Muscle Wasting in Cancer,
Several MDs Linked
If it holds up under further scrutiny, the finding that cancer-associated
muscle wasting may share a molecular pathway with the wasting
seen in several forms of muscular dystrophy may help
increase funding in this area and benefit both groups of patients.
In the November issue of Cancer Cell, Denis Guttridge of Ohio
State University and colleagues suggest that disruption of a
repeated cluster of proteins that rings muscle fibers (cells)
in or near the cell membrane is disrupted in cancer-associated
wasting (cachexia).
In several forms of muscular dystrophy -- Duchenne, Becker, limb-girdle and congenital -- this cluster, known as the dystrophin-glycoprotein complex,
or DGC, is completely or partially lost because of
a mutation in a gene for one of its components.
The first DGC component to be identified was dystrophin.
In 1986, MDA-supported researchers linked defects in the gene
for this muscle protein to the cause of Duchenne muscular dystrophy,
a severe, childhood-onset form of MD, and later linked different
flaws in the same gene to Becker MD, a less severe MD with somewhat
later onset.
In the 1990s, other MDA-funded researchers, particularly Kevin
Campbell at the University of Iowa, contributed to the identification
of the sarcoglycans, four proteins nestled in the cell
membrane, and found that the absence of any one of them can
lead to limb-girdle MD, a disorder of varying severity and age
of onset.
Recently, Campbell’s group demonstrated that a loss of
the usual sugar coating (glycosylation) of another DGC protein,
dystroglycan, can lead to various forms of congenital MD.
Campbell says he thinks the November findings need further
assessment, but that a DGC-cancer link wouldn’t surprise
him. |
