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The role of RICTOR downstream of receptor tyrosine kinase in cancers

Molecular cancer, 2018-02, Vol.17 (1), p.39-39, Article 39

2018

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Atypical BRAF and NRAS Mutations in Mucosal Melanoma

Cancers, 2019-08, Vol.11 (8), p.1133

2019

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Mechanism of RAF isoform switching induced by oncogenic RAS in melanoma

Small GTPases, 2011-09, Vol.2 (5), p.289-292

Dumaz, Nicolas

2011

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Oncogene abnormalities in a series of primary melanomas of the sinonasal tract: NRAS mutations and cyclin D1 amplification are more frequent than KIT or BRAF mutations

Human pathology, 2013-09, Vol.44 (9), p.1902-1911

2013

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Protein Kinase A Blocks Raf-1 Activity by Stimulating 14-3-3 Binding and Blocking Raf-1 Interaction with Ras

The Journal of biological chemistry, 2003-08, Vol.278 (32), p.29819-29823

2003

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Unmasking the tumourigenic role of SIN1/MAPKAP1 in the mTOR complex 2

Clinical and translational medicine, 2023-10, Vol.13 (10), p.e1464-e1464

2023

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Novel treatment strategy for NRAS-mutated melanoma through a selective inhibitor of CD147/VEGFR-2 interaction

Oncogene, 2022-04, Vol.41 (15), p.2254-2264

2022

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ERK and PDE4 cooperate to induce RAF isoform switching in melanoma

Nature structural & molecular biology, 2011-05, Vol.18 (5), p.584-591

2011

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RICTOR Affects Melanoma Tumorigenesis and Its Resistance to Targeted Therapy

Biomedicines, 2021-10, Vol.9 (10), p.1498

2021

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In melanoma, RAS mutations are accompanied by switching signaling from BRAF to CRAF and disrupted cyclic AMP signaling

Cancer research (Chicago, Ill.), 2006-10, Vol.66 (19), p.9483-9491

2006

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TERT promoter mutations in melanoma render TERT expression dependent on MAPK pathway activation

Oncotarget, 2016-08, Vol.7 (33), p.53127-53136

2016

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TERT Expression Induces Resistance to BRAF and MEK Inhibitors in BRAF-Mutated Melanoma In Vitro

Cancers, 2023-05, Vol.15 (11), p.2888

2023

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FGF2 Induces Resistance to Nilotinib through MAPK Pathway Activation in KIT Mutated Melanoma

Cancers, 2020-04, Vol.12 (5), p.1062

2020

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A Melanoma-Tailored Next-Generation Sequencing Panel Coupled with a Comprehensive Analysis to Improve Routine Melanoma Genotyping

Targeted oncology, 2020-12, Vol.15 (6), p.759-771

2020

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Baseline Genomic Features in BRAFV600 -Mutated Metastatic Melanoma Patients Treated with BRAF Inhibitor + MEK Inhibitor in Routine Care

Cancers, 2019-08, Vol.11 (8), p.1203

2019

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Cyclic AMP Blocks Cell Growth through Raf-1-Dependent and Raf-1-Independent Mechanisms

Molecular and Cellular Biology, 2002-06, Vol.22 (11), p.3717-3728

2002

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New perspectives on targeting RAF, MEK and ERK in melanoma

Current opinion in oncology, 2021-03, Vol.33 (2), p.120-126

2021

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Mechanisms of resistance and predictive biomarkers of response to targeted therapies and immunotherapies in metastatic melanoma

Current opinion in oncology, 2020-03, Vol.32 (2), p.91-97

2020

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Targeted therapies in melanoma beyond BRAF: targeting NRAS-mutated and KIT-mutated melanoma

Current opinion in oncology, 2020-03, Vol.32 (2), p.79-84

2020

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Integrating signals between cAMP and the RAS/RAF/MEK/ERK signalling pathways. Based on the anniversary prize of the Gesellschaft für Biochemie und Molekularbiologie Lecture delivered on 5 July 2003 at the Special FEBS Meeting in Brussels

The FEBS journal, 2005-07, Vol.272 (14), p.3491-3504

2005

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Inhibition of the proprotein convertases represses the invasiveness of human primary melanoma cells with altered p53, CDKN2A and N-Ras genes

PloS one, 2010-04, Vol.5 (4), p.e9992-e9992

2010

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Protein kinase CK1 is a p53-threonine 18 kinase which requires prior phosphorylation of serine 15

FEBS letters, 1999-12, Vol.463 (3), p.312-316

1999

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Inactivation of kindlin-3 increases human melanoma aggressiveness through the collagen-activated tyrosine kinase receptor DDR1

Oncogene, 2024-05, Vol.43 (21), p.1620-1630

2024

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The soluble form of CD160 acts as a tumor mediator of immune escape in melanoma

Cancer Immunology, Immunotherapy, 2022-11, Vol.71 (11), p.2731-2742

2022

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Serine15 phosphorylation stimulates p53 transactivation but does not directly influence interaction with HDM2

The EMBO journal, 1999-12, Vol.18 (24), p.7002-7010

1999

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The role of RICTOR downstream of receptor tyrosine kinase in cancers

Atypical BRAF and NRAS Mutations in Mucosal Melanoma

Mechanism of RAF isoform switching induced by oncogenic RAS in melanoma

Oncogene abnormalities in a series of primary melanomas of the sinonasal tract: NRAS mutations and cyclin D1 amplification are more frequent than KIT or BRAF mutations

Protein Kinase A Blocks Raf-1 Activity by Stimulating 14-3-3 Binding and Blocking Raf-1 Interaction with Ras

Unmasking the tumourigenic role of SIN1/MAPKAP1 in the mTOR complex 2

Novel treatment strategy for NRAS-mutated melanoma through a selective inhibitor of CD147/VEGFR-2 interaction

ERK and PDE4 cooperate to induce RAF isoform switching in melanoma

RICTOR Affects Melanoma Tumorigenesis and Its Resistance to Targeted Therapy

In melanoma, RAS mutations are accompanied by switching signaling from BRAF to CRAF and disrupted cyclic AMP signaling

TERT promoter mutations in melanoma render TERT expression dependent on MAPK pathway activation

TERT Expression Induces Resistance to BRAF and MEK Inhibitors in BRAF-Mutated Melanoma In Vitro

FGF2 Induces Resistance to Nilotinib through MAPK Pathway Activation in KIT Mutated Melanoma

A Melanoma-Tailored Next-Generation Sequencing Panel Coupled with a Comprehensive Analysis to Improve Routine Melanoma Genotyping

Baseline Genomic Features in BRAFV600 -Mutated Metastatic Melanoma Patients Treated with BRAF Inhibitor + MEK Inhibitor in Routine Care

Cyclic AMP Blocks Cell Growth through Raf-1-Dependent and Raf-1-Independent Mechanisms

New perspectives on targeting RAF, MEK and ERK in melanoma

Mechanisms of resistance and predictive biomarkers of response to targeted therapies and immunotherapies in metastatic melanoma

Targeted therapies in melanoma beyond BRAF: targeting NRAS-mutated and KIT-mutated melanoma

Integrating signals between cAMP and the RAS/RAF/MEK/ERK signalling pathways. Based on the anniversary prize of the Gesellschaft für Biochemie und Molekularbiologie Lecture delivered on 5 July 2003 at the Special FEBS Meeting in Brussels

Inhibition of the proprotein convertases represses the invasiveness of human primary melanoma cells with altered p53, CDKN2A and N-Ras genes

Protein kinase CK1 is a p53-threonine 18 kinase which requires prior phosphorylation of serine 15

Inactivation of kindlin-3 increases human melanoma aggressiveness through the collagen-activated tyrosine kinase receptor DDR1

The soluble form of CD160 acts as a tumor mediator of immune escape in melanoma

Serine15 phosphorylation stimulates p53 transactivation but does not directly influence interaction with HDM2

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