We are motivated to fund research and find a cure for VHL!

1.  Double Strand is collaborating with top researchers at Massachusetts Institute of Technology and Harvard-Massachusett’s General Hospital on a research project, that with the proper funding, has great potential to dramatically improve the treatment for Central Nervous System (CNS) Hemangioblastomas and many Cancers.

2.  VHL IS GENETICALLY DEFINED – The gene for VHL has been mapped on the short arm of Chromosome 3. Its genetic identity makes VHL an ideal model for research study with its molecular synergies to pathways causing all forms of cancers. VHL can be diagnosed with DNA testing.

3.  VHL AFFECTS MANY ORGANS and breakthroughs in treatments for VHL will have an impact on a wide range of illnesses and cancers in many organs.

4.  20% OF CASES ARE SPORADIC—Everyone has some risk for VHL. The incidence of VHL in a family where one parent has the disease is 50%. 20% of cases are ‘de novo’ meaning a new mutation and no other family member has the illness. This means anyone in the population is susceptible at a rate of 1:32,000.


40/40 RULE: 40% of VHL patients have renal cell cancer by the age of 40

50/25 RULE: 50% OF VHL patients have CHS hemangioblastomas by the age of 25

90% OF VHL patients have disease manifestation by the age of 65

Life expectancy for VHL is 52.5 years of age. Life expectancy since genetic identification has increase by 16 years.


Mutations of the VHL gene, of which there have been more than 1500 identified, cause cells to lose their ability to process information properly and act as if they are starved of oxygen. Surrounding cells produce abnormally high numbers of blood vessels which cause the formation of tumors, cysts, and cancers in many organs.

Our research funding will focus on the following areas and questions:

  • Is it possible to create targeted, precision treatments to kill tumors without causing collateral patient morbidity and mortality?
  • Can we prevent tumor formation and growth in all cancers by repairing the VHL gene and its misfolded protein to restore its ability to stop tumor blood vessel growth?
  • How can we stimulate the body’s own immune system to constrain tumor growth without stimulating a generalized autoimmune response?
  • What causes symptomatic CNS hemangioblastoma tumors to grow 10x faster than asymptomatic?

CURRENT TREATMENT MODALITIES FOR KIDNEY CANCER AND CNS HEMANGIOBLASTOMAS are suboptimal requiring surgery in the absence of truly effective medications or other modalities. In the presence of single or multiple CNS tumors, surgical treatment is indicated only for the symptom producing lesion. in renal cell cancer, active surveillance is recommended in tumors less than 3 centimeters. Ablative techniques have had some success in smaller tumors.

Recent development of anti-angiogenesis medications has been encouraging for clear cell renal cancer but the hope for the future lies in the development of targeted, precise, non-surgical therapies which will become a new standard of care and will eliminate the need for recurrent major surgeries while improving life quality and extension for all patients.