Our Unique Platform

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DNA in the nucleus of your cells consists of instructions (genes) for building all the proteins that make up your body.   However, scientists know the function of only a fraction of the DNA in the cell nucleus; the other approximately 70% is “evolutionary junk”.  We discovered that this “junk” contains small DNA regions (that we have termed Transposon-Associated Gene Sequences (“TAGs”) that are shared by genes coordinating specific pathways.  This allows them to participate in direct gene-to-gene “conversations”.  We can now detect these conversations for potential therapeutic benefit, having identified TAGs for pathways including cancer, heart disease, and Parkinson’s Disease.

The most aggressive cancer cells are those that devolve into a more primitive state, where complex gene-to-gene conversations are lost.  When this happens, an ancient stress response kicks in and cells start proliferating and moving without normal controls, eventually causing metastatic disease.

We developed a small, interfering (si)RNA that can block the critical, final conversation cancer genes are having to survive - stopping cancer right at the source.

The prognosis remains poor for patients with KRAS G12D-mutant pancreatic cancer. There are several targeted KRAS-G12D inhibitors being developed to be used in conjunction with chemo- and immuno-therapies.  However, the ability of these tumors to rapidly proliferate under stress allows evolution of bypass mutations, consistently resulting in therapy breakthrough. Developing novel therapies for this patient population remains of paramount importance.

•  Both low and high doses of our ONCO-TAG inhibit tumor growth in CDX studies in mice

•  High-dose ONCO-TAG inhibited growth by almost 60%, equal to a commercial positive control consisting of a mix of anti-transcription factor siRNA

•  Effect is dose-dependent

Our molecule differs from others because it targets a single long non-coding (lnc) RNA that is required for expression of multiple genes within the HIPPO/Yap1 pathway to function. KRASmut cancers are particularly dependent on this pathway (references 1-5). Inhibiting this lncRNA decreases the chance of bypass mutations and therapy breakthrough, often seen when targeting a single gene in KRASmut cancers. Our molecule would likely be an adjunct to current therapies.

1. Kapoor A, et. al. Yap1 activation enables bypass of oncogenic Kras addiction in pancreatic cancer. Cell. 2014 Jul 3;158(1):185-97.
2. Greten FR. YAP1 takes over when oncogenic K-Ras slumbers. Cell. 2014 Jul 3;158(1):11-2. 
3. Mira A, Ambrogio C. YAP and TAZ orchestrate adaptive resistance to KRAS inhibitors. Nat Cancer. 2023 Jun;4(6):784-6.
4. Zhang, W. et al. Downstream of mutant KRAS, the transcription regulator YAP is essential for neoplastic progression to pancreatic ductal adenocarcinoma. Sci. Signal. 7, ra42 (2014).
5. Zhao B, Wei X, Li W, Udan RS, Yang Q, Kim J, Xie J, Ikenoue T, Yu J, Li L, Zheng P, Ye K, Chinnaiyan A, Halder G, Lai Z, and Guan K. Inactivation of YAP oncoprotein by the Hippo pathway is involved in cell contact inhibition and tissue growth control. Genes Dev. 2007; 21(21):2747-61. 
6. Harvey, K.F., Tang, T.T. Targeting the Hippo pathway in cancer. Nat Rev Drug Discov (2025).