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[Cancer Research 48, 199-205, January 1, 1988]
© 1988 American Association for Cancer Research

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In Situ c-myc Expression and Genomic Status of the c-myc Locus in Infiltrating Ductal Carcinomas of the Breast

Renato Mariani-Costantini, Chantal Escot, Charles Theillet, Annie Gentile, Giorgio Merlo, Rosette Lidereau and Robert Callahan1

Laboratory of Tumor Immunology and Biology, National Cancer Institute, NIH, Bethesda, Maryland 20892, and Centre Rene Huguenin, rue Gaston Latouche, 92211 St. Cloud, France

We have studied the expression of the c-myc protooncogene and the cycle-dependent histone 4 gene at the cellular level by RNA:RNA in situ hybridization in 18 primary breast ductal adenocarcinomas. These tumors have previously been examined by Southern and Northern blot analysis for the genomic status of c-myc and its expression, respectively (Escot et al., Proc. Natl. Acad. Sci. USA, 83: 4834–4838, 1986). Positive c-myc hybridization signals were associated with carcinoma cells in all cases, including tumors which had no apparent alterations of the c-myc locus. Steady-state levels of c-myc mRNA appeared heterogeneous in carcinomas with similar histology. High levels of hybridization were found in four of seven tumors with strong amplification of the c-myc locus. Similarly high levels of c-myc hybridization were detected in two of nine cases which had an apparently normal c-myc locus but comparatively low cellularity. In addition to carcinoma cells, dense clusters of infiltrating lymphocytes, present in three tumors, exhibited c-myc hybridization. The expression of the histone 4 gene failed to correlate with levels of c-myc expression. We conclude that in infiltrating ductal carcinomas: (a) the c-myc protooncogene is transcriptionally activated; (b) c-myc amplification is probably underestimated due to heterogeneous cellularity; (c) high-level c-myc amplification is related to high-level expression, but other unknown factors also may play a role; (d) differences in levels of c-myc expression may not only be attributed to differences in the growth fractions; and (e) c-myc mRNA in total RNA from biopsy samples may be contributed by infiltrating lymphocytes.

1 To whom requests for reprints should be addressed, at Laboratory of Tumor Immunology and Biology, National Cancer Institute, NIH, Building 10, Room 5B50, Bethesda, MD 20892.

Received 3/30/87. Revised 9/22/87. Accepted 9/25/87.




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Cancer Research Clinical Cancer Research
Cancer Epidemiology Biomarkers & Prevention Molecular Cancer Therapeutics
Molecular Cancer Research Cancer Prevention Research
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Annual Meeting Education Book Meeting Abstracts Online
Copyright © 1988 by the American Association for Cancer Research.