A Cause Of Resistance To Colon Cancer Treatment Identified
Doctors and researchers of Hospital del Mar and its research institute, the IMIM, have lead a study describing a new pharmacological resistance to cancer. This new mechanism is a mutation in an oncogene called EGFR (epidermal growth factor receptor) causing resistance to treatment using a drug called cetuximab, a monoclonal antibody which specifically attacks the EGFR. The study proves that, both in lab models and in patients with colon cancer, this mutation appears during the disease and that, when this happens, it stops the drug from being effective and the tumor grows.
Improved Understanding Of Specific Molecular Mechanisms At Work During Cell Stress May Help Create New Therapeutic Approaches To Cancer
The expression of p53 and Mdm2 is closely related. In an article published this week in the Cancer Cell review, Robin Fahraeus and his collaborators from Inserm Unit 940 ("Therapeutic Targets for Cancer"), demonstrate that cellular response to DNA damage requires involvement from the protein kinase ATM so that Mdm2 can positively or negatively control protein p53. Much focus is placed on protein p53 in cancer research. Discovered in 1979, p53 precisely regulates cell proliferation and triggers cell distribution or programmed natural cell death (apoptosis) in accordance with requirements.
In Cancer Metastasis, DGK-Alpha Helps Cancer Cells Gain Traction And Mobilize
Metastasizing cancer cells often express integrins that provide better traction. A new study in The Journal of Cell Biology reveals how a lipid-converting enzyme helps the cells mobilize these integrins. Adhesive integrin proteins continually cycle to and from the cell surface. Invasive cancer cells that carry mutant forms of the tumor suppressor p53 often bias the process, increasing the recycling of a particular integrin that offers a better grip on the fibronectin fibers found in tumors. To make this change, mutant p53 requires the Rab-coupling protein (RCP), which connects the integrins to the Rab GTPases that promote membrane recycling.