International Conference on Systemics, Cybernetics and Informatics
( ICSCI - 2012 )
Conference Dates: February 15 - 18, 2012
Venue: Dr. MCR HRD Institute, Government of Andhra Pradesh, India, Road No. 25, Jubilee Hills, Hyderabad – 500 033
http://www.hrdiap.gov.in ; Ph: +91-40-23548487; Fax:: 23548489; email: adm.ao@hrdiap.gov.in
Organized By: Pentagram Research Centre Pvt Limited
Corporate Address: 201, Venkat Homes, MIGH-59, Mehdipatnam, Hyderabad, Andhra Pradesh, India
Conference Secretariat Address: 1073, Road No. 44, Jubilee Hills, Hyderabad, Andhra Pradesh, India
Web Site: www.icsci.net ; Tel: +91-40-23553986; email: icscimail@yahoo.com
Mission: To Create A Knowledge Based Society
International Conference on Systemics, Cybernetics and Informatics is an event organized by Pentagram Research
Dr. Karunagaran Devarajan
Guest of Honor
Dr. Karunagaran Devarajan
Dr. Karunagaran is a Professor at the Department of Biotechnology, Indian
Institute of Technology Madras, Chennai. He started his career as a lecturer
in Biochemistry at the PSG college of Arts and Science, Coimbatore in 1979
and taught a number of BSc and MSc students for more than a decade.He has
made significant contributions in the field of signal transduction, mediated
by epidermal growth factor receptors (EGFRs) and their ligands implicated in
the development of human cancer. A novel concept proposed by him (with Dr.
Yosef Yarden from Israel) is that ErbB-2 (the second member of EGFR family)
acts as the preferred heterodimeric partner of all the known members of the
EGFR family, and at least, part of the transforming ability of an over
expressed ErbB-2 is due to transactivation of growth factor signaling.
Moderate expression of ErbB-2 is biased for heterodimerization with ErbB-3
and ErbB-4 receptors that bind neu differentiation factor. A monoclonal
antibody against neu differentiation factor raised by him is being marketed
by a U. S. Company. Dr. Karunagaran (with Dr. Mien-Chie Hung from Houston)
discovered that adenoviral E1A suppressed the radiation-induced activation
of Nuclear Factor kappa B (NF-κB), a transcription factor known to protect
cells from cell death. This finding provides a plausible mechanism for the
long-known susceptibility of cells to radiation-induced apoptosis in the
presence of E1A. Dr. Karunagaran joined the Rajiv Gandhi Centre for
Biotechnology, Thiruvananthapuram in December 1997. His laboratory studies
are focused on cervical cancer, an important public health problem for adult
women in India. Cervical cancer causes about 250,000 deaths annually
worldwide, with women in the developing countries accounting for 80% of
these deaths. Although human papilloma virus (HPV) infection is the major
risk factor for cervical cancer, molecular alterations of tumor suppressor
genes and/or oncogenes either associated with HPV infection or independent
of it are necessary for the cervical cancer progression. Dr. Karunagaran has
shown that the transcription factor, nuclear factor-kappa B (NF-κB) is
constitutively activated in high-grade squamous intraepithelial lesions and
squamous cell carcinomas during human cervical cancer progression (cited in
text book “the biology of Cancer” on page 195, by Robert A. Weinberg,
Garland Science http://www.garlandscience.com/textbooks/0815340788.asp).
Many chemopreventive agents induce programmed cell death or apoptosis, a
potent mechanism by which they eliminate preneoplastic or cancer cells.
Curcumin, the yellow pigment derived from Curcuma longa, is a
pharmacologically safe compound and possesses antioxidant, antiinflammatory
and anticancer activities. Curcumin inhibits cell proliferation and induces
apoptosis of several, but not all cancer cells. Dr. Karunagaran has proposed
that differential over expression of certain antiapoptotic proteins may
account for the failure of curcumin to induce apoptosis in some cancer
cells. Results from his laboratory suggest antiapoptotic roles for NF-κB,
Bcl-XL and heat shock proteins such as hsp70 in curcumin-induced apoptosis.
His laboratory has identified that NF-κB can also regulate epidermal growth
factor-induced apoptosis by a similar mechanism. Loss of transforming growth
factor-β (TGF-β) sensitivity is observed in a wide variety of cancers
including cervical cancer. His laboratory has reported a novel Smad 2
mutation in a human cervical tumor sample and loss of expression of Smad 2
and Smad 4 in different stages of cervical cancer progression and also the
mutations of Smad 2 and Smad 4 in two of the six human cervical cancer cell
lines analyzed revealing an important role for Smads in human cervical
cancer for the first time. Two of his research publications are now
recognized as classic citations (more than 400 citations each) and two more
have more than 200 citations each and his ‘h-index’ has now increased to 23.
For further details on current research interests, browse through the
ongoing research projects.
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