISSN: 1476-5551</identifier><identifier>DOI: 10.1038/sj.leu.2400743</identifier><identifier>PMID: 9264373</identifier><identifier>CODEN: LEUKED</identifier><language>eng</language><publisher>London: Nature Publishing</publisher><subject>Abnormalities ; Acute lymphoblastic leukemia ; Acute myeloid leukemia ; Alleles ; Biological and medical sciences ; Blotting, Southern ; Burkitt Lymphoma - genetics ; Child ; Childhood ; Children ; Chromosome 12 ; Chromosomes, Human, Pair 12 ; Deoxyribonucleic acid ; DNA ; DNA-Binding Proteins - genetics ; Etiology ; ETS Translocation Variant 6 Protein ; Gene Deletion ; Gene Rearrangement ; Hematologic and hematopoietic diseases ; Heterozygosity ; Humans ; Leukemia ; Leukemia-Lymphoma, Adult T-Cell - genetics ; Leukemias. Malignant lymphomas. Malignant reticulosis. Myelofibrosis ; Loss of heterozygosity ; Lymphatic leukemia ; Lymphocytes T ; Medical sciences ; Nuclear Proteins - genetics ; Proto-Oncogene Proteins c-ets ; Repressor Proteins ; Sequence Deletion ; Transcription Factors - genetics ; Translocation ; Tumor suppressor genes ; Tumors</subject><ispartof>Leukemia, 1997-08, Vol.11 (8), p.1220-1223</ispartof><rights>1997 INIST-CNRS</rights><rights>Macmillan Publishers Limited 1997.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c378t-2078ba8822f86e069a4a6ce8060fc6314c574e622b1315a0c4e83898fe37da3c3</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27901,27902</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=2780339$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/9264373$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>TAKEUCHI, S</creatorcontrib><creatorcontrib>SERIU, T</creatorcontrib><creatorcontrib>BARTRAM, C. 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The deletion in these two cases includes the helix-loop-helix (HLH) domain. This is consistent with the hypothesis that the normal tel can heterodimerize with the TEL/AML-1 gene product and inhibit the transforming capacity of the chimeric protein. Presumably, loss of the HLH of the normal remaining TEL allele abrogates this tumor suppressor-like function. The case with homozygous deletion of TEL is also consistent with this gene having qualities of a tumor suppressor. One unusual case had T-ALL rather than B-lineage ALL and the leukemic cells had rearrangement of TEL, but they did not have an alteration of the remaining TEL allele suggesting that the etiology of this disease may be different. This analysis further emphasizes the importance of loss of the normal TEL allele in childhood precursor B-lineage ALL.</description><subject>Abnormalities</subject><subject>Acute lymphoblastic leukemia</subject><subject>Acute myeloid leukemia</subject><subject>Alleles</subject><subject>Biological and medical sciences</subject><subject>Blotting, Southern</subject><subject>Burkitt Lymphoma - genetics</subject><subject>Child</subject><subject>Childhood</subject><subject>Children</subject><subject>Chromosome 12</subject><subject>Chromosomes, Human, Pair 12</subject><subject>Deoxyribonucleic acid</subject><subject>DNA</subject><subject>DNA-Binding Proteins - genetics</subject><subject>Etiology</subject><subject>ETS Translocation Variant 6 Protein</subject><subject>Gene Deletion</subject><subject>Gene Rearrangement</subject><subject>Hematologic and hematopoietic diseases</subject><subject>Heterozygosity</subject><subject>Humans</subject><subject>Leukemia</subject><subject>Leukemia-Lymphoma, Adult T-Cell - genetics</subject><subject>Leukemias. 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R</au><au>GOLUB, T. R</au><au>REITER, A</au><au>MIYOSHI, I</au><au>GILLILAND, D. G</au><au>KOEFFLER, H. P</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>TEL is one of the targets for deletion on 12p in many cases of childhood B-lineage acute lymphoblastic leukemia</atitle><jtitle>Leukemia</jtitle><addtitle>Leukemia</addtitle><date>1997-08-01</date><risdate>1997</risdate><volume>11</volume><issue>8</issue><spage>1220</spage><epage>1223</epage><pages>1220-1223</pages><issn>0887-6924</issn><eissn>1476-5551</eissn><coden>LEUKED</coden><abstract>Abnormalities of the short arm of chromosome 12 including loss of heterozygosity (LOH) and TEL/AML-1 fusion resulting from a t(12;21)(p13;q22) translocation are frequently observed in childhood acute lymphoblastic leukemia (ALL). We investigated 21 DNA samples of childhood ALL which had LOH at 12p13. Rearrangement of TEL was observed in eight cases and another case showed a homozygous deletion of TEL. Two informative samples with TEL rearrangement had a deletion localized to the 5' region of this gene. The deletion in these two cases includes the helix-loop-helix (HLH) domain. This is consistent with the hypothesis that the normal tel can heterodimerize with the TEL/AML-1 gene product and inhibit the transforming capacity of the chimeric protein. Presumably, loss of the HLH of the normal remaining TEL allele abrogates this tumor suppressor-like function. The case with homozygous deletion of TEL is also consistent with this gene having qualities of a tumor suppressor. One unusual case had T-ALL rather than B-lineage ALL and the leukemic cells had rearrangement of TEL, but they did not have an alteration of the remaining TEL allele suggesting that the etiology of this disease may be different. This analysis further emphasizes the importance of loss of the normal TEL allele in childhood precursor B-lineage ALL.</abstract><cop>London</cop><pub>Nature Publishing</pub><pmid>9264373</pmid><doi>10.1038/sj.leu.2400743</doi><tpages>4</tpages></addata></record> |
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| subjects | Abnormalities Acute lymphoblastic leukemia Acute myeloid leukemia Alleles Biological and medical sciences Blotting, Southern Burkitt Lymphoma - genetics Child Childhood Children Chromosome 12 Chromosomes, Human, Pair 12 Deoxyribonucleic acid DNA DNA-Binding Proteins - genetics Etiology ETS Translocation Variant 6 Protein Gene Deletion Gene Rearrangement Hematologic and hematopoietic diseases Heterozygosity Humans Leukemia Leukemia-Lymphoma, Adult T-Cell - genetics Leukemias. Malignant lymphomas. Malignant reticulosis. Myelofibrosis Loss of heterozygosity Lymphatic leukemia Lymphocytes T Medical sciences Nuclear Proteins - genetics Proto-Oncogene Proteins c-ets Repressor Proteins Sequence Deletion Transcription Factors - genetics Translocation Tumor suppressor genes Tumors |
| title | TEL is one of the targets for deletion on 12p in many cases of childhood B-lineage acute lymphoblastic leukemia |
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