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Biomedical subjects

P Lebowitz

Publications and source records attributed to P Lebowitz.

43 records · Page 3Linked to original sources
PubMed1973

Preferred site for initiation of RNA transcription by Escherichia coli RNA polymerase within the simian virus 40 DNA segment of the nondefective adenovirus-simian virus 40 hybrid viruses Ad2 + ND 1 and Ad2 + ND 3 .

The DNA of simian virus 40 (SV40) was transcribed into RNA by Escherichia coli RNA polymerase at 18 to 24 C after synchronization of the initiation of RNA synthesis. After a brief synthetic period the RNA product contained relatively large amounts of sequences derived from a limited segment of SV40 DNA. The source for this pulse-labeled RNA was found to be a portion of the segment of SV40 DNA included within the nondefective adenovirus (Ad)-SV40 hybrid viruses, Ad2(+)ND(1) and Ad2(+)ND(3). After synthesis with [gamma-(32)P] ATP, Ad2(+)ND(1) and Ad2(+)ND(3) DNA transcripts contained an initial sequence missing from Ad2 transcripts. This sequence was identified as an initiation sequence for polymerase transcription of the SV40 DNA. Thus, there is a preferred site for initiation of in vitro transcription on the segment of SV40 DNA common to the nondefective Ad2(+)ND(1) and Ad2(+)ND(3) hybrid viruses.

Adenoviridae↗
PubMedDate not supplied

Oncogenic genes and human malignancy.

All vertebrates possess a series of genes which are homologs of the oncogenic genes of acute transforming retroviruses. Two lines of evidence suggest that these genes may play a role in the development of human malignancy: (1) DNA from a variety of human tumors transforms NIH 3T3 mouse fibroblasts and the transforming genes from a number of carcinomas, sarcomas, and hematological malignancies have been identified as members of a family of genes, the ras family, closely related to the oncogenic genes of the Harvey and Kirsten murine sarcoma viruses; and (2) correlations exist between the chromosomal localizations of certain oncogenes and the chromosomal breakpoints in specific translocations and deletions in certain human malignancies. In three separate hematological malignancies, alterations in more than one oncogenic gene may be involved in the neoplastic process.

Animals↗