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Dr. Didier Dréau
Assistant Professor,
Dept. of Biology
Office:
Woodward 490B
Lab:
Woodward 475 East
Phone: (704)687-8314
ddreau@uncc.edu
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Dr. Dréau's Academic Degrees
* Bachelor in Physiology & Cell Biology, University of Rennes
I (France) – 1988.
* Master in Molecular & Cell Biology, University Blaise Pascal,
Clermont-Ferrand (France) – 1990.
* Ph.D. in Molecular & Cell Biology (Immunology), College of Agriculture
of Rennes (France) – 1994.
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Courses Taught
* BIOL 3273L Animal Physiology Lab (Fall 2004)
* BIOL 3273 Animal Physiology (Spring 2005):
The 3273 course (spring
2005) is available through WebCT and 49er [http://www.express.uncc.edu/cp/home/loginf].
If you need help with WebCT, please contact the
Center for Teaching and
e-Learning [http://www.uncc.edu/webct/WCT_STUDENT/index.html]"
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Dr. Dréau Laboratory research
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Professional Experience
• 1994-1996 Research Fellowship in Infection and Immunology,
Carolinas Medical Center, Charlotte.
• 1996-1997 Research Fellowship in Cancer Immunology, Carolinas
Medical Center, Charlotte.
• 1998-2002 Research scientist Dept General Surgery, Carolinas
Medical Center, Charlotte.
• 2002-2002 Director of Immunology & Oncology Research,
Carolinas Medical Center, Charlotte.
• 2003-2004 Research scientist Department of Biology, University
of North Carolina at Charlotte.
• 2004-Present Assistant Professor, Department of Biology, University
of North Carolina at Charlotte.
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Honors, Awards and Memberships
• 1994-2004 Adjunct Assistant Professor, Biology, University
of North Carolina at Charlotte, NC
• 1995-Present Ad hoc reviewer for Am. J. Dermopathol., Gastroenterology and J. Interferon and Cytokine Research
• 1998-Present Member of the American Association for Cancer
research (AACR)
• 2000-Present Member of the Graduate Faculty, University of
North Carolina at Charlotte, NC
• 2001-Present Member (Founding) and user of the Charlotte Genomics
Consortium, a micro-array facility
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Summary of Research Projects:
The Research projects ongoing in Dr. Dréau's laboratory focus
on understanding the molecular, cellular, tissular and physiological
bases of metastases associated with cancers of epithelial origin.
• The cancers of epithelial origin include: the most lethal skin cancer, i.e. melanoma and the most common solid tumor in female i.e., breast cancer.In these cancers as in others, the occurrence of metastases is associated
with a high mortality (see the site of the American Cancer Society
for details on cancer statistics in the US: http://www.cancer.org
). • The development of metastases is a multi-step process, which,
from the tumor standpoint, includes:
- Development of tumor cells with metastatic potentials.
- Detachment, migration of tumor cells generally through the vascular
system (blood, lymph vessels), and anchoring within the host tissue.
- Growth of the metastatic mass requiring the concurrent development
of vessels, i.e. neo-angiogenesis, which provide oxygen and various
nutriments.
- Preventing responses of the immune system throughout all the steps
associated with the development of tumor metastases.
Dr. Dréau's research center on the mechanisms of cancer metastasis, and the vascular and immune interactions associated with cancer growth. More specifically, the following aspects of cancer metastasis are studied:
• Key features of Metastatic Tumors:
What are the mechanisms implicated in the differentiation of a metastatic
tumor cell from non-metastatic tumor cells? What is the combination
of parameters/features associated with a rapid development of metastases?
In the laboratory this research is conducted on melanoma cell lines.
The identification of key features associated with the development
of metastases involves many molecular and cellular technologies and the use of in vivo models. In
addition, in vivo models contribute to the analysis.
The results of these studies may allow a more efficient diagnostic
and treatment of patients with solid tumors including melanoma patients.
• Anchoring and Growth of Metastatic Tumors:
Although some of the protein associated in the detachment, migration
and anchoring within an organ with tissular specificity different
from the tumor cell origin have been defined; the mechanism and the
molecules associated with the development of distant metastases have
not. Moreover, epidemiological data suggests that metastases occur
in different organ based on the tumor origin. Also understanding the
effect of tumor growth within an organ is also crucial.
In the laboratory this research is conducted on a breast cancer bone
metastases in vivo model. Additionally, in collaboration with Dr.
Iain McKillop, the development of distant liver metastases and
their effects of liver functions are analyzed.
From a diagnostic standpoint, an understanding of the minimal features
associated with the development of brain or liver metastases would
be of tremendous help in the clinical setting.
• Vascularization of the Metastatic Tumors:
As the tumor grows, it requires the development of new vessels, i.e.,
neo-angiogenesis. The new vessels transport oxygen and various nutriments
to the tumor cells allowing for additional growth of the tumor mass.
The ability to generate neo-angiogenesis varies greatly between tumors.
These Interactions with the vascular System are critical to the development
of metastases.
In the laboratory, we are interested in these interactions and how
the tumor cells production of angiogenic factors including endothelin-1
(ET-1) and vascular endothelial growth factor (VEGF) stirs the development
of new vessels. These studies are conducted, in collaboration with
Dr. M. G. Clemens, on an in vivo
breast cancer model of the development of bone metastases. This in
vivo model closely mimics the development of breast cancer metastases
to the bone and allows the analysis of the effect of endothelin-1,
a key protein associated with the development of new vessels, a critical
step for tumor growth.
The gathered information will provide a better understanding of the
step associated with the generation of new vessels and may deliver
the bases for the development of angiogenic-based treatments of aggressive
metastatic tumors. Indeed, preventing tumor growth by preventing the
development of new vessels (therefore starving the tumor cells) may
become a clinical option for patients with solid tumor including breast
cancer patients.
• Interactions Immune System and Metastases:
One of the reasons associated with the development of metastases is
the ability of cancer cells to evade the immune system. Although the
interactions immune system and tumor cells are complex, current data
indicate that there is active “fight” between the defense
system and the tumor mass. The mechanisms associated with the ability
of tumor cells to evade the host immune system mechanisms may be active
(e.g., production of cytokines affecting the immune response) and/or
passive (e.g., passive selection of the tumor cell without any recognizable
antigen). In some cancers, like melanoma and renal cell carcinoma,
boosting the immune responses either by the administration of systemic
treatments (e.g., IL-2, IFN) or more specific vaccines has shown some
clinical success. However, mechanisms behind the development of an
immune response resulting in the cancer cure in some cancer patients remain
unknown.
The laboratory is interested in tumor cell expression of genes susceptible
to modulate/redirect the immune response. These genes/proteins may
be clear targets for the development of efficient cancer treatment.
************************************************************************************************** SELECTED PUBLICATIONS
Bruhat A., Dréau D., Drake M.E., Tourmente
S., Chapel S., Couderc J.L., Dastugue B., 1993. Intronic and 5'
flanking sequences of the drosophila ß3
tubulin gene are essential to confer ecdysone responsiveness. Mol.
Cell. Endocr. 94:61-71.
Dréau D., Lallès J.P., Philouze-Romé V.,
Toullec R., Salmon H., 1994. Local and systemic immune responses to
soybean protein ingestion in early weaned pigs. J. Anim. Sci., 72:
2090-2098.
Dréau D., Morton D., Foster M., Swiggett
J.P., Sonnenfeld G., 1997. Immune alterations in male and female mice
after 2-deoxy-D-glucose administration. Physiol Behav, 62 (6):
1325-1331.
Dréau D., Morton D., Fowler N., Foster M.,
Sonnenfeld G., 1998. Effects of 2-deoxy-D-glucose administration on
immune parameters in mice. Immunopharmacology, 39 (3): 201-213.
Dréau D., Bosserhoff A.-K., White R.L.,
Holder W.D, 1999. Melanoma-inhibitory activity protein concentrations
in the blood of melanoma patients treated with immunotherapy. Oncology
Research, 11: 55-61.
Dréau D., Lallès J.P., 1999. Contribution
to the study of gut hypersensitivity reactions to soyabean proteins in
preruminant calves and early-weaned piglets. Livest. Prod. Sci., 60:
209-218.
Dréau D., Sonnenfeld G., Morton D.S.,
Fowler N., Lyte M., 1999. Effects of social conflict on immune
responses and Escherichia coli growth within peritoneal implant
chambers in mice. Physiol Behav, 67: 133-140.
Dréau D., Culberson C., Wyatt S., Holder
W.D, 2000. Human Papilloma virus in melanoma biopsy specimens and its
relation to melanoma progression. Ann. Surg., 231: 664-671.
Dréau D., Foster M., Morton D.S., Fowler
N., Kinney K., Sonnenfeld G, 2000. Immune alterations in three mouse
strains following 2-deoxy-D-glucose administration. Physiol Behav,
70:1-8.
Bosserhoff A.K., Dréau D., Hein R.,
Landthaler M., Holder W.D., Buettner R., 2001. Melanoma inhibitory
activity (MIA), a serological marker of malignant melanoma. Recent
Results in Cancer Res., 158:158-168.
Dréau D., Foster M., Hogg M., Swiggett J.,
Holder W.D., White R.L, 2001. Angiogenic and immune parameters during
Interferon-alpha2b adjuvant treatment in melanoma patients. Oncol. Res,
12:241-251.
Brar S.S., Grigg C., Wilson K.S., Holder
W.D. Jr, Dréau D., Austin C., Foster M., Ghio A.J., Whorton A.R.,
Stowell G.W., Whittall L.B., Whittle R.R., White D.P., Kennedy T.P.,
2004. Disulfiram inhibits activating transcription factor/cyclic
AMP-responsive element binding protein and human melanoma growth in a
metal-dependent manner in vitro, in mice and in a patient with
metastatic disease. Mol Cancer Ther. 3:1049-60.
Carbonell
A.M., Matthews B.D., Dréau D.,
Foster M., Austin C.E., Kercher K.W., Sing R.F., Heniford B.T., 2004.
The susceptibility of prosthetic biomaterials to infection. Surg
Endosc.[Epub ahead of print]"
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