top of page

BLOOD CANCER

Epigenetic Therapy Cancer Treatment

Epigenetic Therapy: A Breakthrough in Blood Cancer Treatment

Traditional cytotoxic drugs often stimulate cancer stem cells making tumor recurrence nearly inevitable. In contrast, epigenetic therapies offer a durable, targeted approach by exploiting underlying cellular alterations to fundamentally change patient outcomes. 

​

​

First FDA Approved Agent

​

Decitabine (a derivative of Azacitidine) revolutionized hematologic care by demonstrating remarkable success in treating myelodysplastic syndromes (MDS) and acute myeloid leukemia (AML)

Proven Survival Benefits ​

​

The landmark AZA001 clinical study established 5-aza as a preferred, high impact treatment for high risk MDS patients, significantly reducing the risk of leukemic transformation

Precision Targeting: EZH2 Inhibitors

Many hematopoietic tumors carry genetic alterations that increase lysine 27 methylation, leading to an adverse prognosis. EZH2 inhibitors directly target these specific mutations.

 

While EZH2 commonly functions as an oncogene, it can also act as a tumor suppressor in myeloid neoplasia, making precise inhibition essential.

The Clinical Challenge of Non-Selectivity

While traditional epigenetic drugs like decitabine show incredible promise, they can become refractory because their DNA-level mechanisms are unselctive.

​

For example, while decitabine successfully demethylates oncosuppressor genes, it can simultaneously activate oncopromters (like S100B), highlighting the strict need for more sophisticated, selective therapies. 

The Promise of MTET: Next Generation Epigenetic Treatment

To overcome the limitations of traditional, unselective drugs, Cancer Research and Life Foundation is pioneering clinical trials for a novel Modified Multi Molecular Targeted Epigenetic Therapy (MTET) protocol.​

​

MTET represents a monumental leap forward in three distinct ways

01

True Selectivity

Designed to precisely target and restore oncosuppressor genes without accidentally unleashing harmful cancer promoter genes

02

Dual Action Mechanism

Successfully combines critical histone epigenetic alterations with DNA epigenetic alterations simultaneously, a long standing hurdle in oncology research. 

03

Dynamic Potency

Offers flexible potency that adapts to the shifting, complex epigenetic platform of cancer aberrancies, including comprehensive targeting of the critical EZH2 gene. 

bottom of page