PT  - JOURNAL ARTICLE
AU  - YOHEI SEKINO
AU  - KENSHIRO TAKEMOTO
AU  - DAIKI MURATA
AU  - TAKASHI BABASAKI
AU  - KOHEI KOBATAKE
AU  - HIROYUKI KITANO
AU  - KENICHIRO IKEDA
AU  - KEISUKE GOTO
AU  - SHOGO INOUE
AU  - TETSUTARO HAYASHI
AU  - DAIKI TANIYAMA
AU  - MASANOBU SHIGETA
AU  - KAZUYA KURAOKA
AU  - KOJI MITA
AU  - MAYUMI KANEKO
AU  - KAZUHIRO SENTANI
AU  - NAOHIDE OUE
AU  - JUN TEISHIMA
TI  - P53 Is Involved in Sunitinib Resistance and Poor Progression-free Survival After Sunitinib Treatment of Renal Cell Carcinoma
AID  - 10.21873/anticanres.15233
DP  - 2021 Sep 01
TA  - Anticancer Research
PG  - 4287--4294
VI  - 41
IP  - 9
4099  - http://ar.iiarjournals.org/content/41/9/4287.short
4100  - http://ar.iiarjournals.org/content/41/9/4287.full
SO  - Anticancer Res2021 Sep 01; 41
AB  - Background/Aim: Sunitinib continues to be administered as a first-line therapeutic agent in metastatic renal cell carcinoma (mRCC). This study examined the potential role of p53 in sunitinib resistance and as a predictive marker in mRCC. Materials and Methods: We analysed the effects of p53 knockout on sunitinib resistance. p53 expression in 53 mRCC patients receiving first-line sunitinib was determined immunohistochemically. We performed in silico analysis to examine the predictive value of p53 in mRCC. Results: WST-1 assays showed that p53 knockout decreased sensitivity to sunitinib. Sunitinib and nutlin-3 together suppressed cell growth. Immunohistochemistry revealed 11 p53-positive cases among 53 patients with mRCC. Kaplan–Meier analysis showed that p53-positive cases tended to be associated with poor progression-free survival (PFS) after first-line sunitinib treatment. In the JAVELIN 101 study, TP53 mutation was significantly associated with poor PFS after sunitinib treatment. Conclusion: p53 may be involved in sunitinib resistance and represent a valuable marker for sunitinib treatment in mRCC.