ASH Clinical News December 2015 | Page 113

FEATURE

groups to review and provide
internal critiques of grants
well in advance of submission
deadlines.
The current funding climate
is still adversely impacting
productivity because inordinate

Carolyn A. Felix, MD,
Children’s Hospital
of Philadelphia,
Philadelphia, PA
Why did you apply for
an ASH Bridge Grant?
My future as a physicianscientist is critically
dependent on being able
to regain federal funding
from the NIH – both in
terms of carrying on with
the research efforts of
my lab and in supporting
my trainees. I applied for
a Bridge Grant to gain
foundational support as I
continue my research in
developing a therapeutic
strategy for infant acute
lymphocytic leukemia to
collect key preliminary
data to revise my R01.
Federal funding has
either remained flat or
decreased over the last
decade while the number
of applications has
increased significantly.
ASH provides a critical
pathway to continue
research when it is
becoming more and more
difficult to get funding
from the NIH.
How are you adjusting
your research
practice in this
decreased funding
environment?
With fewer funding
sources, it takes much
longer to get important
research projects off the
ground. Researchers are
looking for more creative
avenues in seeking
funding and relying on
non-profits or other
funding sources for their
research.
A number of proactive
programs are in place
or are being initiated
at an institutional level
to address the current
funding climate. These
include an increasing
trend in the formation
of self-organizing

potential to force researchers
and institutions to make
difficult choices regarding
which projects will continue
when all have high potential to
change the outcome of diseases
in affected patients. ●

amounts of time are spent
preparing grants, as opposed
to generating new and exciting
data and publishing results,
and this remains the only
avenue to succeed in getting
funded. This ultimately has the

Evasion of apoptosis may
be a question of balance
Increased BCL-2 expression helps
cancer cells to survive1
BCL-2

Release of pro-apoptotic proteins
may trigger apoptosis1

Pro-apoptotic
proteins sequestered
by BCL-2

Free
pro-apoptotic
proteins

Increased expression of BCL-2 impairs the pathway
to programmed cell death
Like normal cells, cancer cells will often induce expression of pro-apoptotic proteins in
response to stressors like limited metabolic resources, rapid cell division, or exposure to
cytotoxic agents.1
Cancer cells may increase expression of the anti-apoptotic protein, BCL-2.1 Pro-apoptotic
proteins are bound and sequestered by BCL-2, helping the cancer cell to avoid
programmed cell death.2
Mitochondria

Pro-apoptotic proteins—if released from BCL-2—have the potential to
trigger apoptosis.1

To learn more about the BCL-2 pathway,

BOOTH #1833

visit
and
at the ASH Annual Meeting.

#547

References: 1. Letai AG. Diagnosing and exploiting cancer’s
addiction to blocks in apoptosis. Nat Rev Cancer. 2008;8(2):121131. 2. Garcia-Saez AJ. The secrets of the Bcl-2 family. Cell
Death Differ. 2012;19(11):1733-1740.

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