Damon Runyon News

Many studies have shown that the cancer cells within a tumor form a remarkably diverse population. These cellular differences play a significant role in how the tumor develops and how it responds to therapy. A technology called flow cytometry (a high-throughput method for characterizing single cells) has been critical for these findings; however, the technology is inherently limited because it can only measure biochemical processes that can be interrogated using a fluorescent molecule.

Aging is the primary risk factor for developing cancer. Despite the growing list of age-associated defects, we do not yet understand why aging is one of the most potent carcinogens.   

Tumors evade the immune system by suppressing the function of T cells otherwise capable of destroying cancer cells. These T cells develop in lymph nodes - specialized tissues that control responses against cancer, infection, and other disease. As T cells become activated against tumors, the cells differentiate and proliferate at much slower rates. This decreased proliferation dramatically reduces the effectiveness of anti-tumor immune responses. 

Clinical testing for inherited cancer risk often leads to identification of rare genetic variants, but it is uncertain if these variants affect cancer risk. This uncertainty is difficult for cancer patients who want to know the best way to prevent future cancers in themselves and their families. 

Many diseases could be cured if the power of our own immune systems could be harnessed. For cancer, the theory of "cancer immunoediting" provides a hypothesis for how tumors escape detection by the immune system. 

Dr. Papapetrou [Edward P. Evans Foundation Innovator] studies a disease called myelodysplastic syndrome (MDS), which often progresses to leukemia. She is using a novel approach to identify the specific genetic alterations involved in the development of MDS, which are not currently known.

Many cancers initially respond to therapy. However, cancers often acquire resistance and stop responding to further treatment. Small cell lung cancer (SCLC) is an example of a cancer that is highly sensitive to initial treatment, but quickly acquires a vicious resistance resulting in a five-year patient survival rate of less than 4%. In order to combat drug resistance and improve the quality of life for patients with SCLC, it is important to understand the key genetic changes and cellular pathways that drive resistance.

[Nadia’s Gift Foundation Innovator]

Tumors evolve from single cells. As they expand to form the tumor mass, the cells diverge and form distinct subpopulations with different genetic mutations. This salient characteristic is called "intratumor heterogeneity" and confounds basic research and clinical diagnostics. The challenge is that standard genomic tools require a large amount of input material and thus are limited to measuring an average signal from a complex population of cells.  

[Island Outreach Foundation Innovator of the Damon Runyon-Rachleff Innovation Award]

Cancer is thought to arise through a series of genetic mutations in the DNA sequence. Depending on the location of these errors and the genes that are affected, these mutations lead to the many different features that characterize cancer cells such as uncontrolled proliferation, escape from cell death and metastasis.

Antibodies have proven to be powerful tools in cancer research, facilitating the elucidation of disease mechanisms and generating novel and effective anti-cancer therapeutics. However, antibody biotechnology is limited by one major factor: the inability of antibodies to effectively cross the cell membrane to reach the inside of the cell, or cytosol. A new strategy is clearly necessary-one based on facile and reliable delivery of active antibody-like molecules into various cell types.