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Please, support our research!
Donating even just $5 or $10, combined with everyone else's donation,
helps us fund research like this...
Our Auckland, New Zealand research team, headed by Dr. Andrew Shelling and his Ph.D. student Roseanne Rosario,
has just published the
first big article
based on the research we have funded. More about that article in a
moment, but first I want to thank everybody who has made a donation to our research fund. We take great pride
in seeing the line near the bottom of page one that says,
"This work is funded by the Sladjana M. Crosley Fund
for GCT Research."
If you have donated, you should also be proud that your contribution is helping science as we search for an effective
treatment of GCT. You can also rest assured that when you made the commitment to support our research, we made
sure that all of that money will go to actual research.
The research (You can get the article
Ever since the ground-breaking paper on FOXL2:C134W (mutant FOXL2) by Shah, et al. in 2009, we have operated under
the assumption that this mutant gene must be part of the means by which the granulosa cell transforms into cancer.
[To recap that work, mutant FOXL2 was found in 97% of adult GCT (AGCT), 10% of juvenile GCT (JGCT), but not in other
ovarian or breast cancers].
That original paper only told us that the mutation was present, but could not tell us anything about what the mutation was
doing. Since then, several research groups are focusing on FOXL2 and how to sort out what it does, in GCT, and
whether controlling (or knocking down) the gene is the key to controlling GCT.
Roseanne's work investigated a significant difference between the 2 usual GCT cell lines, KGN and COV434. KGN is
generally considered similar to AGCT and COV434 is considered similar to JGCT. The
cells (in a dish) look considerably different, and, as other research has shown, KGN expresses mutant FOXL2 while
COV434 expresses normal FOXL2 but at very low levels.
So Roseanne, in general terms, put mutant FOXL2 into COV434 and knocked it down
(effectively removed it) from KGN. Then she analysed what changes occured in the genetic makeup of both cells.
Roseanne's paper can't tell us yet everything we need to know before we can move forward with designing a treatment,
but it does delineate a significant genetic difference between AGCT and JGCT which will need
to be considered in developing therapies, and suggests the key pathway that seems to be involved with AGCT. More work remains,
but we know more today, thanks to all of our research teams around the world, than we knew a year ago.
Speaking of our teams, here is a recap of our current research teams that you have helped through your donations.
Auckland, New Zealand - Dr. Andrew Shelling
Edmonton, Alberta, Canada - Dr. Mary Hitt
Helsinki, Finland - Dr. Mikko Anttonen
Vancouver, British Columbia, Canada - Dr. David Huntsman
Help us keep the findings coming!