Maxime Dhainaut
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
Maxime Dhainaut has a total of 136 co-authors. Here are the top co-authors by number of shared publications:
- Alice Oliffson Kamphorst
Marc and Jennifer Lipschultz Precision Immunology Institute, ISMMS, NY, NY, USA
22 shared publications - Amaia Lujambio
Department of Oncological Sciences, Icahn School of Medicine at Mount Sinai, New York, USA
22 shared publications - Marina Ruiz de Galarreta
Department of Oncological Sciences, Icahn School of Medicine at Mount Sinai, New York, USA
22 shared publications - Katherine E. Lindblad
Marc and Jennifer Lipschultz Precision Immunology Institute, ISMMS, NY, NY, USA
21 shared publications - Alexander M. Tsankov
Icahn School of Medicine at Mount Sinai
12 shared publications - Anthony Lozano
Marc and Jennifer Lipschultz Precision Immunology Institute, ISMMS, NY, NY, USA
12 shared publications
Latest Publications
- Open Access
- 17 June 2026
- Published by American Association for Cancer Research (AACR)
Supplementary Figure S1 from NOTCH1 Drives Sexually Dimorphic Immune Responses in Hepatocellular Carcinoma
Sex-dependent immune responses in NOTCH1-driven liver tumors
- 17 June 2026
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Figure S1 from NOTCH1 Drives Sexually Dimorphic Immune Responses in Hepatocellular Carcinoma
Sex-dependent immune responses in NOTCH1-driven liver tumors
- Open Access
- 17 June 2026
- Published by American Association for Cancer Research (AACR)
Supplementary Figure S3 from NOTCH1 Drives Sexually Dimorphic Immune Responses in Hepatocellular Carcinoma
NOTCH1-driven tumors in females lead to impaired CD8+ T cell priming and activation
- 17 June 2026
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Figure S3 from NOTCH1 Drives Sexually Dimorphic Immune Responses in Hepatocellular Carcinoma
NOTCH1-driven tumors in females lead to impaired CD8+ T cell priming and activation
- Open Access
- 17 June 2026
- Published by American Association for Cancer Research (AACR)
Supplementary Figure S2 from NOTCH1 Drives Sexually Dimorphic Immune Responses in Hepatocellular Carcinoma
Mechanism of immune surveillance in males with NOTCH1 liver tumors
- 17 June 2026
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Figure S2 from NOTCH1 Drives Sexually Dimorphic Immune Responses in Hepatocellular Carcinoma
Mechanism of immune surveillance in males with NOTCH1 liver tumors
- Open Access
- 17 June 2026
- Published by American Association for Cancer Research (AACR)
Supplementary Data from NOTCH1 Drives Sexually Dimorphic Immune Responses in Hepatocellular Carcinoma
- 17 June 2026
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Data from NOTCH1 Drives Sexually Dimorphic Immune Responses in Hepatocellular Carcinoma
- Open Access
- 17 June 2026
- Published by American Association for Cancer Research (AACR)
Supplementary Figure S4 from NOTCH1 Drives Sexually Dimorphic Immune Responses in Hepatocellular Carcinoma
Enhancing DC-T cell axis in females harboring NOTCH1-driven tumors has therapeutic effects
- 17 June 2026
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Figure S4 from NOTCH1 Drives Sexually Dimorphic Immune Responses in Hepatocellular Carcinoma
Enhancing DC-T cell axis in females harboring NOTCH1-driven tumors has therapeutic effects
- Open Access
- 17 June 2026
- Published by American Association for Cancer Research (AACR)
Data from NOTCH1 Drives Sexually Dimorphic Immune Responses in Hepatocellular Carcinoma
Hepatocellular carcinoma presents strong sexual dimorphism, being two to three times more frequent in males than in females; however, the role of sex in response to immunotherapies in HCC remains unknown. We demonstrate that NOTCH1, an understudied oncogene in HCC, elicits sexually dimorphic antitumor immunity and response to FDA-approved immunotherapies. Surprisingly, males harboring NOTCH1-driven tumors displayed enhanced antitumor immune responses, which, in mice, were mediated by dendritic and T cells. Conversely, females harboring NOTCH1-driven tumors presented immune evasion and resistance to immunotherapies through a defect in dendritic cell (DC)–mediated priming and activation of CD8+ T cells in mice, which was restored therapeutically with CD40 agonism. Mechanistically, the sexually dimorphic immunity was mediated by genes in the sex chromosomes but not by sex hormones. Together, our study unravels an unexpected association between NOTCH1 and sex in cancer immunity and highlights the potential of restoring the DC−CD8+ T-cell axis with CD40 agonism to improve outcomes.Significance:Although HCC presents strong sexual dimorphism, the role of sex in response to immunotherapies remains elusive. With a novel HCC mouse model and validation in patients with HCC, we demonstrate that NOTCH1 disrupts antitumor immunity specifically in females through a mechanism mediated by sex chromosome genes, which is reversed with CD40 agonism.See related commentary by Zhu and Koltsova, p. 452
- 17 June 2026
- Published by American Association for Cancer Research (AACR)
Open AccessData from NOTCH1 Drives Sexually Dimorphic Immune Responses in Hepatocellular Carcinoma
Hepatocellular carcinoma presents strong sexual dimorphism, being two to three times more frequent in males than in females; however, the role of sex in response to immunotherapies in HCC remains unknown. We demonstrate that NOTCH1, an understudied oncogene in HCC, elicits sexually dimorphic antitumor immunity and response to FDA-approved immunotherapies. Surprisingly, males harboring NOTCH1-driven tumors displayed enhanced antitumor immune responses, which, in mice, were mediated by dendritic and T cells. Conversely, females harboring NOTCH1-driven tumors presented immune evasion and resistance to immunotherapies through a defect in dendritic cell (DC)–mediated priming and activation of CD8+ T cells in mice, which was restored therapeutically with CD40 agonism. Mechanistically, the sexually dimorphic immunity was mediated by genes in the sex chromosomes but not by sex hormones. Together, our study unravels an unexpected association between NOTCH1 and sex in cancer immunity and highlights the potential of restoring the DC−CD8+ T-cell axis with CD40 agonism to improve outcomes.Significance:Although HCC presents strong sexual dimorphism, the role of sex in response to immunotherapies remains elusive. With a novel HCC mouse model and validation in patients with HCC, we demonstrate that NOTCH1 disrupts antitumor immunity specifically in females through a mechanism mediated by sex chromosome genes, which is reversed with CD40 agonism.See related commentary by Zhu and Koltsova, p. 452
- Open Access
- 3 March 2025
- Published by American Association for Cancer Research (AACR)
Supplementary Figure S1 from NOTCH1 Drives Sexually Dimorphic Immune Responses in Hepatocellular Carcinoma
Sex-dependent immune responses in NOTCH1-driven liver tumors
- 3 March 2025
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Figure S1 from NOTCH1 Drives Sexually Dimorphic Immune Responses in Hepatocellular Carcinoma
Sex-dependent immune responses in NOTCH1-driven liver tumors
- Open Access
- 3 March 2025
- Published by American Association for Cancer Research (AACR)
Supplementary Data from NOTCH1 Drives Sexually Dimorphic Immune Responses in Hepatocellular Carcinoma
- 3 March 2025
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Data from NOTCH1 Drives Sexually Dimorphic Immune Responses in Hepatocellular Carcinoma
- Open Access
- 3 March 2025
- Published by American Association for Cancer Research (AACR)
Supplementary Figure S4 from NOTCH1 Drives Sexually Dimorphic Immune Responses in Hepatocellular Carcinoma
Enhancing DC-T cell axis in females harboring NOTCH1-driven tumors has therapeutic effects
- 3 March 2025
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Figure S4 from NOTCH1 Drives Sexually Dimorphic Immune Responses in Hepatocellular Carcinoma
Enhancing DC-T cell axis in females harboring NOTCH1-driven tumors has therapeutic effects
- Open Access
- 3 March 2025
- Published by American Association for Cancer Research (AACR)
Supplementary Figure S3 from NOTCH1 Drives Sexually Dimorphic Immune Responses in Hepatocellular Carcinoma
NOTCH1-driven tumors in females lead to impaired CD8+ T cell priming and activation
- 3 March 2025
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Figure S3 from NOTCH1 Drives Sexually Dimorphic Immune Responses in Hepatocellular Carcinoma
NOTCH1-driven tumors in females lead to impaired CD8+ T cell priming and activation