Our Research

Unusual (atypical) genes and their products that are specific to disease states are studied at Atypigene Biomedical Research Institute (ABRI), a non-profit medical research facility. Importantly, these genes are not studied by other research entities because proprietary cloning and expression techniques licensed by ABRI are required for study of these genes. It is our belief that targeting these unusual gene expressions will result in less toxic therapies for unmet human medical needs such as cancer.

Our lead target for development of universal anti-cancer therapies is Migration inducting gene-7 (Mig-7); an atypical gene that produces protein in a cancer microenvironment. To date, this gene is not expressed by normal cells in children and adult humans. These data suggest that therapies specifically targeting this gene expression could be non toxic. The only other human “normal” cell type, besides tumor cells, that expresses Mig-7 is an embryonic/fetal cell type known as trophoblast cells that contribute to placenta formation during pregnancy (1-3). Proof-of-principle experiments demonstrate that Mig-7 is targetable (4).

Another potential benefit of future Mig-7 therapies is cost effectiveness because Mig-7 expression is found in 96% of malignant solid-type cancers regardless of the original tumor’s organ site (4;5). Furthermore, Mig-7 expression causes precancer cell lines to become highly invasive (2;4). The most successful treatments of cancer have been those that target precancers such as early detection of cervical intraepithelial neoplasia6 that leads to cervical cancer. There are no current therapies that target the transition of precancer tumor cells (benign) to invasive cancer (malignant and lethal). Therefore, we postulate that Mig-7 based therapies and diagnostics could be used for early detection as well as treatment of precancer to cancer as well as advanced cancer.

References cited 

1. Crouch,S., C.S.Spidel, and J.S.Lindsey. 2004. HGF and ligation of avb5 integrin induce a novel, cancer cell-specific gene expression required for cell scattering. Experimental Cell Research 292:274-287.
2. Petty,A.P., K.L.Garman, V.D.Winn, C.M.Spidel, and J.S.Lindsey. 2007. Overexpression of carcinoma and embryonic cytotrophoblast cell-specific Mig-7 induces invasion and vessel-like structure formation. Am J Pathol 170:1763-1780.
3. Petty,A.P., C.L.Dick, and J.S.Lindsey. 2008. Translation of an atypical human cDNA requires fidelity of a purine-pyrimidine repeat region and recoding. GENE 414:49-59.
4. Petty,A.P., S.E.Wright, K.A.Rewers-Felkins, M.A.Yenderrozos, B.A.Vorderstrasse, and J.S.Lindsey. 2009. Targeting migration inducting gene-7 inhibits carcinoma cell invasion, early primary tumor growth, and stimulates monocyte oncolytic activity. Mol Cancer Ther 8:2412-2423.
5. Phillips,T.M. and J.S.Lindsey. 2005. Carcinoma cell-specific Mig-7: A new potential marker for circulating and migrating cancer cells. Oncology Reports 13:37-44.
6. Berman,J.J. and G.W.Moore. 2010. Precancer: The beginning and the end of cancer. Jones and Bartlett, Sudbury, MA.

Patent applications

"Mig-7 as a specific anticancer target" – PCT/US2007/068078 filed May 2, 2006; U.S. 12/299,160 filed October 31, 2008
"Mig-7 as a specific anticancer target" – PCT/US2008/080809 filed October 22, 2008