The SCL (tal-l, TCLS) gene is a member of the basic domain, helix-loop-helix (bHLH) class of putative transcription factors. We found that (i) the SCL promoter for exon Ia contains a potential recognition site for GATA-binding transcription factors, (ii) SCL mRNA is expressed in all erythroid tissues and cell lines examined, and (iii) SCL mRNA increases upon induced differentiation of murine erythroleukemia (MEL) cells, and inferred that SCL may play a physiologic role in erythroid differentiation. We used gel shift and transfection assays to demonstrate that the GATA motif in the SCL promoter binds GATA-1 (and GATA-2), and also mediates transcriptional transactivation. To identify a role for SCL in erythroid differentiation, we generated stable transfectants of MEL and K562 (a human chronic myelogenous leukemia cell line that can differentiate along the erythroid pathway) cells overexpressing wildtype, antisense or mutant SCL cDNA. Increasing the level -of SCL expression in two independent MEL lines (F4-6 and C19, a 745 derivative) and K562 cells increased the rate of spontaneous (i.e. in the absence of inducer) erythroid differentiation. Conversely, induced differentiation was inhibited in MEL transfectants expressing either antisense SCL cDNA or a mutant SCL lacking the basic domain. Our experiments suggest that the SCL gene can be a target for the erythroid transcription factor GATA-1 and that the SCL gene product serves as a positive regulator of erythroid differentiation.

We have studied a leukemic stem-cell line,

Genetic counseling and testing offers the potential to focus cancer screening resources in individuals truly at increased risk, thereby reducing mortality and morbidity. Fears of discrimination and concerns about psychological and psychosocial issues may present barriers to the use of current cancer prevention strategies, including genetic counseling and testing.

The serological analysis and the restriction enzyme pattern of the tick isolates leave little doubt that the viruses were IBR virus. To our knowledge, this is the only reported example of a mammal-infecting herpesvirus isolated from an arthropod host. It is not known whether the presence of the virus in the ticks is a result of biological replication or mechanical transmission. The source of the virus that infected the ticks is also in question. We have found antibodies to IBR virus in both deer and cattle in the area of the Sierra Nevada (9) where the ticks were collected. Since the viremic stage of disease in an animal is relatively short, there must be very few animals in an area at a particular time capable of transmitting virus to ticks; consequently, it is puzzling that virus was isolated from three separate collections of ticks obtained over a 3-year period. The presence of IBR virus in each of these collections would be even more remarkable if the ticks were mechanically infected, since one would expect the virus to be present for only brief intervals. Hence it is important to determine (i) whether IBR virus can replicate in ticks, (ii) how long the virus remains infectious in ticks, (iii) whether ticks can be infected with IBR virus from feeding on viremic cattle and can then transmit the disease to normal cattle, (iv) whether IBR virus can be observed in the tick with the electron microscope, and (v) whether the virus can be mechanically transmitted without replication of the virus. Abstract. A human immunoglobulin heavy chain (y4) gene is mapped by chromosome hybridization in situ. This gene is located at band J4q32, a site commonly involved in a chromosomal translocation characteristic of malignant B cells.

A clinical trial was recently conducted to evaluate the safety and efficacy of a selective inhibitor of cyclooxygenase-2