Localization of the oncogene c‐<i>erb</i>A1 immediately proximal to the acute promyelocytic leukaemia breakpoint on chromosome 17

Sheer, Denise; Sheppard, David M.; Beau, MM Le; Rowley, Janet D.; Román, Carlos; Solomon, Ellen

doi:10.1111/j.1469-1809.1985.tb01690.x

Cited by 32 publications

(9 citation statements)

References 15 publications

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“…Other genes that have been previously mapped to this region of chromosome 17 include the HOX2 homeobox gene cluster, the procollagen al(I) gene, the galactokinase gene, and the ERBA oncogene (32)(33)(34)(35). A region of conserved synteny for all of these genes exists on mouse chromosome 11 (36), baboon chromosome 16 (37), and African green monkey chromosome 19 (37); and it would not be surprising if subunit genes for the fibrinogen receptor in these other species are also physically linked.…”

Section: Discussionmentioning

confidence: 99%

Physical linkage of the genes for platelet membrane glycoproteins IIb and IIIa.

Bray

Barsh

Rosa

et al. 1988

Proc. Natl. Acad. Sci. U.S.A.

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The fibrinogen receptor on human platelets is a prototypic member of the integrin family and is composed of subunit glycoproteins Ub (gpilb) and lila (gplIa) in a 1:1 stoichiometric ratio. We have isolated cDNA clones for gpIlb and gpIIIa and localized both genes to chromosome 17. In the current study, several approaches were used to localize and map the genes for gpIlb and gpIlla. A preliminary evaluation of subchromosomal localization was performed by using a panel of mouse-human somatic cell hybrids that contain different amounts of the long arm of human chromosome 17. Southern hybridization to the DNA of these hybrids shows that both genes map near the thymidine kinase gene. In situ hybridization to intact human chromosomes localized both genes to the 17q21-22 region. To better define the physical distance between the two genes, we examined the genomic hybridization pattern of each cDNA probe to high molecular weight restriction fragments separated by pulsed-field gel electrophoresis. Serial hybridizations of the same frter have allowed construction of long-range Mlu I and Sfi I restriction maps spanning more than 500 kilobases. Finally, nonoverlapping portions of the cDNAs for both gpilb and gplIa were used to probe Sfi I digests of genomic DNA separated by fieldinversion gels. This confirmed that the genes are physically linked within the same 260-kilobase Sfi I fragment and suggests that the gene for gpilb is located on the 3' side of the gene for gpIla. These results suggest that coordinate expression of gpilb and gpilla may depend on physical proximity.

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Section: Discussionmentioning

confidence: 99%

Physical linkage of the genes for platelet membrane glycoproteins IIb and IIIa.

Bray

Barsh

Rosa

et al. 1988

Proc. Natl. Acad. Sci. U.S.A.

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“…Two genes, a (8) and d (9), each ofwhich codes for two alternatively spliced forms of the thyroid hormone receptor, designated al, a2 ( 10), ( 1, and (32 ( 1 ), have been identified. The a 1, (1, and (32 forms bind thyroid hormone, whereas the a2 does not.…”

Section: Introductionmentioning

confidence: 99%

Differential expression of mutant and normal beta T3 receptor alleles in kindreds with generalized resistance to thyroid hormone.

Mixson

Hauser²,

Tennyson³

et al. 1993

J. Clin. Invest.

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Thyroid hormone resistance (THR) is primarily an autosomal dominant inherited disease characterized by resistance of pituitary and peripheral tissues to the action of thyroid hormone. We investigated whether the heterogeneous phenotypic features that occur not only among kindreds but also within the same kindred might be due to the expression of differing ratios of mutant and normal receptors in tissues. Using an allele-specific primer extension method, we determined the relative expression of normal and mutant mRNAs from the fibroblasts of affected and unaffected members of two kindreds with TRH: A-H and N-N. While two affected members of A-H, as expected, had nearly equal amounts of normal and mutant hTR(3 mRNA, two other members had mutant mRNA levels that accounted for at least 70% of the hTR# mRNA. Phenotypic variability within and between kindreds with generalized resistance to thyroid hormone GRTH may be due to this differential expression of the mutant and wild type mRNA. Furthermore, when several clinical parameters of THR were compared in several affected members from two kindreds with GRTH, we found that two cases in one kindred exhibited a high mutant-tonormal hTR68 ratio and had considerably more bone resistance during their development. In certain kindreds with THR, differing ratios of normal and mutant hTR receptors may be age and growth related and may account for the reported attenuation of phenotypic symptoms with age. (J. Clin. Invest. 1993.

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“…The translocation has not been reported in any other type of malignancy (Mitelman, 1984), other than in a promyelocytic form of chronic myeloid leukaemia blast crisis (Berger et al, 1983). The oncogene c-erbAl has been localised immediately proximal to the APL breakpoint on chromosome 17 (Sheer et al, 1985). The specificity and incidence of the translocation suggest the presence of a gene which plays a role in myeloid differentiation at the promyelocyte stage, at one of the translocation breakpoints on chromosome 15 or 17.…”

Section: Methodsmentioning

confidence: 85%

Incidence of the 15q+;17q- chromosome translocation in acute promyelocytic leukaemia (APL)

Sheer¹,

Lister²,

Amess³

et al. 1985

Br J Cancer

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Summary Cytogenetic analysis was carried out on peripheral blood cultures from seven patients with acute promyelocytic leukaemia . A reciprocal 15;17 chromosome translocation, t(lSq +; 17q -), was found in all cases, and the breakpoints estimated to be 15q22 and 17ql2-21. In addition to the t(15q+;17q-), trisomy 10 was found in 50% of cells analysed in one case. These results suggest that the 15;17 chromosome translocation may be observed in most cases of APL where the leukaemic cells are cultured before cytogenetic analysis is performed. The use of conditioned media in the culture of leukaemic cells is also described.

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Localization of the oncogene c‐erbA1 immediately proximal to the acute promyelocytic leukaemia breakpoint on chromosome 17

Cited by 32 publications

References 15 publications

Physical linkage of the genes for platelet membrane glycoproteins IIb and IIIa.

Physical linkage of the genes for platelet membrane glycoproteins IIb and IIIa.

Differential expression of mutant and normal beta T3 receptor alleles in kindreds with generalized resistance to thyroid hormone.

Incidence of the 15q+;17q- chromosome translocation in acute promyelocytic leukaemia (APL)

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