OncoLog, Volume 60, Number 3, March 2015 Page: 2
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Small Cell Lung Cancer Studies
[Continued from page 1]lung cancer, there's often a single driver
oncogene that we can target with new
drugs," he said. "But small cell lung
cancer is wired differently. Small cell
lung cancer doesn't seem to have these
driver oncogenes. We think what drives
it is the loss of tumor suppressor genes
RBJ and TP53."
PARP inhibitors
To identify new therapeutic targets
for small cell lung cancer, researchers
led by Lauren Byers, M.D., an assistant
professor in the Department of Tho-
racic/Head and Neck Medical Oncol-
ogy, conducted a proteomic analysis
of both small cell and non-small cell
lung cancer cell lines to systematically
assess the activation of critical intra-
cellular signaling pathways. "Because
there haven't been any approved tar-
geted drugs for small cell lung cancer,
we wanted to identify differences be-
tween small cell and non-small cell
lung cancer that could help us identify
new drugs that could work against small
cell lung cancer," Dr. Byers said.
The researchers found that PARPI,
an enzyme involved in DNA repair,
was expressed at high levels in small
cell lung cancer cells. Dr. Heymach
said these high levels may be related
to the loss of RB 1 and TP53.
The discovery of elevated PARPI
expression in small cell lung cancer
was exciting because drugs that inhibit
PARP proteins are available; such drugs
are sometimes used to treat breast or
ovarian cancers in patients with BRCA1
or BRCA2 mutations. "The idea is that
since tumors with BRCA mutations al-
ready have a defect that inhibits their
ability to repair DNA damage, the
PARP inhibitor will further impair
the cells' ability to repair DNA damage
and cause the cells to die," Dr. Byers
said. When further experiments showed
that PARP inhibitors used to treat
breast and ovarian cancers also killed
small cell lung cancer cells, Dr. Byers
said, "We saw the opportunity to take
our observation into the clinic quickly."
Dr. Byers is leading or participating
in three ongoing clinical trials of PARP
inhibitors for lung cancer treatment-/l
"In non-small cell
lung cancer, there's often a single
driver oncogene that we can tar-
get with new drugs. Small cell
lung cancer doesn't seem to have
these driver oncogenes."
- Dr. John Heymachone for non-small cell and two for small
cell lung cancer. Currently enrolling
patients with relapsed or refractory
small cell lung cancer is a multicenter
phase II trial of the PARP inhibitor
veliparib (previously called ABT-888)
with the cytotoxic drug temozolomide.
Patients in the study are randomly as-
signed to receive temozolomide with
veliparib or placebo.
The study's goal is to learn whether
the addition of veliparib will extend
progression-free survival. "The idea
is that the cytotoxic drug causes DNAdamage in the cancer cells, and the
PARP inhibitor prevents the cancer
from repairing the damage," Dr. Byers
said. "It's still early, but we're excited
by some of the results we're seeing."
The second study of PARP inhib-
itors in small cell lung cancer is a first-
in-human study of the PARP inhibitor
BMN 673. The goals of this study are
to find the maximum tolerated dose
of BMN 673 and to assess the drug's
efficacy in patients with advanced
or recurrent solid tumors. The trial
recently reached its enrollment goal.Shrinkage of small cell lung cancer (arrows) can be seen in computed tomography
scans taken before (left) and after 4 weeks of single-agent treatment with the PARP
inhibitor BMN 673 (right). Image courtesy of Dr Lauren Byers.2 OncoLog March 2015
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University of Texas M.D. Anderson Cancer Center. OncoLog, Volume 60, Number 3, March 2015, periodical, March 2015; Houston, Texas. (https://texashistory.unt.edu/ark:/67531/metapth639488/m1/2/?q=%22Business%2C+Economics+and+Finance+-+Medicine%22: accessed July 9, 2024), University of North Texas Libraries, The Portal to Texas History, https://texashistory.unt.edu; crediting UNT Libraries Government Documents Department.