cell of choice by virtue of the selectable marker 
gene within them. STFs might also eventually prove 
useful for cloning other types of genes, such as those 
involved in cellular aging, since they do not require 
a selective growth advantage in complementation 
experiments. (This work was supported in part by 
the National Institutes of Health.) 
The laboratory constructed a library of STFs from 
llpl5. Several of these caused in vitro growth 
arrest of WT and rhabdomyosarcoma cells, demon- 
strating that tumor suppressor genes can be isolated 
and transferred in this manner. The tumor suppres- 
sor activity was localized within a region of 2 Mb 
adjacent to, but apparently distinct from, the BWS 
chromosomal breakpoints. The laboratory is now 
looking for genes in this region and determining 
whether it might represent yet a third Hp WT- 
related locus. 
Finally, WT is made even more complex by the 
fact that some non-BWS families with WT do not 
show linkage of this trait to chromosome 1 1 . Re- 
cently, Dr. Feinberg's group, with a former sabbati- 
cal member of the laboratory. Dr. Anthony E. Reeve 
(University of Otago, New Zealand), found involve- 
ment of chromosome 16 in WT. 
Dr. Feinberg is also Associate Professor of Inter- 
nal Medicine and Human Genetics at the Univer- 
sity of Michigan Medical School. 
Books and Chapters of Books 
Deisseroth, A.B., Herst, C.V., Wedrychowski, A., 
Sims, S., Seong, D., Johnson, E., Yuan, T., Romine, 
M., Paslidis, N., Emerson, S., Feinberg, A.P., 
Gao, P., Huston, L., Claxton, D., Kornblau, S., 
LeMaistre, F., Kantarjian, H., Talpaz, M., Reading, 
C, and Spitzer, G. 1991 . Novel approaches to the 
therapy of CML. In New Strategies in Bone 
Marrow Transplantation (Champlin, R.E., and 
Gale, R.P., Eds.). New York: Wiley-Liss, pp 163- 
169. 
Articles 
Maw, M.A., Grundy, P.E., Millow, L.J., Eccles, M.R., 
Dunn, R.S., Smith, P.J., Feinberg, A.P., Law, 
D.J., Paterson, M.C., Telzerow, P.E., Callen, D.F., 
Thompson, A.D., Richards, R.I., and Reeve, A.E. 
1992. A third Wilms' tumor locus on chromo- 
some I6q. Cancer /?e5 52:3094-3098. 
Upadhyaya, G., Guba, S.C., Sih, S.A., Feinberg, 
A.P., Talpaz, M., Kantarjian, H.M., Deisseroth, 
A.B., and Emerson, S.G. 1991. Interferon-alpha re- 
stores the deficient expression of the cytoadhe- 
sion molecule lymphocyte function antigen-3 by 
chronic myelogenous leukemia progenitor cells. 
J Clin Invest 88:2131-2136. 
HUMAN MOLECULAR GENETICS AND COMPARATIVE GENE MAPPING 
UtaFrancke, M.D., Investigator 
The mapping of genes on human and mouse chro- 
mosomes has been a long-standing activity in Dr. 
Francke's laboratory. With focus on cloned genes of 
known function that are expressed specifically in 
the nervous system or other differentiated tissues, 
mapping results are obtained that are relevant in dif- 
ferent respects. Comparative mapping of chromo- 
somes within and between species reveals insight 
into genome evolution and leads to the detection of 
new members of gene families. Mapping informa- 
tion is used to define candidate genes for human 
inherited disorders or phenotypic mutations in 
mice. Furthermore, understanding of the pheno- 
typic consequences of chromosome aneuploidy is 
facilitated by knowledge of specific genes located in 
the aneuploid segment. 
By Southern hybridization or polymerase chain re- 
action (PGR) analysis of somatic cell hybrid panels 
with defined subsets of human and mouse chromo- 
somes, and by in situ hybridization of cloned genes 
to chromosomes using fluorescence detection 
methods, as well as by genetic mapping with recom- 
binant inbred strains of mice, the laboratory has de- 
termined the chromosomal map positions for nu- 
merous genes in both species. 
Mapping Studies Identify Disease Genes 
The gene for a peripheral myelin protein (PMP- 
22), which had been independently isolated as a 
growth-arrest gene, was assigned to mouse chromo- 
some 1 1 and human chromosome 17p. By virtue of 
these localizations and the gene's function in the 
peripheral nervous system, it became a candidate 
for involvement in the mouse mutation Trembler 
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