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Blood, Vol. 95 No. 7 (April 1), 2000:
pp. 2372-2377
Delineation of a minimal interval and identification of 9 candidates for a tumor suppressor gene in malignant myeloid disorders
on 5q31
Stephen K. Horrigan,
Zarema H. Arbieva,
Hong Yan Xie,
Jelena Kravarusic,
Noreen C. Fulton,
Haley Naik,
Tiffany T. Le, and
Carol A. Westbrook
From the Department of Pediatrics, Lombardi Cancer Center,
Georgetown Medical Center, Washington, DC, and the Section of
Hematology/Oncology, Department of Medicine, University of Illinois at
Chicago, Chicago, IL.
Interstitial deletion or loss of chromosome 5 is frequent in
malignant myeloid disorders, including myelodysplasia (MDS) and acute
myeloid leukemia (AML), suggesting the presence of a tumor suppressor
gene. Loss of heterozygosity (LOH) analysis was used to define a
minimal deletion interval for this gene. Polymorphic markers on 5q31
were identified using a high-resolution physical and radiation hybrid
breakpoint map and applied to a patient with AML with a subcytogenetic
deletion of 5q. By comparing the DNA from leukemic cells to buccal
mucosa cells, LOH was detected with markers D5S476 and D5S1372 with
retention of flanking markers D5S500 to D5S594. The D5S500-D5S594
interval, which covers approximately 700 kb, thus represents a minimal
localization for the tumor suppressor gene. Further refinement of the
physical map enabled the specification of 9 transcription units within
the encompassing radiation hybrid bins and 7 in flanking bins. The 9 candidates include genes CDC25, HSPA9, EGR1, CTNNA1, and 5 unknown ESTs. Reverse-transcription polymerase chain
reaction confirms that all of them are expressed in normal human bone
marrow CD34+ cells and in AML cell lines and thus
represent likely candidates for the MDS-AML tumor suppressor gene at 5q31.
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