The Future of Cancer Research is Here

Advancing innovative tumor-specific therapies through revolutionary research to shatter the global cancer burden

Current cancer research needs supercharging so that leaps in next-generation therapies become commonplace. At Institute 53, we dream bigger, we flip the script on cancer, and we definitely don't play by the rules. Institute 53 scientists are not content with the next step — they are going far beyond “taking it up another notch.”

Microscope

Pioneering the Next Generation of p53 Cancer Therapeutics

Cell research

A Case of Dr. Jekyll and Mr. Hyde

The p53 gene and p53 protein have been a major focus in cancer research for more than 45 years, and much has been learned to leverage discoveries into clever strategies for killing cancer. This continues to remain a challenge that results from the remarkable ability of p53 to play the dichotomous role of Dr. Jekyll fighting against cancer and Mr. Hyde causing cancer. Throughout the years of scientists trying to target p53 therapeutically, the Mr. Hyde in p53 has stayed a step ahead, so at Institute 53, we have veered off in a completely new direction; to trick the Mr. Hyde of p53 to do the cancer killing for us.

THE SCIENCE BEHIND INSTITUTE 53

The Science Supporting Institute 53

p53 was first discovered as an oncogene and oncoprotein when mutated, and later as a tumor suppressor in its wildtype form, earning it the moniker Guardian of the Genome. This dichotomy — suppressing cancer and promoting cancer — is unique in the field of cancer research.

There are two general types of p53 mutations that cause cancer: those that merely knockout the p53 gene (such as a deletion), and missense mutations predominantly within p53's DNA Binding Domain that not only eliminate p53's tumor suppressor function but also unleash p53's cancer-promoting properties. These missense mutations are referred to as Gain-Of-Function (GOF), in which new transcriptional activation of genes results — many of which drive cancer development, metastasis, and drug resistance.

It has long been intriguing how so many different missense mutations in p53 could generate the same type of novel gene activation properties. GOF mutated p53 exhibits promoter binding for activated genes not through direct DNA binding as wildtype p53 does, but through interaction with transcription factors such as Sp1 and ETS1. At least two factors define promoters that bind GOF mutated p53: multiplicity of transcription factor binding sites and appropriate spacing of these sites.

With this mechanistic insight, investigators at Institute 53 have developed therapeutically beneficial genes driven by GOF mutated p53 to create cancer-killing agents. A new era of gene therapy for cancer treatment is now on the horizon.

Cancers in Our Sights

  • Lung Cancer (including the deadly Small Cell Lung Cancer)
  • Ovarian Cancer
  • Pancreatic Cancer
  • Esophageal Cancer
  • Head and Neck Cancer

INSTITUTE 53 STRATEGIC PILLARS

Transforming Tumor Biology into Targeted Therapies

Precision Oncology

Restoring the tumor-suppressive power of p53 to develop therapies that target cancer cells with unmatched genomic precision.

Global Translation

Driving the reach of oncology advancements to healthcare systems worldwide, reducing the global cancer burden through strategic translation.