Jeffrey A. Frenster, Michael M. Papalian, Marilyn A. Masek, and John H. Frenster
Department of Medicine, Stanford University, Stanford Calif. and
The Institute for Medical Research, San Jose, Calif. 

DNA helix openings within extended euchromatin provide active DNA templates for RNA and DNA synthesis (Cancer Res. 36: 2294 (1976). Such DNA templates decrease markedly in size and number during normal bone marrow cell differentiation and maturation (Nature 248: 334 (1974), accompanied by a progressive conversion of transcription-active extended euchromatin to transcription-inactive condensed heterochromatin (Advan. Cell Molec. Biol. 3:1 (1974). Lymph nodes biopsied from untreated patients with Hodgkin's Disease during original staging of the disease were examined by high-resolution electron microscopic probe analysis of the DNA helix openings as previously described (J. Cell Biol. 67: 123a (1975). Neoplastic Hodgkin's and Reed-Sternberg cells were observed to undergo nuclear maturation sequences consisting of nuclear hypersegmentation, blebbing, pocket and projection formation, simultaneous with extreme degrees of inactivation of DNA template activity, but unaccompanied by any significant degree of conversion of extended euchromatin to condensed heteochromatin. Adjacent lymphocytes displayed high DNA template activity despite significant heterochromatinization, while macrophages revealed intermediate degrees of both. These quantitative single-cell data suggest that neoplastic cells may inactivate DNA templates without converting extended euchromatin to condensed heterochromatin in-vivo.

Supported in part by Research Grants CA-10174 and CA-13524 from the National Cancer Institute, by Research Grant IC-45 from the American Cancer Society, and by a Research Scholar Award from the Leukemia Society.

Top Of Page - Euchromatin Network - Current Research - Forums - Other Sites - Future Events -