Why EGFR drugs stop working in glioblastoma
Original title: Breaking adaptive oncogenic resistance in glioblastoma via targeting the EGFR-STAT3 axis.
How far along is this research?
- Lab cells
- Animals
- Review
- Tested in people
This looks across many earlier studies rather than running a new one.
This is a review of past research and an idea for future work, not a treatment people can get.
The short version
This paper looks at how glioblastoma: A glioma that is given grade 4. Grade 4 is the highest grade there is. The tumor grows fast. Treatment usually starts soon after it is found. It often means surgery, and then radiation and chemotherapy. See the glossary tumors get around drugs aimed at EGFR.
What was studied. This is a review of past research, not a new study. The authors looked at two signals inside glioblastoma: A glioma that is given grade 4. Grade 4 is the highest grade there is. The tumor grows fast. Treatment usually starts soon after it is found. It often means surgery, and then radiation and chemotherapy. See the glossary cells, called EGFR and STAT3.
What they found. Many glioblastoma: A glioma that is given grade 4. Grade 4 is the highest grade there is. The tumor grows fast. Treatment usually starts soon after it is found. It often means surgery, and then radiation and chemotherapy. See the glossary tumors have extra or changed EGFR. But trials of drugs aimed at EGFR have given poor results. The authors say a second signal, STAT3, stays switched on and keeps the tumor growing even when EGFR is blocked.
What this means, and what it doesn't
What it could mean: It may help explain why past EGFR drugs did not help much. It points researchers toward blocking both signals instead of one.
What it doesn't mean: This is not a new treatment, and it was not tested in people. It is one team's reading of past work plus an idea for what to try next. It is not a cure, and it does not change the care a doctor can offer today.
Source: PubMed, October 8, 2026 · Read the original
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