Final answer:
Cancer cells with elevated EGFR levels will have an increased sensitivity to EGF, leading to more binding and a stronger affinity, thereby promoting excessive cell growth. Blocking the EGF-EGFR interaction could interfere with cancer cell proliferation by halting the pathway promoting division and growth.
Step-by-step explanation:
Many cancer cells have elevated levels of the EGF receptor (EGFR), which means that they will respond to lower levels of EGF, and as a result, they may bind much more EGF and bind EGF with higher affinity. This overexpression of EGFR leads to an increased sensitivity to the epidermal growth factor, thereby triggering the signaling pathways that promote cell division and growth more frequently than in normal cells. Therefore, cancer cells can thrive even with minimal amounts of growth factors present.
EGFR is a receptor tyrosine kinase involved in many cellular processes, including cell growth, wound healing, and tissue repair. When EGF binds to the EGFR, it activates a cascade of downstream phosphorylation events, leading to cell growth and division. However, the inappropriate activation of EGFR, such as in cancer cells, can result in uncontrolled cell growth and division, contributing to the proliferation of cancer.
In relation to blocking the EGF-EGFR interaction in cancer therapy, a chemical that inhibits the binding of EGF to EGFR would block the EGFR pathway, thus potentially interfering with the replication of cancerous cells that overexpress EGFR.