American Association for Cancer Research

Memorial Fund Continues Korsmeyer Legacy in Cell Death Research

 

In March of 2005, the AACR and the cancer research field lost a pioneer in the area of apoptosis, also known as programmed cell death. An outstanding mentor to his students, Stanley J. Korsmeyer, M.D., was well known for his significant contributions to our understanding of the mechanisms that regulate apoptosis.

AACR recognized Korsmeyer's scientific accomplishments in 2004 with the Pezcoller Foundation-AACR International Award for Cancer Research for work that has helped to establish certain cell death regulators as a new category of oncogenes and tumor suppressor genes. "Dr. Korsmeyer's research has had widespread impact, not only in advancing our understanding of the genesis of cancer, but also more broadly on biology and medicine," said Margaret Foti, Ph.D., M.D. (h.c.), AACR chief executive officer.

Born in 1951 and raised in the town of Beardstown, Illinois, Korsmeyer was the son of livestock farmers. His early experience raising a pair of prizewinning Hampshire hogs through his involvement with the 4H Club made him think about becoming a veterinarian. Those early aspirations evolved into an education in biological sciences and ultimately a stellar career in cancer research.

Korsmeyer demonstrated that the abnormal cells in B-cell lymphoma contained a genetic mutation that enabled them to survive apoptosis, the body's normal process for eliminating cells. Suzanne Cory, Ph.D., The Walter and Eliza Hall Institute of Medical Research, Melbourne, Australia, said," His contributions to our field are enormous and he is sorely missed, both as a person and a scientist. I know that I speak for all of us when I say that his untimely death makes us all the more determined to conquer cancer." She remembered the elegance of his talks and papers. "As well as his science being excellent," she said, "it was beautiful. The knowledge that he has helped to build about bcl-2 (a novel oncogene that blocks cell death) and this pathway may well prove to be the Achilles' heel in conquering many kinds of cancer." In addition to this discovery, Korsmeyer discovered other members of the bcl-2 gene family and their involvement in cell death.

After Korsmeyer's untimely death, AACR received contributions in his memory from family members, friends, colleagues, organizations and foundations totaling more than $120,000. To honor his memory and continue his legacy, the Memorial Fund sponsored the first Stanley J. Korsmeyer Memorial Symposium: Apoptotic and Non-Apoptotic Cell Death in Cancer at AACR's 2007 Annual Meeting. This important symposium will be presented at the AACR Annual Meeting for at least ten years. In this way, Korsmeyer's legacy will continue to inspire his colleagues and countless young investigators.

Eileen P. White, Ph.D., AACR board member, Korsmeyer Symposium chair and a molecular biologist at the Cancer Institute of New Jersey and Rutgers University, said, "Stan's contribution to our understanding of this pathway is enormous. His scientific footprint is all over this pathway. It is our responsibility to honor his life by facilitating his legacy."

A member of the AACR since 1992, Korsmeyer served as associate editor of Cell Growth & Differentiation (now titled Molecular Cancer Research), program committee chair for the 2001 AACR Annual Meeting, and member of the Board of Directors, among other appointments. "Stan was deeply committed to AACR, and we benefited from his dedication, expertise and guidance in many ways over the years," said Foti.

Addressing the attendees at the 2007 symposium, Susan Korsmeyer, his wife of 25 years, emotionally thanked the scientists in the audience for dedicating their lives to cancer research. "I understand," she said, "in a profoundly personal way the essential and urgent need to conquer the ravages of cancer and hope that you will continue to be inspired to perform the next experiment."  With the help of AACR, through the Stanley J. Korsmeyer Memorial Fund, the support will be there.