Cancer / Oncology News

Georgetown Researchers Lead Discovery Expected To Significantly Change Biomedical Research

In a major step that could revolutionize biomedical research, scientists have discovered a way to keep normal cells as well as tumor cells taken from an individual cancer patient alive in the laboratory - which previously had not been possible. Normal cells usually die in the lab after dividing only a few times, and many common cancers will not grow, unaltered, outside of the body.

Tissue Structure Delays Cancer Development

Cancer growth normally follows a lengthy period of development. Over the course of time, genetic mutations often accumulate in cells, leading first to pre-cancerous conditions and ultimately to tumour growth. Using a mathematical model, scientists at the Max Planck Institute for Dynamics and Self-Organization in Göttingen, University of Pennsylvania and University of California San Francisco, have now shown that spatial tissue structure, such as that found in the colon, slows down the accumulation of genetic mutations, thereby delaying the onset of cancer. Their model could help in the assessment of tissue biopsies and improve predictions of the progression of certain cancer types.

Researchers Find Potential Target For Treating Metastatic Cancer

Finding ways to counteract or disrupt the invasive nature of cancer cells, called "metastasis," has been a long-term goal of cancer researchers. Now, researchers at Moffitt Cancer Center in Tampa, Fla., have identified an interactive pathway that regulates metastases in some cancers that may be vulnerable to chemical targeting in order to prevent cancer cell proliferation and tumor growth.

Ongoing collaboration by researchers in Moffitt's Departments of Tumor Biology and Drug Discovery has revealed the potential for combating metastatic disease by disrupting the interaction between the retinoblastoma tumor suppressor protein (Rb) and Raf-1 (a gene with a potential to cause cancer) with RRD-251, a selective, chemical disrupter of Rb-Raf-1 interaction.


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