Dilong Yu
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Research Subjects
Dilong Yu has a total of 12 co-authors. Here are the top co-authors by number of shared publications:
- Chuanming Zheng
Zhejiang Provincial People’s Hospital 1 Otolaryngology & Head and Neck Center, Cancer Center, Department of Head and Neck Surgery Affiliated People’s Hospital, Hangzhou Medical College, Hangzhou, China
15 shared publications - Jiafeng Wang
Zhejiang Key Laboratory of Precision Medicine Research on Head & Neck Cancer, Hangzhou, 310014, China; Zhejiang Provincial Clinical Research Center for Malignant Tumor, Hangzhou, 310014, China; Key Laboratory for Cancer Prevention and Treatment of Guizhou Province, Bijie, 551700, China; Otolaryngology & Head and Neck Center, Cancer Center, Department of Head and Neck Surgery, Zhejiang Provincial People's Hospital (Affiliated People's Hospital), Hangzhou Medical College, Hangzhou, 310014, China
15 shared publications - Jiajie Xu
Otolaryngology & Head and Neck Center, Cancer Center, Department of Head and Neck Surgery, Zhejiang Provincial People's Hospital (Affiliated People's Hospital), Hangzhou Medical College, Hangzhou 310014, China.
15 shared publications - Liehao Jiang
Zhejiang Provincial People’s Hospital 1 Otolaryngology & Head and Neck Center, Cancer Center, Department of Head and Neck Surgery Affiliated People’s Hospital, Hangzhou Medical College, Hangzhou, China
15 shared publications - Minghua Ge
Otolaryngology & Head and Neck Center, Cancer Center, Department of Head and Neck Surgery, Zhejiang Provincial People’s Hospital (Affiliated People’s Hospital), Hangzhou Medical College, Hangzhou, China
15 shared publications - Ping Huang
Center for Clinical Pharmacy, Cancer Center, Department of Pharmacy, Zhejiang Provincial People’s Hospital (Affiliated People’s Hospital), Hangzhou Medical College, Hangzhou 310014, China
15 shared publications
Latest Publications
- Open Access
- 17 June 2026
- Published by American Association for Cancer Research (AACR)
Figure S1 from Androgen Receptor Signaling Induces CD8+ T-cell Dysfunction That Is Reversed by Androgen Deprivation Therapy in Male Head and Neck Squamous Cell Carcinoma
Sex differences in clinical features of HNSCC; Related to Fig. 1.
- 17 June 2026
- Published by American Association for Cancer Research (AACR)
Open AccessFigure S1 from Androgen Receptor Signaling Induces CD8+ T-cell Dysfunction That Is Reversed by Androgen Deprivation Therapy in Male Head and Neck Squamous Cell Carcinoma
Sex differences in clinical features of HNSCC; Related to Fig. 1.
- Open Access
- 17 June 2026
- Published by American Association for Cancer Research (AACR)
Data from Androgen Receptor Signaling Induces CD8+ T-cell Dysfunction That Is Reversed by Androgen Deprivation Therapy in Male Head and Neck Squamous Cell Carcinoma
Head and neck squamous cell carcinoma (HNSCC) exhibits a distinct sex disparity in incidence, with a higher incidence in males than in females. Recent studies have suggested that this difference persists even after accounting for smoking and alcohol use, highlighting the need to elucidate the underlying biological mechanisms. In this study, we demonstrated that sex differences in HNSCC are androgen dependent and identified androgen receptor (AR) signaling as a key regulator of the tumor immune microenvironment by modulating CD8+ T-cell differentiation and function. Mechanically, early growth response 4 functioned as a direct downstream transcriptional effector of AR that induced CD8+ T-cell dysfunction. Clinically, androgen deprivation therapy (ADT) was an effective therapeutic strategy in HNSCC, suppressing tumor growth in mice while improving intratumoral CD8+ T-cell function. Moreover, combining ADT with immune checkpoint inhibitors led to improved antitumor efficacy. Together, these findings reveal ADT as a promising therapeutic approach to enhance the antitumor activity of sex-biased CD8+ T cells in HNSCC, which could inform the development of sex-biased immunotherapies for treating patients with HNSCC.Significance:Androgen receptor engenders a sex-biased tumor microenvironment in head and neck cancer by suppressing CD8+ T-cell function, which can be overcome with androgen deprivation therapy to delay tumor progression.
- 17 June 2026
- Published by American Association for Cancer Research (AACR)
Open AccessData from Androgen Receptor Signaling Induces CD8+ T-cell Dysfunction That Is Reversed by Androgen Deprivation Therapy in Male Head and Neck Squamous Cell Carcinoma
Head and neck squamous cell carcinoma (HNSCC) exhibits a distinct sex disparity in incidence, with a higher incidence in males than in females. Recent studies have suggested that this difference persists even after accounting for smoking and alcohol use, highlighting the need to elucidate the underlying biological mechanisms. In this study, we demonstrated that sex differences in HNSCC are androgen dependent and identified androgen receptor (AR) signaling as a key regulator of the tumor immune microenvironment by modulating CD8+ T-cell differentiation and function. Mechanically, early growth response 4 functioned as a direct downstream transcriptional effector of AR that induced CD8+ T-cell dysfunction. Clinically, androgen deprivation therapy (ADT) was an effective therapeutic strategy in HNSCC, suppressing tumor growth in mice while improving intratumoral CD8+ T-cell function. Moreover, combining ADT with immune checkpoint inhibitors led to improved antitumor efficacy. Together, these findings reveal ADT as a promising therapeutic approach to enhance the antitumor activity of sex-biased CD8+ T cells in HNSCC, which could inform the development of sex-biased immunotherapies for treating patients with HNSCC.Significance:Androgen receptor engenders a sex-biased tumor microenvironment in head and neck cancer by suppressing CD8+ T-cell function, which can be overcome with androgen deprivation therapy to delay tumor progression.
- Open Access
- 17 June 2026
- Published by American Association for Cancer Research (AACR)
Figure S9 from Androgen Receptor Signaling Induces CD8+ T-cell Dysfunction That Is Reversed by Androgen Deprivation Therapy in Male Head and Neck Squamous Cell Carcinoma
Transcriptomic changes and pathway enrichment analysis following flutamide treatment; Related to Fig.6.
- 17 June 2026
- Published by American Association for Cancer Research (AACR)
Open AccessFigure S9 from Androgen Receptor Signaling Induces CD8+ T-cell Dysfunction That Is Reversed by Androgen Deprivation Therapy in Male Head and Neck Squamous Cell Carcinoma
Transcriptomic changes and pathway enrichment analysis following flutamide treatment; Related to Fig.6.
- Open Access
- 17 June 2026
- Published by American Association for Cancer Research (AACR)
Table S1 from Androgen Receptor Signaling Induces CD8+ T-cell Dysfunction That Is Reversed by Androgen Deprivation Therapy in Male Head and Neck Squamous Cell Carcinoma
The antibodies used in this article.
- 17 June 2026
- Published by American Association for Cancer Research (AACR)
Open AccessTable S1 from Androgen Receptor Signaling Induces CD8+ T-cell Dysfunction That Is Reversed by Androgen Deprivation Therapy in Male Head and Neck Squamous Cell Carcinoma
The antibodies used in this article.
- Open Access
- 17 June 2026
- Published by American Association for Cancer Research (AACR)
Figure S7 from Androgen Receptor Signaling Induces CD8+ T-cell Dysfunction That Is Reversed by Androgen Deprivation Therapy in Male Head and Neck Squamous Cell Carcinoma
Effects of enzalutamide and degarelix on tumor progression and tumor-infiltrating CD8⁺ T cell responses; Related to Fig. 3.
- 17 June 2026
- Published by American Association for Cancer Research (AACR)
Open AccessFigure S7 from Androgen Receptor Signaling Induces CD8+ T-cell Dysfunction That Is Reversed by Androgen Deprivation Therapy in Male Head and Neck Squamous Cell Carcinoma
Effects of enzalutamide and degarelix on tumor progression and tumor-infiltrating CD8⁺ T cell responses; Related to Fig. 3.
- Open Access
- 17 June 2026
- Published by American Association for Cancer Research (AACR)
Table S2 from Androgen Receptor Signaling Induces CD8+ T-cell Dysfunction That Is Reversed by Androgen Deprivation Therapy in Male Head and Neck Squamous Cell Carcinoma
The information about HNSCC patients in this article.
- 17 June 2026
- Published by American Association for Cancer Research (AACR)
Open AccessTable S2 from Androgen Receptor Signaling Induces CD8+ T-cell Dysfunction That Is Reversed by Androgen Deprivation Therapy in Male Head and Neck Squamous Cell Carcinoma
The information about HNSCC patients in this article.
- Open Access
- 17 June 2026
- Published by American Association for Cancer Research (AACR)
Figure S5 from Androgen Receptor Signaling Induces CD8+ T-cell Dysfunction That Is Reversed by Androgen Deprivation Therapy in Male Head and Neck Squamous Cell Carcinoma
Hormone receptor profiling and AR-associated functional regulation of tumor-infiltrating CD8⁺ T cells in HNSCC; Related to Fig.2.
- 17 June 2026
- Published by American Association for Cancer Research (AACR)
Open AccessFigure S5 from Androgen Receptor Signaling Induces CD8+ T-cell Dysfunction That Is Reversed by Androgen Deprivation Therapy in Male Head and Neck Squamous Cell Carcinoma
Hormone receptor profiling and AR-associated functional regulation of tumor-infiltrating CD8⁺ T cells in HNSCC; Related to Fig.2.
- Open Access
- 17 June 2026
- Published by American Association for Cancer Research (AACR)
Figure S2 from Androgen Receptor Signaling Induces CD8+ T-cell Dysfunction That Is Reversed by Androgen Deprivation Therapy in Male Head and Neck Squamous Cell Carcinoma
The effect of tumor immune microenvironment on sex-biased HNSCC; Related to Fig. 1.
- 17 June 2026
- Published by American Association for Cancer Research (AACR)
Open AccessFigure S2 from Androgen Receptor Signaling Induces CD8+ T-cell Dysfunction That Is Reversed by Androgen Deprivation Therapy in Male Head and Neck Squamous Cell Carcinoma
The effect of tumor immune microenvironment on sex-biased HNSCC; Related to Fig. 1.
- Open Access
- 17 June 2026
- Published by American Association for Cancer Research (AACR)
Figure S3 from Androgen Receptor Signaling Induces CD8+ T-cell Dysfunction That Is Reversed by Androgen Deprivation Therapy in Male Head and Neck Squamous Cell Carcinoma
Sex differences in tumor growth and CD8+ T cell infiltration in murine models; Related to Fig.1.
- 17 June 2026
- Published by American Association for Cancer Research (AACR)
Open AccessFigure S3 from Androgen Receptor Signaling Induces CD8+ T-cell Dysfunction That Is Reversed by Androgen Deprivation Therapy in Male Head and Neck Squamous Cell Carcinoma
Sex differences in tumor growth and CD8+ T cell infiltration in murine models; Related to Fig.1.
- Open Access
- 17 June 2026
- Published by American Association for Cancer Research (AACR)
Figure S6 from Androgen Receptor Signaling Induces CD8+ T-cell Dysfunction That Is Reversed by Androgen Deprivation Therapy in Male Head and Neck Squamous Cell Carcinoma
Androgen targeted therapies modulate CD8+ T cell immune landscape; Related to Fig.3.
- 17 June 2026
- Published by American Association for Cancer Research (AACR)
Open AccessFigure S6 from Androgen Receptor Signaling Induces CD8+ T-cell Dysfunction That Is Reversed by Androgen Deprivation Therapy in Male Head and Neck Squamous Cell Carcinoma
Androgen targeted therapies modulate CD8+ T cell immune landscape; Related to Fig.3.