VEGF165b Inhibits Bevacizumab Treatment in Colorectal Cancer
Author Information
Author(s): Varey A H R, Rennel E S, Qiu Y, Bevan H S, Perrin R M, Raffy S, Dixon A R, Paraskeva C, Zaccheo O, Hassan A B, Harper S J, Bates D O
Primary Institution: University of Bristol
Hypothesis
The balance of pro- and antiangiogenic VEGF-A isoforms regulates tumor growth rates and affects the sensitivity of tumors to bevacizumab.
Conclusion
The study shows that VEGF165b expression can inhibit the effectiveness of bevacizumab treatment in colorectal cancer.
Supporting Evidence
- VEGF165b overexpression inhibited colon carcinoma growth in mouse models.
- Bevacizumab was effective against tumors expressing VEGF165 but not against those expressing VEGF165b.
- VEGF165b binds to bevacizumab with similar affinity as VEGF165.
Takeaway
This study found that a specific protein, VEGF165b, can stop a cancer treatment from working, which is important for understanding how to treat colon cancer better.
Methodology
The study used enzyme-linked immunosorbent assay, quantitative polymerase chain reaction, and mouse xenograft models to analyze VEGF isoform expression and tumor growth.
Potential Biases
Potential bias in sample selection and the interpretation of results based on the specific focus on VEGF isoforms.
Limitations
The study primarily focuses on a specific isoform of VEGF and its effects, which may not encompass all factors influencing colorectal cancer treatment outcomes.
Participant Demographics
Mean patient age was 71.5 years, with 62% male subjects.
Statistical Information
P-Value
p<0.01
Confidence Interval
95% CI
Statistical Significance
p<0.05
Digital Object Identifier (DOI)
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