Cancer treatments were designed to keep cancer cells at bay by preventing their growth, survival, and spread throughout the body. However, even today there are many cancers that, for some reason, support the action of the drugs used, managing to spread without remedy in many patients. Why can’t these drugs stop some cancers?
The epidermal growth factor receptor (EGFR) is the cellular receptor whose mutations that affect EGFR expression or activity can lead to cancer . Starting from this premise, Xiaojun Tan, a student at the University of Wisconsin-Madison (USA), has found the solution while investigating the places where this receptor can be found: he discovered that cancer evades the action of drugs by infiltration through a back door of cells . “What we see here is quite different. It is an alternative strategy to promote the survival of cancer cells, ”explains Tan.
Cancer cells are therefore able to thrive, breaking through before the onslaught of drugs. “Hundreds of thousands of patients each year have EGFR-related tumors. This discovery has implications for millions of cancer patients around the world ”, clarifies Richard A. Anderson, leader of the study.
The researchers explain that, just as healthy cells use “autophagy” as a means of “tightening their belts” when resources are scarce, cancer cells also use it to survive under stress conditions , that is, when a drug threatens their survival. The excess of the inactive EGFR receptor helps cancer cells to locate within healthy cells where autophagy begins, also triggering a series of cellular changes that promote the survival of cancer cells.
The study results, which have been published in the journal Cell , suggest that to stop cancer, original drugs developed to inactivate the EGFR receptor could be combined with drugs that block autophagy of cancer cells to seal both the front and back doors. and prevent these from developing in any way possible.
