Amplification of the erbB/EGF receptor and a structurally related gene, designated erbB‐2, have previously been detected in a variety of human tumors. In a series of human mammary tumor cell lines, analysis of transcripts of these genes revealed elevated levels of one or the other in more than 60% of tumors analyzed. Eight cell lines demonstrated erbB‐2 mRNA levels ranging from 4‐ to 128‐fold above those of normal controls. erbB‐2 expression was evaluated in comparison to the expression level of actin observed in these cell lines. There was no evidence of an aberrantly sized erbB‐2 transcript in any of these lines. Immunoblot analysis indicated elevation in levels of the 185‐kd product of the erbB‐2 gene expressed by these cells. In four lines erbB‐2 gene amplification in the absence of an apparent gene rearrangement was demonstrated. In a representative cell line of this type, SK‐BR‐3, the amplified erbB‐2 gene copies were located in an aberrant chromosomal location. Four additional cell lines, which demonstrated 4‐ to 8‐fold overexpression of erbB‐2 mRNA, did not exhibit gene amplification. In a representative cell line of this type ZR‐75‐1, an apparently normal chromosomal location was found for the erbB‐2 gene. Our findings indicate that overexpression of the erbB‐2 gene in mammary tumor cell lines is frequent and associated with different genetic abnormalities.

Human papillomaviruses (HPV) 16 and 18 are closely linked with human genital cancer. In most cervical carcinomas, viral sequences are integrated into the host genome. HeLa, a cervical carcinoma cell line, has multiple copies of integrated HPV 18 DNA. In this study, in situ chromosome hybridization was used to assign the integration sites of HPV 18 DNA sequences on HeLa cell chromosomes. Four sites of hybridization were identified at 8q23→q24, 9q31→q34, p11→p13 on an abnormal chromosome 5, and q12→q13 on an abnormal 22. Three of these sites correspond with the locations of MYC, ABL, and SIS protooncogenes, and are at or in close proximity to fragile sites. The chromosomal localization of HPV 18 DNA may be useful in assessing the role of viral integration in the development of this malignancy.

Three human ras family protooncogenes, c-Ki-ras-1, and c-Ki-ras-2, and N-ras, have been mapped to chromosome bands 6p11-12, 12p11.1-12.1, and 1p11-13, respectively by in situ molecular hybridization. Certain human cancers display consistent and specific alterations involving chromosomes 1, 6, and 12. The precise chromosomal localization of ras genes will permit evaluation of the possible effect of these chromosome changes on the structure and activities of ras protooncogenes in human neoplasia.

solar energy deposition into its atmosphere by a factor of 2.5 (17). The periodicity of albedo variations appears to provide an input to global planetary weather systems on a short time scale relative to Neptune's 164-year period of revolution around the sun. Neptune's orbit is almost perfectly circular, so its changing distance from the sun caused only an insignificant 0.5% decrease in total insolation since 1972. What appears remarkable is the extraordinary sensitivity of Neptune's atmosphere to the modulation of the solar output.

The cell-derived domain of Gardner-Rasheed feline sarcoma virus (GR-FeSV) consists of a y-actin-and a tyrosine-specific protein kinase-encoding sequence designated v-fgr. By utilizing a v-fgr probe, it was possible to detect related sequences present at low copy number in DNAs of a variety of mammalian species and to isolate a human fgr homologue. Comparative studies revealed that this human DNA clone represented all but 200 base pairs of v-fgr. Analysis of human genomic DNA demonstrated that thefgr protooncogene was distinct from the cellular homologues of other retrovirus onc genes. In addition, the fgr protooncogene was localized to the distal portion of the short arm of human chromosome 1 at p36.1-36.2 by in situ hybridization. Taken together, our findings establish that thefgr protooncogene is a unique member of the tyrosine kinase gene family.