American Association for Cancer Research
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Supplemental Tables S1-S3 from VEGF-A Expression Correlates with TP53 Mutations in Non–Small Cell Lung Cancer: Implications for Antiangiogenesis Therapy

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journal contribution
posted on 2023-03-30, 23:31 authored by Maria Schwaederlé, Vladimir Lazar, Pierre Validire, Johan Hansson, Ludovic Lacroix, Jean-Charles Soria, Yudi Pawitan, Razelle Kurzrock

Supplemental Tables S1-S3. Number/Frequency of mutations in 123 patients with lung cancer (S1); List of genes used in transcriptomic analysis (S2); Expression levels of VEGF-A in mutated (M) vs. wild-type (WT) TP53 lung cancer by histology (S3).



Bevacizumab is one of the most widely used antiangiogenic drugs in oncology, but the overall beneficial effects of this VEGF-A targeting agent are relatively modest, in part due to the lack of a biomarker to select patients most likely to respond favorably. Several molecular aberrations in cancer influence angiogenesis, including mutations in the tumor suppressor gene TP53, which occur frequently in many human malignancies. In this study, we present a multiple regression analysis of transcriptomic data in 123 patients with non–small cell lung cancer (NSCLC) showing that TP53 mutations are associated with higher VEGF-A expression (P = 0.006). This association was interesting given a recent retrospective study showing longer progression-free survival in patients with diverse tumors who receive bevacizumab, if tumors harbor mutant TP53 instead of wild-type TP53. Thus, our current findings linking TP53 mutation with VEGF-A upregulation offered a mechanistic explanation for why patients exhibit improved outcomes after bevacizumab treatment when their tumors harbor mutant TP53 versus wild-type TP53. Overall, this work warrants further evaluation of TP53 as a ready biomarker to predict bevacizumab response in NSCLC and possibly other tumor types. Cancer Res; 75(7); 1187–90. ©2015 AACR.

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