News and Events BMDCR
Huggins Lecture Series
Saturdays, January 15 through March 5, 2005
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Despite significant advances in our understanding of tumor formation and growth, the formation of metastases (the spread of cancer cells to other organs) remains the lethal aspect of cancer. For the majority of tumors, presence of clinically detectable metastases is the hallmark of incurable disease. The process of metastasis is a complex and multi-step process where a cancer cell leaves the tumor, survives transport in the circulation, and establishes a secondary tumor in another organ, such as the liver, brain, or bone.
Metastasis research has recently shown that a critical step in the development of metastatic disease is the growth of disseminated cancer cells at the secondary site, or "metastatic colonization." Metastasis suppressor genes are a family of genes that block the ability of a tumor to spread, and these genes can serve as important markers for predicting cancer recurrence and the development of metastases. Moreover, metastasis suppressor genes have the potential to become effective targets for anti-metastatic therapy.
The work conducted in the laboratory of Dr. Carrie Rinker-Schaeffer focuses on the metastasis suppressor gene MAP Kinase Kinase 4, or MKK4. Our lab identified MKK4 as a metastasis suppressor gene and showed that it has an important role in prostate and ovarian cancer. MKK4 is an important gene in cellular stress signaling and cell proliferation and survival. My thesis work was aimed at identifying the mechanism by which MKK4 suppressed metastasis using a mouse model of prostate cancer.
| The Problem, The Prostate, and The Man | January 15, 2005 |
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| What is Cancer? | January 22, 2005 |
| The Cause of Prostate Cancer | January 29, 2005 |
| Diagnosing Prostate Cancer | February 5, 2005 |
| Treating Prostate Cancer | February 12, 2005 |
| Prostate Cancer Metastasis | February 19, 2005 |
| Hormones and Prostate Cancer | February 26, 2005 |
| Emerging and Novel Treatment Techniques - Hope for the Future |
March 5, 2005 |