From
big lizards to astrocytomas
(continued)
Several
years, many experiments and a million what-ifs later, Cala arrived
at his current area of research: the sodium-proton exchanger in
tumor growth and proliferation.
Cells
that thrive in an oxygen-deprived environment - notably, cancer
cells - have increased rates of hydrogen production. "Tumor
cells are greedy; they generate lots of hydrogen," says Cala.
"It is essential that they get rid of these hydrogen ions efficiently
if they are to continue to rely upon anaerobic metabolism."
But
if researchers could jerry-rig the sodium-proton exchanger to make
cancer cells go acidic, they might be able to interfere with their
viability. Or so Cala thought.
In
work that Cala's lab is about to publish, Anderson, graduate student
Lee Anne McLean and professor of neurology Fred Gorin inhibited
the sodium proton exchanger in normal brain cells (astrocytes) from
rats and malignant glioma cells from cancer patients. Just as they
hypothesized, the intracellular environment became acidic. The tumor
cells died while the healthy cells were unharmed.
The
next phase of studies has just begun. Cala and his co-workers are
performing animal studies involving a little-used diuretic that
inhibits the sodium-proton exchanger. They want to see if inhibiting
the sodium-proton exchange alters tumor growth in animals.
"I'd
been interested in exploring whether inhibiting the sodium-proton
exchange might be lethal to glial tumor cells and dilly-dallying
around with this project for years," Cala says. "But Lazaro's
death finally got me off the dime."
Of
course, the road from promising studies to effective treatments
is filled with detours, stalls, and unfulfilled expectations. Back
at his laboratory, Cala watches the microscopic reactions of glial
cells to the sodium proton exchanger, takes a breath and waits -
a lasting homage to an old friend.
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