Association of Expression Levels or Activation Status of STAT3 with Treatment Outcomes of Sunitinib in Patients with Renal Cell Carcinoma

Yamamoto, Kazuhiro; Hara, Takuji; Nakagawa, Tsutomu; Hirai, Midori; Fujisawa, Masato; Yano, Ikuko

doi:10.1007/s11523-018-0563-4

Cited by 6 publications

(1 citation statement)

References 33 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Fortunately, growing evidence has demonstrated that angiogenesis-directed treatment can reverse this suppressive effect ( 53 ), and the knockdown of VEGFR-1 can decrease the frequency of the suppressors in RCC ( 54 ). Likewise, Yamamoto et al ( 55 ) and Guislain et al ( 56 ) showed that sunitinib could reduce MDSC accumulation in the tumor compartment and improve the suppressive TME through blocking the signal transducer and activator of transcription 3 (STAT3) signaling pathways, thus increasing the apoptotic rate of MDSCs in mice. Coincidently, sunitinib could decrease the frequency of Tregs both in the TME and the whole body subsequently to the first cycle of treatment.…”

Section: Conversation Between Targeted Therapy and The Immune Tumor Mmentioning

confidence: 99%

RCC Immune Microenvironment Subsequent to Targeted Therapy: A Friend or a Foe?

2020

View full text Add to dashboard Cite

Renal cell carcinoma (RCC) is composed of different subtypes with distinct molecular and histological tumor heterogeneity. Although the advent of various targeted therapies has improved the survival of patients with advanced RCC over the past 15 years (since 2006), few cases experienced complete response due to drug resistance. Recent studies have demonstrated that the outcomes following targeted therapies are potentially associated with intricate cross-links between immune responses and suppressors in the tumor microenvironment (TME). In addition, progress on drug research and development enhances our awareness and understanding about immunotherapy and combined treatment. In this review article, we intend to make a comprehensive summary about TME and its alterations following targeted therapies, provide valid evidence in this aspect, and discuss optimal matches between targeted therapy and immunotherapy.

show abstract