I've quoted the breastcancerchoices.org comment below on the lung study....this is really good stuff.
Cited below is the first study referenced by Dr. Flechas, a UCLA study in which not only the NIS symporter, but thyroperoxidase (TPO) as well were put into a retrovirus that was put into mice with oat cell lung cancer.
The significance of adding TPO to the NIS is that TPO helps to oxidize iodide to form iodine to make hormones and bind to fats to form iodolactones to kill cancer cells.
Then iodide was given to the mice - NONRADIOACTIVE IODIDE!
With all of the NIS to help the iodide get in, more than 95% of the mice's oat cell lung cancer cells were killed. Way cool.
What great UCLA researchers to try using nonradioactive iodide to kill the lung cancer!
Nonradioactive Iodide Effectively Induces Apoptosis in Genetically Modified Lung Cancer Cells1
Ling Zhang , Sherven Sharma , Li X. Zhu , Takahiko Kogai , Jerome M. Hershman , Gregory A. Brent , Steven M. Dubinett2 and Min Huang2
Division of Pulmonary and Critical Care Medicine [L. Z., S. S., L. X. Z., S. M. D., M. H.], Division of Endocrinology and Metabolism, Department of Medicine [T. K., J. M. H., G. A. B.], Lung Cancer Research Program of the Jonsson Comprehensive Cancer Center [S. M. D.], and Department of Pathology, David Geffen School of Medicine [M. H.], University of California Los Angeles and Veterans Affairs Greater Los Angeles Healthcare System, California 90073
We assessed a nonradioactive approach to induce apoptosis innon-small cell lung cancer by a novel iodide uptake and retentionmechanism. To enhance tumor apoptosis, we transduced non-smallcell lung cancer cells with retroviral vectors containing thesodium iodide symporter (NIS) and thyroperoxidase (TPO) genes.Expression of NISand TPOfacilitated concentration of iodidein tumors. As a consequence of the marked increase in intracellularlevels of iodide, apoptosis was seen in >95% of NIS/TPO-modifiedlung cancer cells. Intraperitoneal injection of potassium iodideresulted in significant tumor volume reduction in NIS/TPO-modifiedtumor xenografts without apparent adverse effects in SCID mice.Iodide induced an increase in the level of reactive oxygen species.Iodide-induced apoptosis is sensitive to N-acetylcysteine inhibition,suggesting an important role by reactive oxygen species in thisapoptotic process. In addition, iodide-induced apoptosis isassociated with overexpression of CDKN1A (p21/Waf1)and down-regulationof survivin at both mRNA and protein levels. This is the firstreport demonstrating that a therapeutic dose of nonradioactiveiodide has potent efficacy and high selectivity against lungcancer when used in combination with genetic modification ofcancer cells to express the NIS/TPOgenes.