OF O ~ ~aBErlS: A m ~ L ~ . T.C. Hsu, The University of Texas M.D. Ander~cn Hospital at Houston, Houston, ~e.~as. The Boveri hypothesis that csne~- starts from genetic changes of a cell remained untested f ~ more than 3 Oeca~es, mainly because of technical d~/~ficulties in studylng vertebrate ~ . Prohably the esrliest attempt was made ~y Biesele et al. (1942) on mouse tumors. In the early 1950's, the use of ascites tumor ceils enabled Makino and Levan and Hausd~ka to ~ropose the stealine concept. Afte~ the application of the hypotcnic solution treatment method, the problem of identifying diploid ~ number and ~oss cfrcmssames mcrphologF was solved. An important discovery was the correction of the diploid dm-~mc~me number of man in 1956. From this startlng point, a standard human karyotype was reoammended by a oc~m~ttee, and ~ i c etiologF of many human c c ~ t a l s ~ was established. Several discoveries Qn osno~~ cyot~enetics suggested specific c~r~oscme aberrations in specific tumors, including ~ e myelogenous leukemia, neurobl~st~ma, menir~ioma, and several less olesr-~/t oases. H~4ever, si~niflcant progresses in csnoer cytogenetics and r~l~ted studies were made after the invention of various banding techniques. Many subjects oould not have advenoed without d~rom~sc~e banding teelmiques. Many current subjects will be discussed individually in detail at this ocnfe~nce. The progresses in eanoer c y t o ~ i c s em~naticslly indicate speclfic genetic alteraticns in target tissues, and m~qy of these can be i~entifie~ as constitutional lesions. Genetic predispositicm to esncer also includes cases of ct~cm~ome fragility and sensitivity to environmental mutagens, k~ predict that genetic etiology will be established in all types of neopl~,~ and atris~ individuals can be identified at early ages.
* MECHANISMS OF GENE AMPLIFICATION. R. Schimke, Stanford U n i v e r s i t y , Stanford,
CA. Abstract not received.
HEAT-INDUCED CHROMOSOME DAMAGE IN CHO K1 CELLS IS ALTERED BY TREATMENT WITH METABOLIC INHIBITORS. Steven Daggett Department Sciences,
W. and
Sherwood, Robert T.
of Stanford
Ann S. Schimke.
Biological University.
The survival of cultured mammalian cells following moderate heat shock is increased significantly when cells are treated with protein synthesis inhibitors prior to and during heat shock. We have found that this effect is c o r r e l a t e d with a strong reduction in t h e frequency and extent of chromosome damage when cells are treated with I0 mcg/ml cycloheximide. This reduction in the frequency of cells with heat-induced chromosome damage is slightly greater than the increase in c e l l s u r v i v a l . An important aspect of this effect appears to be the strong inhibition of DNA replication (measured as 3H-TdR incorporation) induced by cycloheximide. These data are consistent with the proposal that the S-phase sensitivity o f c e l l s to h e a t s h o c k is d u e t o h e a t - i n d u c e d DNA damage.