Alex's Lemonade Stand Foundation for Childhood Cancer

Background

Cell metabolism is a key aspect of cell biology. Tumors frequently have significant alterations in the specific types of nutrients they require and the way in which they use these nutrients. Certain genes are often associated with driving these critical changes in tumor cell metabolism, which in turn define their aggressive nature. In particular, MYCN, a potent gene that is altered in several pediatric cancers, such as neuroblastoma, is capable of driving defined changes in tumor metabolism.

Background

Background

Our laboratory is interested in finding better treatments for osteosarcoma (OS), the most common malignant primary bone tumor in children and adolescents. Survival rates for patients with OS have not changed for more than 30 years. We have been studying a rare genetic disorder called Rothmund-Thomson syndrome (RTS) as a model for OS development, where 2/3 of patients have germline mutations in a gene called RECQL4 (Type II RTS). These patients have an extremely high and specific risk for developing OS.

Background

T-cells have proved safe and effective for the treatment of certain types of cancer. However, T-cell efficacy against most solid tumors is limited by the immunosuppressive microenvironment generated by tumor cells and their infiltrating stroma. Myeloid-derived cells are potent controllers of the tumor microenvironment and can alter the fate of tumor-specific T-cells.

Background

Langerhans cell histiocytosis (LCH) is a rare form of cancer that occurs mostly in children. The incidence of LCH is 3 to 5 cases per million children, similar to that observed in Hodgkin Lymphoma or acute myeloid leukemia. Despite similar incidence and survival, LCH patients have benefited from far less research funding and attention than other childhood hematologic neoplasias, likely due to incomplete understanding of the disease. LCH is caused by abnormal proliferation of cells derived from bone marrow.