Scott Lowe

Cancer Biology & Genetics

Cancer Researcher

Self Exam

  • Occupation: Research Scientist
  • Alternative career choice: Never thought about it
  • What do rock stars and scienctists have in common: Both try to make the world a better place by helping to improve the quality of lives.
  • Musical Instrument I Play: Guitar, trumpet
  • I tend to approach life: Head on, attending to each obstacle as it comes and focusing on the bigger picture.
  • Biggest misconceptions about me or my work: People think scientists are serious and boring, not true, we know how to have a good time. Many work hard and play hard.
  • Worst part-time job ever: None
  • Longest med school study session: Crash session for graduate school entrance exam
  • Best moment in medicine/research: Demonstrating that the p53 gene, which is inactivated through mutation in many cancers, normally can eliminate damaged cells through a process called apoptosis

About My Research

Disease Area: Cancer

Research Area: My laboratory is interested in understanding cancer genetics and biology, and through this identifying more effective ways to treat cancer

Science Impact/Accomplishments or Goal: Our work has contributed to the understanding of a broad class of genes called tumor suppressor genes whose action naturally suppresses the development of cancer.  We have identified tumor suppressor genes, shown what biological processes they participate in to prevent cancer, and shown how they can influence (or be exploited) to improve how cancers respond to treatment

Research Description: We use new genetic and genomic technologies to identify genes that cause and maintain cancer


“Scott Lowe, PhD, Geoffrey Beene Senior Chair, Chair Geoffrey Beene Cancer Research Center Executive Committee

Cancer arises through an evolutionary process whereby normal cells acquire mutations that erode growth controls, leading to the inappropriate expansion of aberrantly proliferating cells. Such mutations can involve activation of oncogenes or inactivation of tumor-suppressor genes, each contributing new capabilities to the developing cancer cell. However, cancer is not an inevitable consequence of oncogenic mutations; instead, cells acquiring such mutations can be eliminated or kept in check by innate tumor-­- suppressor programs that can be activated in these damaged cells.

Our laboratory studies tumor-suppressor networks controlling apoptosis and senescence and how their disruption influences malignant behavior. We previously showed that apoptosis and cellular senescence are potent barriers to oncogene-driven tumorigenesis and that each contributes to the antitumor action of many chemotherapeutic drugs. Thus, not only do mutations that disrupt apoptosis and senescence promote tumor progression, they can also reduce the efficacy of cancer therapy.

To facilitate our research, we are combining genetic and genomic tools that enable us to explore various aspects of cancer biology in a comprehensive way. We have recently developed mouse cancer models by genetically manipulating stem and progenitor cells ex vivo and then transplanting the altered cells into the appropriate organ of syngeneic recipient mice. This approach allows us to study the impact of many genes and gene combinations on tumorigenesis in a “mosaic” setting where tumor-initiating cells are embedded in normal tissues.

Furthermore, we have developed powerful methods for using RNA interference (RNAi) to suppress gene function in vivo in either a stable or reversible manner. Current efforts strive to integrate mosaic mouse models, RNA interference, and genomics to identify new components of these networks and characterize their impact on tumorigenesis and treatment response. In addition, we are developing new RNAi methods to explore the role of tumor suppressor genes in tumor maintenance, and cell death mechanisms involved in tumor regression. “