PRESENTATION TITLE

Mechanisms of Malignant Progression

PRESENTER(S)

Robert A. Weinberg, Ph.D.

VIEWING LOCATIONS
Zoom Registration Link

LEARNING OBJECTIVES

• Demonstrate the role of epigenetics in malignant progression.
• Describe the role of tissue microenvironment in promoting progression.
• Review the EMT:  Cell-biological program.

PRESENTERS BIO

Robert A. Weinberg, Ph.D., received both his undergraduate- and graduate-level education in the Department of Biology of the Massachusetts Institute of Technology (MIT) in the years 1960 to 1969. After post-doctoral stays at The Weizmann Institute in Israel and the Salk Institute in California, he was asked to return to MIT where he assumed a faculty-level position in 1974. He has continued as a member of the MIT Department of Biology since that time with the additional association with the affiliated Whitehead Institute for Biomedical Research since 1982.

His research has been focused over the past four decades on the molecular and biochemical determinants of neoplastic cell transformation and led to the discovery of the first functionally validated human oncogene (Ras) in 1979-81 and the isolation of the first validated tumor suppressor gene, RB, in 1986. This work led in subsequent years to the first experimental transformation of normal human cells into neoplastic cells in 1999. Since 2004, his group has been increasingly focused on the mechanisms by which the cell-biological program termed the epithelial-mesenchymal transition (EMT) confers on carcinoma cells many of the traits that are required for invasion and metastasis formation. Among other discoveries, they demonstrated in 2008 that the EMT program can create de novo carcinoma cells with the properties of cancer stem cells.

In recent years, the overlap between the EMT program and cancer stemness has been explored in greater detail, leading to the discovery in 2015 that activation of a previously latent EMT program enables both normal and neoplastic epithelial cells to enter a stem-cell like state through distinct mechanisms. Most recently (2022), the lab has also identified distinct, intermediate cancer cell-states within the E-M spectrum that have different metastatic capabilities, underscoring the importance of cellular plasticity during cancer progression. Intriguingly, the lab has also recently discovered that the residence of cancer cells within different parts of the E-M spectrum influence their ability to differentially dictate their immune microenvironment and response to immune checkpoint blockade therapy while also making them differentially vulnerable to an iron-dependent form of cell death, known as ferroptosis. The lab is also actively exploring the molecular mechanisms underlying these phenomena.

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TRANSCRIPT
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