Xixi Zhang
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Previous Organizations / Institutes
The organizations / institutes from the scholar's other articles in the past ten years
Research Subjects
Xixi Zhang has a total of 30 co-authors. Here are the top co-authors by number of shared publications:
- Jason W. Pyrdol
Department of Cancer Immunology and Virology, Dana-Farber Cancer Institute, Boston, Massachusetts
104 shared publications - Kai W. Wucherpfennig
Department of Cancer Immunology and Virology, Dana-Farber Cancer Institute, Boston, MA, USA
104 shared publications - Deng Pan
Tsinghua-Peking Center for Life Sciences, Department of Basic Medical Sciences, Tsinghua University, Beijing, China
103 shared publications - John G. Doench
Genetic Perturbation Platform, Broad Institute, Cambridge, USA
103 shared publications - Oleksandr Kyrysyuk
Department of Cancer Immunology and Virology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA
103 shared publications - Tiffany Y. Juan
Department of Cancer Immunology and Virology, Dana-Farber Cancer Institute, Boston, Massachusetts
103 shared publications
Latest Publications
- 9 July 2026
- Published by American Association for the Advancement of Science (AAAS) in Science
- Vol. 393 (6807) , eaea1200
The CARM1 epigenetic enzyme inhibits cross-presenting dendritic cell function in cancer immunity
The cancer-immunity cycle requires cross-presenting type I conventional dendritic cells (cDC1s) that induce T cell–mediated immunity, but therapeutic strategies for enhancing intratumoral cDC1 function are currently inadequate. We found the epigenetic enzyme CARM1 (coactivator-associated arginine methyltransferase 1) to be a selective negative regulator of cancer antigen presentation by cDC1s but not cDC2s. Inactivation of the Carm1 gene promoted cDC1 antigen cross-presentation, activation, and accumulation in tumors, and a CARM1 inhibitor enhanced cDC1-mediated priming of T cells by means of a cancer neoantigen vaccine. CARM1 inhibition increased chromatin accessibility at BATF3-Jun and RelA sites that are critical for cDC1 function and activation. Transforming growth factor–β regulated Carm1 expression, which suggests that CARM1 inactivation enhanced intratumoral cDC1 function without altering cDC1 homeostasis. These studies identify CARM1 as a potential therapeutic target for enhancing the antitumor function of mouse and human cDC1s.
- 9 July 2026
- Published by American Association for the Advancement of Science (AAAS) in Science
- Vol. 393 (6807) , eaea1200
The CARM1 epigenetic enzyme inhibits cross-presenting dendritic cell function in cancer immunity
The cancer-immunity cycle requires cross-presenting type I conventional dendritic cells (cDC1s) that induce T cell–mediated immunity, but therapeutic strategies for enhancing intratumoral cDC1 function are currently inadequate. We found the epigenetic enzyme CARM1 (coactivator-associated arginine methyltransferase 1) to be a selective negative regulator of cancer antigen presentation by cDC1s but not cDC2s. Inactivation of the Carm1 gene promoted cDC1 antigen cross-presentation, activation, and accumulation in tumors, and a CARM1 inhibitor enhanced cDC1-mediated priming of T cells by means of a cancer neoantigen vaccine. CARM1 inhibition increased chromatin accessibility at BATF3-Jun and RelA sites that are critical for cDC1 function and activation. Transforming growth factor–β regulated Carm1 expression, which suggests that CARM1 inactivation enhanced intratumoral cDC1 function without altering cDC1 homeostasis. These studies identify CARM1 as a potential therapeutic target for enhancing the antitumor function of mouse and human cDC1s.
- Open Access
- 11 December 2025
- Published by American Association for Cancer Research (AACR)
Supplementary Fig. S7 from Addressing Tumor Heterogeneity by Sensitizing Resistant Cancer Cells to T cell–Secreted Cytokines
Supplementary Fig. S7 shows effect of PD-1 inhibition on treatment of tumors containing a B2m-/- population.
- 11 December 2025
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Fig. S7 from Addressing Tumor Heterogeneity by Sensitizing Resistant Cancer Cells to T cell–Secreted Cytokines
Supplementary Fig. S7 shows effect of PD-1 inhibition on treatment of tumors containing a B2m-/- population.
- Open Access
- 11 December 2025
- Published by American Association for Cancer Research (AACR)
Supplementary Fig. S8 from Addressing Tumor Heterogeneity by Sensitizing Resistant Cancer Cells to T cell–Secreted Cytokines
Supplementary Fig. S8 shows CD8 T cell-dependent control of tumors containing a B2m-/- population with inactivated Rnf31 and Atg5 genes.
- 11 December 2025
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Fig. S8 from Addressing Tumor Heterogeneity by Sensitizing Resistant Cancer Cells to T cell–Secreted Cytokines
Supplementary Fig. S8 shows CD8 T cell-dependent control of tumors containing a B2m-/- population with inactivated Rnf31 and Atg5 genes.
- Open Access
- 11 December 2025
- Published by American Association for Cancer Research (AACR)
Supplementary Fig. S3 from Addressing Tumor Heterogeneity by Sensitizing Resistant Cancer Cells to T cell–Secreted Cytokines
Supplementary Fig. S3 generation of tumor cell lines with multiple gene edits.
- 11 December 2025
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Fig. S3 from Addressing Tumor Heterogeneity by Sensitizing Resistant Cancer Cells to T cell–Secreted Cytokines
Supplementary Fig. S3 generation of tumor cell lines with multiple gene edits.
- Open Access
- 11 December 2025
- Published by American Association for Cancer Research (AACR)
Supplementary Fig. S5 from Addressing Tumor Heterogeneity by Sensitizing Resistant Cancer Cells to T cell–Secreted Cytokines
Supplementary Fig. S5 shows association of Atg5-KO and Rnf31/Atg5-dKO signatures with patient survival.
- 11 December 2025
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Fig. S5 from Addressing Tumor Heterogeneity by Sensitizing Resistant Cancer Cells to T cell–Secreted Cytokines
Supplementary Fig. S5 shows association of Atg5-KO and Rnf31/Atg5-dKO signatures with patient survival.
- Open Access
- 11 December 2025
- Published by American Association for Cancer Research (AACR)
Supplementary Fig. S10 from Addressing Tumor Heterogeneity by Sensitizing Resistant Cancer Cells to T cell–Secreted Cytokines
Supplementary Fig. S10 shows pharmacological sensitization to T cell cytokines in vitro and in vivo.
- 11 December 2025
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Fig. S10 from Addressing Tumor Heterogeneity by Sensitizing Resistant Cancer Cells to T cell–Secreted Cytokines
Supplementary Fig. S10 shows pharmacological sensitization to T cell cytokines in vitro and in vivo.
- Open Access
- 11 December 2025
- Published by American Association for Cancer Research (AACR)
Supplementary Fig. S6 from Addressing Tumor Heterogeneity by Sensitizing Resistant Cancer Cells to T cell–Secreted Cytokines
Supplementary Fig. S6 shows functional links between autophagy and cytokine signaling pathways.
- 11 December 2025
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Fig. S6 from Addressing Tumor Heterogeneity by Sensitizing Resistant Cancer Cells to T cell–Secreted Cytokines
Supplementary Fig. S6 shows functional links between autophagy and cytokine signaling pathways.
- Open Access
- 11 December 2025
- Published by American Association for Cancer Research (AACR)
Supplementary Fig. S11 from Addressing Tumor Heterogeneity by Sensitizing Resistant Cancer Cells to T cell–Secreted Cytokines
Supplementary Fig. S11 shows pharmacological sensitization of human melanoma cell line to T cell cytokines.
- 11 December 2025
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Fig. S11 from Addressing Tumor Heterogeneity by Sensitizing Resistant Cancer Cells to T cell–Secreted Cytokines
Supplementary Fig. S11 shows pharmacological sensitization of human melanoma cell line to T cell cytokines.
- Open Access
- 11 December 2025
- Published by American Association for Cancer Research (AACR)
Supplementary Fig. S4 from Addressing Tumor Heterogeneity by Sensitizing Resistant Cancer Cells to T cell–Secreted Cytokines
Supplementary Fig. S4 shows differentially expressed genes revealed by RNA-seq analysis.
- 11 December 2025
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Fig. S4 from Addressing Tumor Heterogeneity by Sensitizing Resistant Cancer Cells to T cell–Secreted Cytokines
Supplementary Fig. S4 shows differentially expressed genes revealed by RNA-seq analysis.
- Open Access
- 11 December 2025
- Published by American Association for Cancer Research (AACR)
Table S1 from Addressing Tumor Heterogeneity by Sensitizing Resistant Cancer Cells to T cell–Secreted Cytokines
Supplementary Table S1: # Raw count of the genome-wide CRISPR screen for identifying T cell-mediated tumor killing in B2m-deficient cells. # MAGeCK results (Gene summary) for the genome-wide CRISPR screen from the B2m-deficient cells. # Gene log2FC in CRISPR screens from B2m-WT cells and B2m-KO cells. ## Common regulators of T cell mediated tumor killing in both B2m-WT and B2m-KO cells
- 11 December 2025
- Published by American Association for Cancer Research (AACR)
Open AccessTable S1 from Addressing Tumor Heterogeneity by Sensitizing Resistant Cancer Cells to T cell–Secreted Cytokines
Supplementary Table S1: # Raw count of the genome-wide CRISPR screen for identifying T cell-mediated tumor killing in B2m-deficient cells. # MAGeCK results (Gene summary) for the genome-wide CRISPR screen from the B2m-deficient cells. # Gene log2FC in CRISPR screens from B2m-WT cells and B2m-KO cells. ## Common regulators of T cell mediated tumor killing in both B2m-WT and B2m-KO cells