Gamini received his BS from the University of Sri Lanka,
MS from Colorado State University and PhD from the University of Hawaii. He was a Post-Doctoral Fellow at both Colorado
State University and the University of Wyoming at Laramie. He began working as a Professional Research
Assistant at the University of Colorado and between 1991 and late 2004 he
worked in the Department of General Internal Medicine, the Division of
Hematology, Renal and Pediatrics. He
returned to the Seligman Lab in 2004.
The iron (Fe) chelator desferrioxamine (DFO) has been
found to be effective as a treatment for neuroblastoma which is a childhood
cancer. Iron is a co-factor needed for the enzyme ribonucleotide reductase to
convert ribose to deoxyribose during DNA syntheses. Hence a block at late G1
phase of the cell cycle is expected in cells undergoing mitosis. However
another block at early G1 has been observed with a variety of the treatment
with DFO in cancer cell lines. This effect has been observed with many other
iron chelators implying that this block is related to Fe deprivation and not
due to DFO through some other mechanism. No explanation for this effect has
been provided thus far in spite of many research publications on this subject.
Gamini’s project in General Hematology primarily involves
pinpointing the cause of early G1 cell cycle arrest using neuroblastoma cell
lines as a model. The work is primarily based on using molecular biology tools
such as specific inhibitors of proteins, mutant plasmids, small interfering RNA
(siRNA), techniques involving signal transduction, western analyses, cell cycle
analyses, PCR procedures.
Publications have been made based on this research, the
most recent being on better differentiation of the two arrest points by iron
chelation and the molecular events involved with the two distinct blocks.