Jeremy RAYMOND

Verified @ludwig.ox.ac.uk

Ludwig Institute for Cancer Research
University of Oxford

Jeremy RAYMOND


            Download Compact PDF  
https://researchid.co/j_raymond

RESEARCH, TEACHING, or OTHER INTERESTS

Cancer Research, Cell Biology
11

Scopus Publications

139

Scholar Citations

7

Scholar h-index

6

Scholar i10-index

Scopus Publications

  • Proneural–mesenchymal hybrid glioblastoma cells are resistant to therapy and dependent on nuclear import
    Guillaume Bourmeau, Oceane Anezo, Jeremy Raymond, Alberto Ballestín, Cathy Pichol-Thievend, Juliette Reveilles, Adrien Thomas, Lin Wang, Melanie Miranda, Eve Moutaux, Stephane Liva, Valentino Ribecco, Laetitia Besse, Florent Dingli, Damarys Loew, Celine Vallot, Gaetano Gargiulo, Vidhya M Ravi, Kevin Joseph, Giorgio Seano
    Neuro Oncology, 2025
    Background Despite extensive research efforts, glioblastoma (GBM) remains a deadly disease with poor prognosis. Although previous studies have identified various cell states within GBM tumors, the molecular mechanism underlying adaptive GBM cell plasticity induced by conventional therapy remains unclear. Methods We used fluorescent reporters for proneural (PN) and mesenchymal (MES) subtypes to monitor GBM cell plasticity in real-time across multiple patient-derived cell lines. This approach revealed cells that concurrently expressed both PN and MES markers. To investigate this unique hybrid population, we implemented a comprehensive methodological approach encompassing bulk and single-cell RNA sequencing, single-cell ChIP sequencing, nuclear proteomics, high-resolution imaging, orthotopic mouse models, clinical dataset analysis, and pharmacological and genetic techniques. This multifaceted strategy allowed us to gain functional and molecular insights into this distinct cellular population. Results We showed that these hybrid cells are increased by conventional therapies, and are resistant to these therapies. At the molecular level, hybrid cells display significant alterations in chromatin structure and nuclear protein composition, elevated transcriptional activity, Myc activation, and improved transport between the nucleus and cytoplasm. Genetic and pharmaceutical inhibition of the nuclear import/export shuttling machinery, increased in hybrid cells, effectively suppressed adaptive GBM cell plasticity and hybrid identity, thereby enhancing the sensitivity of GBM cells to therapies. Conclusions Our results indicate that GBM hybrid cells play a crucial role in chemoradiation resistance. The nuclear transport machinery presents a potential therapeutic target for hybrid cells, offering a way to counteract the typical resistance to treatment observed in GBM.
  • Publisher Correction: Targeting GRPR for sex hormone-dependent cancer after loss of E-cadherin (Nature, (2025), 643, 8072, (801-809), 10.1038/s41586-025-09111-x)
    Jérémy H. Raymond, Zackie Aktary, Marie Pouteaux, Valérie Petit, Flavie Luciani, Maria Wehbe, Patrick Gizzi, Claire Bourban, Didier Decaudin, Fariba Nemati, Igor Martianov, Irwin Davidson, Catherine-Laure Tomasetto, Richard M. White, Florence Mahuteau-Betzer, Béatrice Vergier, Lionel Larue, Véronique Delmas
    Nature, 2025
    This article was originally published under standard Springer Nature license (© The Author(s), under exclusive licence to Springer Nature Limited). It is now available as an open-access paper under a Creative Commons Attribution 4.0 International license, © The Author(s).
  • Targeting GRPR for sex hormone-dependent cancer after loss of E-cadherin
    Jérémy H. Raymond, Zackie Aktary, Marie Pouteaux, Valérie Petit, Flavie Luciani, Maria Wehbe, Patrick Gizzi, Claire Bourban, Didier Decaudin, Fariba Nemati, Igor Martianov, Irwin Davidson, Catherine-Laure Tomasetto, Richard M. White, Florence Mahuteau-Betzer, Béatrice Vergier, Lionel Larue, Véronique Delmas
    Nature, 2025
    Abstract Sex inequalities in cancer are well documented, but the current limited understanding is hindering advances in precision medicine and therapies 1 . Consideration of ethnicity, age and sex is essential for the management of cancer patients because they underlie important differences in both incidence and response to treatment 2,3 . Age-related hormone production, which is a consistent divergence between the sexes, is underestimated in cancers that are not recognized as being hormone dependent 4–6 . Here, we show that premenopausal women have increased vulnerability to cancers, and we identify the cell–cell adhesion molecule E-cadherin as a crucial component in the oestrogen response in various cancers, including melanoma. In a mouse model of melanoma, we discovered an oestrogen-sensitizing pathway connecting E-cadherin, β-catenin, oestrogen receptor-α and GRPR that promotes melanoma aggressiveness in women. Inhibiting this pathway by targeting GRPR or oestrogen receptor-α reduces metastasis in mice, indicating its therapeutic potential. Our study introduces a concept linking hormone sensitivity and tumour phenotype in which hormones affect cell phenotype and aggressiveness. We have identified an integrated pro-tumour pathway in women and propose that targeting a G-protein-coupled receptor with drugs not commonly used for cancer treatment could be more effective in treating E-cadherin-dependent cancers in women. This study emphasizes the importance of sex-specific factors in cancer management and offers hope of improving outcomes in various cancers.
  • The Lipid Droplet Protein DHRS3 Is a Regulator of Melanoma Cell State
    Eleanor Johns, Yilun Ma, Pakavarin Louphrasitthiphol, Christopher Peralta, Miranda V. Hunter, Jeremy H. Raymond, Henrik Molina, Colin R. Goding, Richard M. White
    Pigment Cell and Melanoma Research, 2025
    Lipid droplets are fat storage organelles composed of a protein envelope and lipid‐rich core. Regulation of this protein envelope underlies differential lipid droplet formation and function. In melanoma, lipid droplet formation has been linked to tumor progression and metastasis, but it is unknown whether lipid droplet proteins play a role. To address this, we performed proteomic analysis of the lipid droplet envelope in melanoma. We found that lipid droplet proteins were differentially enriched in distinct melanoma states; from melanocytic to undifferentiated. DHRS3, which converts all‐trans‐retinal to all‐trans‐retinol, is upregulated in the MITFLO/undifferentiated/neural crest‐like melanoma cell state and reduced in the MITFHI/melanocytic state. Increased DHRS3 expression is sufficient to drive MITFHI/melanocytic cells to a more undifferentiated/invasive state. These changes are due to retinoic acid‐mediated regulation of melanocytic genes. Our data demonstrate that melanoma cell state can be regulated by expression of lipid droplet proteins which affect downstream retinoid signaling.
  • UVB radiation suppresses Dicer expression through β-catenin
    Zackie Aktary, Valérie Petit, Irina Berlin, Jeremy Raymond, Frederique Berger, Nisamanee Charoenchon, Evelyne Sage, Juliette Bertrand, Lionel Larue
    Journal of Cell Science, 2024
    Ultraviolet (UV) rays prompt a natural response in epidermal cells, particularly within melanocytes. The changes in gene expression and related signaling pathways in melanocytes following exposure to UV radiation are still not entirely understood. Our findings reveal that UVB irradiation suppresses the expression of Dicer (also known as Dicer1). This repression is intricately linked to the activation of the phosphoinositide 3-kinase (PI3K), ribosomal S6 kinase (RSK) and Wnt–β-catenin signaling pathways, and is directly associated with transcriptional repression by β-catenin (also known as CTNNB1). Notably, we have identified specific binding sites for the TCF/LEF–β-catenin complex in the Dicer promoter. Collectively, these results emphasize the significance of the UV-induced pathway involving the TCF/LEF–β-catenin complex, which impacts Dicer expression. UV radiation also reduced the levels of specific microRNAs known to be important in the biology of melanocytes. This pathway holds potential importance in governing melanocyte physiology.
  • Derivation and Use of Cell Lines from Mouse Models of Melanoma
    Zackie Aktary, Jeremy H. Raymond, Marie Pouteaux, Véronique Delmas, Valérie Petit, Lionel Larue
    Journal of Investigative Dermatology, 2023
  • Targeting GPCRs and Their Signaling as a Therapeutic Option in Melanoma
    Jérémy H. Raymond, Zackie Aktary, Lionel Larue, Véronique Delmas
    Cancers, 2022
    G-protein-coupled receptors (GPCRs) serve prominent roles in melanocyte lineage physiology, with an impact at all stages of development, as well as on mature melanocyte functions. GPCR ligands are present in the skin and regulate melanocyte homeostasis, including pigmentation. The role of GPCRs in the regulation of pigmentation and, consequently, protection against external aggression, such as ultraviolet radiation, has long been established. However, evidence of new functions of GPCRs directly in melanomagenesis has been highlighted in recent years. GPCRs are coupled, through their intracellular domains, to heterotrimeric G-proteins, which induce cellular signaling through various pathways. Such signaling modulates numerous essential cellular processes that occur during melanomagenesis, including proliferation and migration. GPCR-associated signaling in melanoma can be activated by the binding of paracrine factors to their receptors or directly by activating mutations. In this review, we present melanoma-associated alterations of GPCRs and their downstream signaling and discuss the various preclinical models used to evaluate new therapeutic approaches against GPCR activity in melanoma. Recent striking advances in our understanding of the structure, function, and regulation of GPCRs will undoubtedly broaden melanoma treatment options in the future.
  • CLEC12B Decreases Melanoma Proliferation by Repressing Signal Transducer and Activator of Transcription 3
    Henri Montaudié, Laura Sormani, Bérengère Dadone-Montaudié, Marjorie Heim, Nathalie Cardot-Leccia, Meri K. Tulic, Guillaume Beranger, Anne-Sophie Gay, Delphine Debayle, Yann Cheli, Jérémy H. Raymond, Pierre Sohier, Valérie Petit, Stéphane Rocchi, Franck Gesbert, Lionel Larue, Thierry Passeron
    Journal of Investigative Dermatology, 2022
  • BRN2 is a non-canonical melanoma tumor-suppressor
    Michael Hamm, Pierre Sohier, Valérie Petit, Jérémy H. Raymond, Véronique Delmas, Madeleine Le Coz, Franck Gesbert, Colin Kenny, Zackie Aktary, Marie Pouteaux, Florian Rambow, Alain Sarasin, Nisamanee Charoenchon, Alfonso Bellacosa, Luis Sanchez-del-Campo, Laura Mosteo, Martin Lauss, Dies Meijer, Eirikur Steingrimsson, Göran B. Jönsson, Robert A. Cornell, Irwin Davidson, Colin R. Goding, Lionel Larue
    Nature Communications, 2021
    While the major drivers of melanoma initiation, including activation of NRAS/BRAF and loss of PTEN or CDKN2A, have been identified, the role of key transcription factors that impose altered transcriptional states in response to deregulated signaling is not well understood. The POU domain transcription factor BRN2 is a key regulator of melanoma invasion, yet its role in melanoma initiation remains unknown. Here, in a BrafV600EPtenF/+ context, we show that BRN2 haplo-insufficiency promotes melanoma initiation and metastasis. However, metastatic colonization is less efficient in the absence of Brn2. Mechanistically, BRN2 directly induces PTEN expression and in consequence represses PI3K signaling. Moreover, MITF, a BRN2 target, represses PTEN transcription. Collectively, our results suggest that on a PTEN heterozygous background somatic deletion of one BRN2 allele and temporal regulation of the other allele elicits melanoma initiation and progression.
  • Efficacy of targeted radionuclide therapy using [131I]ICF01012 in 3D pigmented BRAF-and NRAS-mutant melanoma models and in vivo NRAS-mutated melanoma
    Hussein Akil, Mercedes Quintana, Jérémy H. Raymond, Tommy Billoux, Valentin Benboubker, Sophie Besse, Philippe Auzeloux, Véronique Delmas, Valérie Petit, Lionel Larue, Michel D’Incan, Françoise Degoul, Jacques Rouanet
    Cancers, 2021
    Purpose: To assess the efficiency of targeted radionuclide therapy (TRT), alone or in combination with MEK inhibitors (MEKi), in melanomas harboring constitutive MAPK/ERK activation responsible for tumor radioresistance. Methods: For TRT, we used a melanin radiotracer ([131I]ICF01012) currently in phase 1 clinical trial (NCT03784625). TRT alone or combined with MEKi was evaluated in three-dimensional melanoma spheroid models of human BRAFV600E SK-MEL-3, murine NRASQ61K 1007, and WT B16F10 melanomas. TRT in vivo biodistribution, dosimetry, efficiency, and molecular mechanisms were studied using the C57BL/6J-NRASQ61K 1007 syngeneic model. Results: TRT cooperated with MEKi to increase apoptosis in both BRAF- and NRAS-mutant spheroids. NRASQ61K spheroids were highly radiosensitive towards [131I]ICF01012-TRT. In mice bearing NRASQ61K 1007 melanoma, [131I]ICF01012 induced a significant extended survival (92 vs. 44 days, p < 0.0001), associated with a 93-Gy tumor deposit, and reduced lymph-node metastases. Comparative transcriptomic analyses confirmed a decrease in mitosis, proliferation, and metastasis signatures in TRT-treated vs. control tumors and suggest that TRT acts through an increase in oxidation and inflammation and P53 activation. Conclusion: Our data suggest that [131I]ICF01012-TRT and MEKi combination could be of benefit for advanced pigmented BRAF-mutant melanoma care and that [131I]ICF01012 alone could constitute a new potential NRAS-mutant melanoma treatment.
  • C57BL/6 congenic mouse NRASQ61K melanoma cell lines are highly sensitive to the combination of Mek and Akt inhibitors in vitro and in vivo
    Valérie Petit, Jeremy Raymond, Christophe Alberti, Marie Pouteaux, Stuart J. Gallagher, Mai Q. Nguyen, Andrew E. Aplin, Véronique Delmas, Lionel Larue
    Pigment Cell and Melanoma Research, 2019

RECENT SCHOLAR PUBLICATIONS

  • Targeting GRPR for sex hormone-dependent cancer after loss of E-cadherin (Jun, 10.1038/s41586-025-09111-x, 2025)
    JH Raymond, Z Aktary, M Pouteaux, V Petit, F Luciani, M Wehbe, P Gizzi, ...
    NATURE 643 (8074), E28-E28 , 2025
    2025
  • Targeting GRPR for sex hormone-dependent cancer after loss of E-cadherin
    JH Raymond, Z Aktary, M Pouteaux, V Petit, F Luciani, M Wehbe, P Gizzi, ...
    Nature 643 (8072), 801-809 , 2025
    2025
    Citations: 11
  • Proneural–mesenchymal hybrid glioblastoma cells are resistant to therapy and dependent on nuclear import
    G Bourmeau, O Anezo, J Raymond, A Ballestín, C Pichol-Thievend, ...
    Neuro-oncology, noaf160 , 2025
    2025
    Citations: 3
  • The lipid droplet protein DHRS3 is a regulator of melanoma cell state
    E Johns, Y Ma, P Louphrasitthiphol, C Peralta, MV Hunter, JH Raymond, ...
    Pigment cell & melanoma research 38 (1), e13208 , 2025
    2025
    Citations: 6
  • 459 Melanocytes lacking BRN2 are radiosensitive: the iltimate guardian of melanocyte stem cells
    Z Aktary, V Petit, JH Raymond, M Pouteaux, R Ballotti, L Larue
    Journal of Investigative Dermatology 144 (12), S307 , 2024
    2024
  • 391 Targeting GRPR for sex-hormone dependent cancer after E-cadherin loss
    Z Aktary, JH Raymond, M Pouteaux, V Petit, V Delmas, L Larue
    Journal of Investigative Dermatology 144 (12), S295 , 2024
    2024
  • UVB radiation suppresses Dicer expression through β-catenin
    Z Aktary, V Petit, I Berlin, J Raymond, F Berger, N Charoenchon, E Sage, ...
    Journal of Cell Science 137 (22), jcs261978 , 2024
    2024
    Citations: 1
  • Derivation and use of cell lines from mouse models of melanoma
    Z Aktary, JH Raymond, M Pouteaux, V Delmas, V Petit, L Larue
    Journal of Investigative Dermatology 143 (4), 538-544. e2 , 2023
    2023
    Citations: 9
  • The E-cadherin-ESR1-GRPR axis defines a sex-specific metastatic pathway in melanoma
    JH Raymond, M Pouteaux, V Petit, Z Aktary, F Luciani, M Wehbe, P Gizzi, ...
    BioRxiv, 2022.12. 02.518844 , 2022
    2022
  • 425 GRPR is an effective target for melanoma
    J Raymond, M Pouteaux, V Petit, Z Aktary, L Larue, V Delmas
    Journal of Investigative Dermatology 142 (12), S254 , 2022
    2022
  • 478 MICAL2, upregulated by β-catenin, induces invasion in melanoma
    P Sohier, N Zidi, J Raymond, Z Aktary, N Charoenchon, V Petit, L Larue
    Journal of Investigative Dermatology 142 (12), S263 , 2022
    2022
  • CLEC12B decreases melanoma proliferation by repressing signal transducer and activator of transcription 3
    H Montaudie, L Sormani, B Dadone-Montaudie, M Heim, N Cardot-Leccia, ...
    Journal of Investigative Dermatology 142 (2), 425-434 , 2022
    2022
    Citations: 11
  • Targeting GPCRs and their signaling as a therapeutic option in melanoma
    JH Raymond, Z Aktary, L Larue, V Delmas
    Cancers 14 (3), 706 , 2022
    2022
    Citations: 19
  • Role de GRPR dans la formation des métastases de mélanome
    J Raymond
    Université Paris sciences et lettres , 2021
    2021
  • BRN2 is a non-canonical melanoma tumor-suppressor
    M Hamm, P Sohier, V Petit, JH Raymond, V Delmas, M Le Coz, F Gesbert, ...
    Nature communications 12 (1), 3707 , 2021
    2021
    Citations: 16
  • Efficacy of Targeted Radionuclide Therapy Using [ 131 I]ICF01012 in 3D Pigmented BRAF- and NRAS-Mutant Melanoma Models and In Vivo NRAS-Mutant Melanoma
    H Akil, M Quintana, JH Raymond, T Billoux, V Benboubker, S Besse, ...
    Cancers 13 (6), 1421 , 2021
    2021
    Citations: 12
  • Efficacy of targeted radionuclide therapy using [131I] ICF01012 in 3D pigmented BRAF-and NRAS-mutant melanoma models and in vivo NRAS-mutated melanoma. Cancers. 2021; 13: 1–20
    H Akil, M Quintana, JH Raymond, T Billoux, V Benboubker, S Besse, ...
    s Note: MDPI stays neutral with regard to jurisdictional claims in published … , 2021
    2021
    Citations: 2
  • C57BL/6 congenic mouse NRAS Q61K melanoma cell lines are highly sensitive to the combination of Mek and Akt inhibitors in vitro and in vivo
    V Petit, J Raymond, C Alberti, M Pouteaux, SJ Gallagher, MQ Nguyen, ...
    Pigment cell & melanoma research 32 (6), 829-841 , 2019
    2019
    Citations: 44
  • BRN2 is a Non-Canonical Melanoma Tumor-Suppressor
    M Hamm, L Larue
    JOURNAL OF INVESTIGATIVE DERMATOLOGY 139 (9), S290-S290 , 2019
    2019
  • 487 C57BL/6 Congenic Mouse NRASQ61K Melanoma Cell Lines are Highly Sensitive to the Combination of MEK and AKT Inhibitors In Vitro and In Vivo
    JH Raymond
    Journal of Investigative Dermatology 139 (9), S298 , 2019
    2019

MOST CITED SCHOLAR PUBLICATIONS

  • C57BL/6 congenic mouse NRAS Q61K melanoma cell lines are highly sensitive to the combination of Mek and Akt inhibitors in vitro and in vivo
    V Petit, J Raymond, C Alberti, M Pouteaux, SJ Gallagher, MQ Nguyen, ...
    Pigment cell & melanoma research 32 (6), 829-841 , 2019
    2019.0
    Citations: 44
  • Targeting GPCRs and their signaling as a therapeutic option in melanoma
    JH Raymond, Z Aktary, L Larue, V Delmas
    Cancers 14 (3), 706 , 2022
    2022.0
    Citations: 19
  • BRN2 is a non-canonical melanoma tumor-suppressor
    M Hamm, P Sohier, V Petit, JH Raymond, V Delmas, M Le Coz, F Gesbert, ...
    Nature communications 12 (1), 3707 , 2021
    2021.0
    Citations: 16
  • Efficacy of Targeted Radionuclide Therapy Using [ 131 I]ICF01012 in 3D Pigmented BRAF- and NRAS-Mutant Melanoma Models and In Vivo NRAS-Mutant Melanoma
    H Akil, M Quintana, JH Raymond, T Billoux, V Benboubker, S Besse, ...
    Cancers 13 (6), 1421 , 2021
    2021.0
    Citations: 12
  • Targeting GRPR for sex hormone-dependent cancer after loss of E-cadherin
    JH Raymond, Z Aktary, M Pouteaux, V Petit, F Luciani, M Wehbe, P Gizzi, ...
    Nature 643 (8072), 801-809 , 2025
    2025.0
    Citations: 11
  • CLEC12B decreases melanoma proliferation by repressing signal transducer and activator of transcription 3
    H Montaudie, L Sormani, B Dadone-Montaudie, M Heim, N Cardot-Leccia, ...
    Journal of Investigative Dermatology 142 (2), 425-434 , 2022
    2022.0
    Citations: 11
  • Derivation and use of cell lines from mouse models of melanoma
    Z Aktary, JH Raymond, M Pouteaux, V Delmas, V Petit, L Larue
    Journal of Investigative Dermatology 143 (4), 538-544. e2 , 2023
    2023.0
    Citations: 9
  • The lipid droplet protein DHRS3 is a regulator of melanoma cell state
    E Johns, Y Ma, P Louphrasitthiphol, C Peralta, MV Hunter, JH Raymond, ...
    Pigment cell & melanoma research 38 (1), e13208 , 2025
    2025.0
    Citations: 6
  • Targeting GPCRs and their signaling as a therapeutic option in melanoma. Cancers (Basel). 2022; 14 (3): 706
    JH Raymond, Z Aktary, L Larue, V Delmas
    Citations: 5
  • Proneural–mesenchymal hybrid glioblastoma cells are resistant to therapy and dependent on nuclear import
    G Bourmeau, O Anezo, J Raymond, A Ballestín, C Pichol-Thievend, ...
    Neuro-oncology, noaf160 , 2025
    2025.0
    Citations: 3
  • Efficacy of targeted radionuclide therapy using [131I] ICF01012 in 3D pigmented BRAF-and NRAS-mutant melanoma models and in vivo NRAS-mutated melanoma. Cancers. 2021; 13: 1–20
    H Akil, M Quintana, JH Raymond, T Billoux, V Benboubker, S Besse, ...
    s Note: MDPI stays neutral with regard to jurisdictional claims in published … , 2021
    2021.0
    Citations: 2
  • UVB radiation suppresses Dicer expression through β-catenin
    Z Aktary, V Petit, I Berlin, J Raymond, F Berger, N Charoenchon, E Sage, ...
    Journal of Cell Science 137 (22), jcs261978 , 2024
    2024.0
    Citations: 1
  • Targeting GRPR for sex hormone-dependent cancer after loss of E-cadherin (Jun, 10.1038/s41586-025-09111-x, 2025)
    JH Raymond, Z Aktary, M Pouteaux, V Petit, F Luciani, M Wehbe, P Gizzi, ...
    NATURE 643 (8074), E28-E28 , 2025
    2025.0
  • 459 Melanocytes lacking BRN2 are radiosensitive: the iltimate guardian of melanocyte stem cells
    Z Aktary, V Petit, JH Raymond, M Pouteaux, R Ballotti, L Larue
    Journal of Investigative Dermatology 144 (12), S307 , 2024
    2024.0
  • 391 Targeting GRPR for sex-hormone dependent cancer after E-cadherin loss
    Z Aktary, JH Raymond, M Pouteaux, V Petit, V Delmas, L Larue
    Journal of Investigative Dermatology 144 (12), S295 , 2024
    2024.0
  • The E-cadherin-ESR1-GRPR axis defines a sex-specific metastatic pathway in melanoma
    JH Raymond, M Pouteaux, V Petit, Z Aktary, F Luciani, M Wehbe, P Gizzi, ...
    BioRxiv, 2022.12. 02.518844 , 2022
    2022.0
  • 425 GRPR is an effective target for melanoma
    J Raymond, M Pouteaux, V Petit, Z Aktary, L Larue, V Delmas
    Journal of Investigative Dermatology 142 (12), S254 , 2022
    2022.0
  • 478 MICAL2, upregulated by β-catenin, induces invasion in melanoma
    P Sohier, N Zidi, J Raymond, Z Aktary, N Charoenchon, V Petit, L Larue
    Journal of Investigative Dermatology 142 (12), S263 , 2022
    2022.0
  • Role de GRPR dans la formation des métastases de mélanome
    J Raymond
    Université Paris sciences et lettres , 2021
    2021.0
  • BRN2 is a Non-Canonical Melanoma Tumor-Suppressor
    M Hamm, L Larue
    JOURNAL OF INVESTIGATIVE DERMATOLOGY 139 (9), S290-S290 , 2019
    2019.0