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100 1 a| Hedgebeth, Tamara L.,e| author.?| UNAUTHORIZED;

245 10 a| Molecular detection of INV(16)(p13q22) in acute myeloid leukemia /c| by Tamara L. Hedgebeth.;

264 0 c| 2002.;

300 a| vi, 62 leaves :b| illustrations (some color) ;c| 28 cm;

336 a| textb| txt2| rdacontent;

337 a| unmediatedb| n2| rdamedia;

338 a| volumeb| nc2| rdacarrier;

502 b| M.S.c| East Carolina Universityd| 2002;

500 a| Presented to the faculty of the Department of Biology.;

500 a| Advisor: John E. Wiley;

520 3 a| Acute myeloid leukemia (AML) is a malignancy of immature bone marrow cells resulting from a block in differentiation of myeloid cells. The most typical chromosome 16 rearrangement is inv(16)(pl3q22) [inv(16)], which accounts for approximately 8% of AML cases. In this rearrangement, the core binding factor beta (CBFB) gene, located on 16q22 is fused to the myosin heavy chain gene (MYH11), located on 16pl3. Several different CBFB/MYH11 transcripts have been identified by RT-PCR, and the type A transcript is the most common. Genomic PCR and DNA sequencing were employed in order to detect this fusion type on the genomic level in inv(16) and putative mosaic inv(16) patient material. Primers were designed so that they spanned intron 30 of MYH11, with the forward primer located in exon 30 of MYH11 and the reverse primer located in exon 31 of MYH11. It was expected that the absence of a band would indicate an inversion and that the presence of a band would indicate the absence of an inversion. A 592 bp PCR product was generated, cloned, and sequenced. Sequencing results confirmed that there was no inversion of chromosome 16 for the three patients. Alignment results revealed extensive homology between the inv(16), putative mosaic inv(16), and normal patient sequences, with only a few differences in nucleotides. Inherent problems associated with the use of chromosome microdissection, DOP-PCR, and genomic PCR in the characterization of inv (16) and CBFB/MYHl1 are also discussed.;

504 a| Includes bibliographical references (leaves 53-62).;

650 0 a| Acute myeloid leukemiax| Genetic aspects.=| ^A863193;

650 0 a| Microdissection.=| ^A444455;

650 0 a| Human chromosomes.=| ^A1468;

650 2 a| Chromosomes, Human.0| (DNLM)D002877=| ^A920601;

655 2 a| Academic Dissertation.0| (DNLM)D019478?| UNAUTHORIZED;

650 7 a| Human chromosomes.2| fast0| (OCoLC)fst00962918;

650 7 a| Microdissection.2| fast0| (OCoLC)fst01019726;

655 7 a| dissertations.2| aat0| (CStmoGRI)aatgf300028029;

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655 7 a| Thèses et écrits académiques.2| rvmgf0| (CaQQLa)RVMGF-000001173;

700 1 a| Wiley, John E.,e| degree supervisor.=| ^A788626;

710 2 a| East Carolina University.b| Department of Biology.=| ^A637467;

856 41 z| Access via ScholarShipu| http://hdl.handle.net/10342/12040;

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Molecular detection of INV(16)(p13q22) in acute myeloid leukemia / by Tamara L. Hedgebeth.

Author/creator	Hedgebeth, Tamara L. author.
Other author	Wiley, John E., degree supervisor.
Other author	East Carolina University. Department of Biology.
Format	Theses and dissertations
Production	2002.
Description	vi, 62 leaves : illustrations (some color) ; 28 cm
Supplemental Content	Access via ScholarShip
Subjects	Acute myeloid leukemia--Genetic aspects. Microdissection. Human chromosomes. Chromosomes, Human.

Summary	Acute myeloid leukemia (AML) is a malignancy of immature bone marrow cells resulting from a block in differentiation of myeloid cells. The most typical chromosome 16 rearrangement is inv(16)(pl3q22) [inv(16)], which accounts for approximately 8% of AML cases. In this rearrangement, the core binding factor beta (CBFB) gene, located on 16q22 is fused to the myosin heavy chain gene (MYH11), located on 16pl3. Several different CBFB/MYH11 transcripts have been identified by RT-PCR, and the type A transcript is the most common. Genomic PCR and DNA sequencing were employed in order to detect this fusion type on the genomic level in inv(16) and putative mosaic inv(16) patient material. Primers were designed so that they spanned intron 30 of MYH11, with the forward primer located in exon 30 of MYH11 and the reverse primer located in exon 31 of MYH11. It was expected that the absence of a band would indicate an inversion and that the presence of a band would indicate the absence of an inversion. A 592 bp PCR product was generated, cloned, and sequenced. Sequencing results confirmed that there was no inversion of chromosome 16 for the three patients. Alignment results revealed extensive homology between the inv(16), putative mosaic inv(16), and normal patient sequences, with only a few differences in nucleotides. Inherent problems associated with the use of chromosome microdissection, DOP-PCR, and genomic PCR in the characterization of inv (16) and CBFB/MYHl1 are also discussed.
General note	Presented to the faculty of the Department of Biology.
General note	Advisor: John E. Wiley
Dissertation note	M.S. East Carolina University 2002
Bibliography note	Includes bibliographical references (leaves 53-62).
Genre/form	dissertations.
Genre/form	Academic theses.
Genre/form	Academic theses.
Genre/form	Thèses et écrits académiques.

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Molecular detection of INV(16)(p13q22) in acute myeloid leukemia / by Tamara L. Hedgebeth.

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