The modern era of our nation's effort to understand and treat cancer, which began with the signing of a new National Cancer Institute Act by President Nixon in December of 1971, is now 30 years old. Although the National Cancer Institute first came into existence in 1937 with the signing of an act by President Franklin D. Roosevelt, only a revolution in biological research in the latter half of the twentieth century enabled cancer to be studied in a rational way and with confidence that success might be possible. During the past 20 years, basic research into the causes that underlie cancer has opened the door to opportunities for diagnosis and treatment such that now, as we enter a new era in cancer research, meaningful progress is possible. To fully exploit these opportunities, however, academic research institutions and the private sector must approach the cancer problem in a fundamentally new way. Although investigator-initiated research should remain the backbone of publicly funded research, large projects that move basic research results into the clinic, commonly called "translational research," require close cooperation between academia and the private sector. Interdisciplinary approaches are the future for research that will make a real difference to patients, but achieving ambitious goals solely with public funds may not be possible. It is now time to re-think how translational cancer research should be assessed, supported, and performed.

The roots of the modern understanding of cancer came from a number of sources. Prominent among these was the study of viruses that caused tumors at the site of inoculation in experimental animals. These viruses carried genes that could change a normal cell into a cancer cell. Research using both RNA and DNA tumor viruses, with Cold Spring Harbor Laboratory preeminent among institutes studying DNA tumor viruses, showed that a small set of genes could transform otherwise healthy cells into cells that grew into a lethal tumor, eventually metastasizing and killing the animal. But relatively few virus genes proved to have any part in inducing human cancers. Notable exceptions were the transforming genes present in the DNA-containing papillomaviruses that, when carried into the epithelial or glandular cells of the cervix, initiate cervical cancer in women.

A few cancer-causing genes were found in RNA tumor viruses that had direct orthologs in human cells. These virus-related human genes, when altered by mutation or when overexpressed, contributed to human cancer. Michael Wigler codiscovered here at CSHL, at the same time as Robert Weinberg at the Massachusetts Institute of Technology, one such gene in 1981, the so-called ras oncogene. Another notable example was the v-myc gene that was first defined in an avian retrovirus that caused myelocytic leukemia in chickens. Later, a related human gene called c-myc was found to be overexpressed in a variety of tumors, including lymphomas, leukemias, and lung, cervical, ovarian, breast, and gastric cancers. The c-myc gene was converted into an oncogene either as a result of chromosome translocation (the aberrant exchange between two unrelated chromosomes), by gene amplification, or by mutation directly in the gene itself.