Researcher Bios

Bruce Stillman, PhD

Bruce Stillman, PhD, president of Cold Spring Harbor Laboratory (CSHL) and Director of the National Cancer Institute-designated CSHL Cancer Center, has been a cancer researcher at CSHL for 30 years. A native of Australia, Stillman received his PhD from the John Curtin School of Medical Research at the Australian National University. He came to CSHL as a Postdoctoral Fellow in 1979.

Stillman’s research focuses on how DNA is copied within cells before they divide in two. His laboratory is studying the mechanism that initiates the entire process of DNA replication. Errors in DNA replication and in the intricate, multistep process by which cells duplicate themselves occur in cancers.

Stillman has received many awards, including the Alfred P. Sloan, Jr. Prize from the General Motors Cancer Research Foundation in 2004, the American Cancer Society Basic Science Award from the Society of Surgical Oncology in 2006 and the Curtin Medal from the Australian National University in 2007.

In 1994, Stillman succeeded Nobel Laureate James D. Watson as Director of CSHL and was appointed President in 2003. Under Stillman’s leadership, CSHL has grown to more than 1,000 employees. Stillman is committed to keeping CSHL’s work on cancer and neurodevelopmental disorders at the cutting edge. Discoveries in basic science, he strongly believes, are the key to making significant diagnostic and therapeutic advances.


Scott Lowe, PhD,

Scott Lowe, PhD, Deputy Director of the Cold Spring Harbor Laboratory (CSHL) Cancer Center, and his multidisciplinary team of cancer researchers and clinicians are working toward finding ways to control cancers in more powerful yet less toxic ways.

After receiving his PhD and doing post-doctoral work at the MIT Center for Cancer Research, Lowe came to CSHL in 1995. He was accepted into the CSHL Fellows Program, focusing on apoptosis, a genetic program used in many chemotherapies that moves cells to destroy themselves.

Lowe moved quickly from the Fellows Program to Assistant, then Associate Investigator, and was named a full professor at CSHL in 2000. In 2001, he became the Deputy Director of the Cancer Center. His research has made important contributions to the understanding of the p53 tumor suppressor pathway, as well as the processes of multi-step carcinogenesis, cellular senescence and tumor-cell drug resistance. Lowe’s current research focuses on understanding the processes that allow normal cells to resist becoming cancerous, and how defects in these processes lead to cancer development and alter the response of cancer cells to chemotherapy.

He has received several awards, including a Sydney Kimmel Foundation Scholar Award, a Rita Allen Foundation Scholar Award, the AACR Outstanding Investigator Award, the AACR-NFCR Professorship in Basic Cancer Research and the Paul Marks Prize for Cancer Research.


Mona Spector, PhD,

Mona Spector, PhD, a researcher in the Tita Monti Cancer Research Laboratory at Cold Spring Harbor Laboratory (CSHL), brings a special perspective to cancer research – that of a survivor. Six years ago, Spector was diagnosed with breast cancer. The experience has left her with a renewed sense of purpose.

Spector earned her doctorate studying cell-division control at Memorial Sloan-Kettering Cancer Center. At CSHL, she first studied programmed cell death — another process that cancer disrupts — before moving into her current cancer research. Spector is digging into the genetic changes that are abundant in cancer. She takes advantage of primary human clinical samples processed by a research nurse at North Shore University Hospital, who is funded through The Don Monti Memorial Research Foundation. The nurse annotates the tissue type and the details of the cancer, but obscures any personal information about the patients, who have consented to this research use of their tissue.

In the future, she will be exploiting powerful next-generation sequencing technology to look for changes in the DNA sequence of cancer cells. Genes that are frequently mutated as cancer advances might make good “targets” for therapy.


Dr. Johannes (Hannes) Zuber

Dr. Johannes (Hannes) Zuber is a post-doctoral fellow working in the Tita Monti Cancer Research Laboratory at Cold Spring Harbor Laboratory (CSHL). He has developed several mouse models of acute myeloid leukemia (AML) to study the genetics of this devastating cancer. These mouse models have already identified several genes that will help physicians make therapeutic decisions for cancer patients and may also identify potential targets for novel therapeutic drugs.

Zuber’s past experience as a hematology oncologist in Berlin, Germany, helps drive his passion for research. The standard protocols used to treat AML patients employed very high doses of chemotherapeutics, which resulted in 10% of patients dying from toxicity. Researching the genetics of leukemia that respond to lower-dose therapy and those that do not could help tailor therapies to the specific genetic composition of leukemia in each patient, sparing some the devastating side effects of high-dose chemotherapy.


Amy Rappaport

Amy Rappaport is a graduate student in the Watson School of Biological Sciences at CSHL. Dr. Lowe calls her a “pioneer” for her use of two recently developed technologies to unravel the complex genetic and biochemical networks that cause acute myeloid leukemia (AML), a cancer in which certain white blood cells proliferate out of control in the bone marrow.

For a few years now, scientists have known that AML patients who respond poorly to treatment carry mutations in genes embedded in chromosomes 5 and 7. But there are many genes in these regions, and despite years of hard work it is not yet clear which are specifically associated with AML.

Rappaport is using a revolutionary technique called RNA interference, or RNAi, developed in part by CSHL scientist Greg Hannon, to switch genes “off” on the two chromosomes. Her test subjects are mice that have been engineered by Dr. Lowe’s group to develop AML-like disease. The scientists predict that combining this animal model with the power of RNAi will enable them to develop a more comprehensive scan of most of the potential leukemia-causing genetic culprits, which in turn will help drive the development of effective drug treatments.