All Solid Tumors

Epigenetic therapies have been extensively studied for treating all solid tumors with varying outcomes. Unfortunately, as solo therapy, they have shown minimal activity in improving patient survival at end-stage disease. The cancer epigenome is characterized by global DNA methylation and chromatin changes, such as the hypermethylation of specific CpG island promoters. Epigenetic agents like DNA methyltransferase or histone deacetylase inhibitors induce phenotype changes by reactivating epigenetically silenced tumor suppressor genes. Despite initial promise in hematologic malignancies, epigenetic agents have not shown significant efficacy as monotherapy against solid tumors. Recent trials demonstrate that epigenetic agents exert favorable modifier effects when combined with chemotherapy, hormonal therapy, or other epigenetic agents.

​

However, there is promising news. Cancer stem cells can be effectively targeted by this modality, as extensively documented in literature. Epigenetic therapies have been shown to enhance response to chemotherapy agents and significantly reduce the chances of cancer recurrence. Therefore, epigenetic therapies are increasingly recommended as a "backbone" therapy to support all other treatment modalities, including surgery, radiation, and chemotherapy.

One of the foundation's key projects involves developing the Modified Multi Molecular Targeted Epigenetic Therapy (MTET) protocol, which has demonstrated overwhelming preclinical data supporting its activity in chemorefractory disease and, most importantly, in advanced cancer cases.

​

A major development in recent cancer research involves rethinking the relationship between tumor size and patient survival. For years, it was believed that larger tumors caused shorter survival. We now understand that because tumors can spread at smaller sizes—when they are more compact and hypoxic—larger tumor size does not necessarily mean shorter survival. This paradigm shift in understanding tumor cell biology has caused a major change in cancer care. We no longer push exclusively for tumor size reduction as we once did. For example, the use of cytotoxic agents is now questioned in advanced stages of disease when patient survival is not simply dependent on tumor size. Interestingly, the RECIST criteria used to define treatment response has not changed, meaning a patient with a smaller post-therapy tumor is still considered a responder, even when the patient may not survive beyond what would be expected without therapy.

​

The role of epigenetic therapies has been further highlighted by these findings. Epigenetic therapies target the root cause of disease and cancer stem cells, working to differentiate cancer stem cells into a lower plasticity phase where they commit to certain cell lineages with reduced capacity to reproduce and re-engage in cell cycles. This approach is believed to translate to better outcomes and improved survival in many cases.