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Article ; Online: The electrochemical corrosion behaviour of compacted (Bi, Pb)-2223 superconductors in aqueous solutions.

Abdel-Gaber, Ashraf M / Najem, Ahmad / Awad, Ramadan

2022 Volume 12, Issue 1, Page(s) 17941

Abstract: The corrosion behaviour of (Bi, Pb)-2223 samples compacted at 0.3-1.9 GPa in 0.5 M of HCl, NaCl, and NaOH solutions at 30 °C was investigated using potentiodynamic polarization curves measurements and electrochemical impedance spectroscopy (EIS) ... ...

Abstract	The corrosion behaviour of (Bi, Pb)-2223 samples compacted at 0.3-1.9 GPa in 0.5 M of HCl, NaCl, and NaOH solutions at 30 °C was investigated using potentiodynamic polarization curves measurements and electrochemical impedance spectroscopy (EIS) technique as well as scanning electron microscopy (SEM) and energy dispersive X-ray emission spectroscopy (EDX). Polarization results showed that the increase in compaction decreases both cathodic hydrogen evolution or oxygen reduction and anodic (BiPb)-2223 superconductor dissolution in 0.5 M HCl, and 0.5 M NaOH. On the other hand, compaction mainly affects the anodic part of the polarization curves of (Bi, Pb)-2223 in 0.5 M NaCl solution. EIS measurements revealed that the highest protection of the superconductors was achieved in 0.5 M NaCl, while the lowest degree of protection was observed in 0.5 M HCl. SEM images show a random plate-like morphology fitted with the marker of (Bi, Pb)-2223 material. The compacted sample at 1.9 GPa indicates deformation of the grains and the formation of a micro-crack. The corrosion mechanism of the superconductor at different pH values was also discussed.
Language	English
Publishing date	2022-10-26
Publishing country	England
Document type	Journal Article
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-022-22663-6
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Targeting Prohibitins to Inhibit Melanoma Growth and Overcome Resistance to Targeted Therapies.

Najem, Ahmad / Krayem, Mohammad / Sabbah, Serena / Pesetti, Matilde / Journe, Fabrice / Awada, Ahmad / Désaubry, Laurent / Ghanem, Ghanem E

Cells

2023 Volume 12, Issue 14

Abstract: Despite important advances in the treatment of metastatic melanoma with the development of MAPK-targeted agents and immune checkpoint inhibitors, the majority of patients either do not respond to therapies or develop acquired resistance. Furthermore, ... ...

Abstract	Despite important advances in the treatment of metastatic melanoma with the development of MAPK-targeted agents and immune checkpoint inhibitors, the majority of patients either do not respond to therapies or develop acquired resistance. Furthermore, there is no effective targeted therapy currently available for BRAF wild-type melanomas (approximately 50% of cutaneous melanoma). Thus, there is a compelling need for new efficient targeted therapies. Prohibitins (PHBs) are overexpressed in several types of cancers and implicated in the regulation of signaling networks that promote cell invasion and resistance to cell apoptosis. Herein, we show that PHBs are highly expressed in melanoma and are associated with not only poor survival but also with resistance to BRAFi/MEKi. We designed and identified novel specific PHB inhibitors that can inhibit melanoma cell growth in 3D spheroid models and a large panel of representative cell lines with different molecular subtypes, including those with intrinsic and acquired resistance to MAPKi, by significantly moderating both MAPK (CRAF-ERK axis) and PI3K/AKT pathways, and inducing apoptosis through the mitochondrial pathway and up-regulation of p53. In addition, autophagy inhibition enhances the antitumor efficacy of these PHB ligands. More important, these ligands can act in synergy with MAPKi to more efficiently inhibit cell growth and overcome drug resistance in both BRAF wild-type and mutant melanoma. In conclusion, targeting PHBs represents a very promising therapeutic strategy in melanoma, regardless of mutational status.
MeSH term(s)	Humans ; Melanoma/pathology ; Skin Neoplasms/drug therapy ; Prohibitins ; Phosphatidylinositol 3-Kinases ; Proto-Oncogene Proteins B-raf/metabolism ; Ligands ; Protein Kinase Inhibitors/pharmacology ; Drug Resistance, Neoplasm
Chemical Substances	Prohibitins ; Phosphatidylinositol 3-Kinases (EC 2.7.1.-) ; Proto-Oncogene Proteins B-raf (EC 2.7.11.1) ; Ligands ; Protein Kinase Inhibitors
Language	English
Publishing date	2023-07-14
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2661518-6
ISSN	2073-4409 ; 2073-4409
ISSN (online)	2073-4409
ISSN	2073-4409
DOI	10.3390/cells12141855
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Macrophage Profiling in Head and Neck Cancer to Improve Patient Prognosis and Assessment of Cancer Cell-Macrophage Interactions Using Three-Dimensional Coculture Models.

Mhaidly, Nour / Journe, Fabrice / Najem, Ahmad / Stock, Louis / Trelcat, Anne / Dequanter, Didier / Saussez, Sven / Descamps, Géraldine

International journal of molecular sciences

2023 Volume 24, Issue 16

Abstract: Tumor-associated macrophages are key components of the tumor microenvironment and play important roles in the progression of head and neck cancer, leading to the development of effective strategies targeting immune cells in tumors. Our study demonstrated ...

Abstract	Tumor-associated macrophages are key components of the tumor microenvironment and play important roles in the progression of head and neck cancer, leading to the development of effective strategies targeting immune cells in tumors. Our study demonstrated the prognostic potential of a new scoring system (Macroscore) based on the combination of the ratio and the sum of the high and low densities of M1 (CD80+) and M2 (CD163+) macrophages in a series of head and neck cancer patients, including a training population (
MeSH term(s)	Humans ; Coculture Techniques ; Head and Neck Neoplasms ; Cell Communication ; Macrophages ; Tumor-Associated Macrophages ; Immunosuppressive Agents ; Tumor Microenvironment
Chemical Substances	Immunosuppressive Agents
Language	English
Publishing date	2023-08-15
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms241612813
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Article: ATP1A1 is a promising new target for melanoma treatment and can be inhibited by its physiological ligand bufalin to restore targeted therapy efficacy.

Soumoy, Laura / Genbauffe, Aline / Mouchart, Lena / Sperone, Alexandra / Trelcat, Anne / Mukeba-Harchies, Léa / Wells, Mathilde / Blankert, Bertrand / Najem, Ahmad / Ghanem, Ghanem / Saussez, Sven / Journe, Fabrice

Cancer cell international

2024 Volume 24, Issue 1, Page(s) 8

Abstract: Despite advancements in treating metastatic melanoma, many patients exhibit resistance to targeted therapies. Our study focuses on ATP1A1, a sodium pump subunit associated with cancer development. We aimed to assess ATP1A1 prognostic value in melanoma ... ...

Abstract	Despite advancements in treating metastatic melanoma, many patients exhibit resistance to targeted therapies. Our study focuses on ATP1A1, a sodium pump subunit associated with cancer development. We aimed to assess ATP1A1 prognostic value in melanoma patients and examine the impact of its ligand, bufalin, on melanoma cell lines in vitro and in vivo. High ATP1A1 expression (IHC) correlated with reduced overall survival in melanoma patients. Resistance to BRAF inhibitor was linked to elevated ATP1A1 levels in patient biopsies (IHC, qPCR) and cell lines (Western blot, qPCR). Additionally, high ATP1A1 mRNA expression positively correlated with differentiation/pigmentation markers based on data from The Cancer Genome Atlas (TCGA) databases and Verfaillie proliferative gene signature analysis. Bufalin specifically targeted ATP1A1 in caveolae, (proximity ligation assay) and influenced Src phosphorylation (Western blot), thereby disrupting multiple signaling pathways (phosphokinase array). In vitro, bufalin induced apoptosis in melanoma cell lines by acting on ATP1A1 (siRNA experiments) and, in vivo, significantly impeded melanoma growth using a nude mouse xenograft model with continuous bufalin delivery via an osmotic pump. In conclusion, our study demonstrates that ATP1A1 could serve as a prognostic marker for patient survival and a predictive marker for response to BRAF inhibitor therapy. By targeting ATP1A1, bufalin inhibited cell proliferation, induced apoptosis in vitro, and effectively suppressed tumor development in mice. Thus, our findings strongly support ATP1A1 as a promising therapeutic target, with bufalin as a potential agent to disrupt its tumor-promoting activity.
Language	English
Publishing date	2024-01-04
Publishing country	England
Document type	Journal Article
ZDB-ID	2091573-1
ISSN	1475-2867
ISSN	1475-2867
DOI	10.1186/s12935-023-03196-y
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Article: RTK Inhibitors in Melanoma: From Bench to Bedside.

Sabbah, Malak / Najem, Ahmad / Krayem, Mohammad / Awada, Ahmad / Journe, Fabrice / Ghanem, Ghanem E

Cancers

2021 Volume 13, Issue 7

Abstract: MAPK (mitogen activated protein kinase) and PI3K/AKT (Phosphatidylinositol-3-Kinase and Protein Kinase B) pathways play a key role in melanoma progression and metastasis that are regulated by receptor tyrosine kinases (RTKs). Although RTKs are mutated in ...

Abstract	MAPK (mitogen activated protein kinase) and PI3K/AKT (Phosphatidylinositol-3-Kinase and Protein Kinase B) pathways play a key role in melanoma progression and metastasis that are regulated by receptor tyrosine kinases (RTKs). Although RTKs are mutated in a small percentage of melanomas, several receptors were found up regulated/altered in various stages of melanoma initiation, progression, or metastasis. Targeting RTKs remains a significant challenge in melanoma, due to their variable expression across different melanoma stages of progression and among melanoma subtypes that consequently affect response to treatment and disease progression. In this review, we discuss in details the activation mechanism of several key RTKs: type III: c-KIT (mast/stem cell growth factor receptor); type I: EGFR (Epidermal growth factor receptor); type VIII: HGFR (hepatocyte growth factor receptor); type V: VEGFR (Vascular endothelial growth factor), structure variants, the function of their structural domains, and their alteration and its association with melanoma initiation and progression. Furthermore, several RTK inhibitors targeting the same receptor were tested alone or in combination with other therapies, yielding variable responses among different melanoma groups. Here, we classified RTK inhibitors by families and summarized all tested drugs in melanoma indicating the rationale behind the use of these drugs in each melanoma subgroups from preclinical studies to clinical trials with a specific focus on their purpose of treatment, resulted effect, and outcomes.
Language	English
Publishing date	2021-04-02
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2527080-1
ISSN	2072-6694
ISSN	2072-6694
DOI	10.3390/cancers13071685
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Understanding Molecular Mechanisms of Phenotype Switching and Crosstalk with TME to Reveal New Vulnerabilities of Melanoma.

Najem, Ahmad / Soumoy, Laura / Sabbah, Malak / Krayem, Mohammad / Awada, Ahmad / Journe, Fabrice / Ghanem, Ghanem E

Cells

2022 Volume 11, Issue 7

Abstract: Melanoma cells are notorious for their high plasticity and ability to switch back and forth between various melanoma cell states, enabling the adaptation to sub-optimal conditions and therapeutics. This phenotypic plasticity, which has gained more ... ...

Abstract	Melanoma cells are notorious for their high plasticity and ability to switch back and forth between various melanoma cell states, enabling the adaptation to sub-optimal conditions and therapeutics. This phenotypic plasticity, which has gained more attention in cancer research, is proposed as a new paradigm for melanoma progression. In this review, we provide a detailed and deep comprehensive recapitulation of the complex spectrum of phenotype switching in melanoma, the key regulator factors, the various and new melanoma states, and corresponding signatures. We also present an extensive description of the role of epigenetic modifications (chromatin remodeling, methylation, and activities of long non-coding RNAs/miRNAs) and metabolic rewiring in the dynamic switch. Furthermore, we elucidate the main role of the crosstalk between the tumor microenvironment (TME) and oxidative stress in the regulation of the phenotype switching. Finally, we discuss in detail several rational therapeutic approaches, such as exploiting phenotype-specific and metabolic vulnerabilities and targeting components and signals of the TME, to improve the response of melanoma patients to treatments.
MeSH term(s)	Epigenesis, Genetic ; Humans ; Melanoma/pathology ; MicroRNAs/genetics ; Phenotype ; Tumor Microenvironment
Chemical Substances	MicroRNAs
Language	English
Publishing date	2022-03-29
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2661518-6
ISSN	2073-4409 ; 2073-4409
ISSN (online)	2073-4409
ISSN	2073-4409
DOI	10.3390/cells11071157
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Article: Correction: Krayem et al. The Benefit of Reactivating p53 under MAPK Inhibition on the Efficacy of Radiotherapy in Melanoma.

Krayem, Mohammad / Sabbah, Malak / Najem, Ahmad / Wouters, An / Lardon, Filip / Simon, Stephane / Sales, François / Journe, Fabrice / Awada, Ahmad / Ghanem, Ghanem E / Van Gestel, Dirk

Cancers

2023 Volume 15, Issue 24

Abstract: In the original article [ ... ]. ...

Abstract	In the original article [...].
Language	English
Publishing date	2023-12-15
Publishing country	Switzerland
Document type	Published Erratum
ZDB-ID	2527080-1
ISSN	2072-6694
ISSN	2072-6694
DOI	10.3390/cancers15245860
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article: The benefit of co-targeting PARP-1 and c-Met on the efficacy of radiotherapy in wild type BRAF melanoma.

Sabbah, Malak / Najem, Ahmad / Vanderkerkhove, Christophe / Kert, Fabien / Jourani, Younes / Journe, Fabrice / Awada, Ahmad / Van Gestel, Dirk / Ghanem, Ghanem E / Krayem, Mohammad

Frontiers in medicine

2023 Volume 10, Page(s) 1149918

Abstract: Melanoma is known to be a radioresistant cancer. Melanoma radioresistance can be due to several factors such as pigmentation, antioxidant defenses and high Deoxyribonucleic acid (DNA) repair efficacy. However, irradiation induces intracellular ... ...

Abstract	Melanoma is known to be a radioresistant cancer. Melanoma radioresistance can be due to several factors such as pigmentation, antioxidant defenses and high Deoxyribonucleic acid (DNA) repair efficacy. However, irradiation induces intracellular translocation of RTKs, including cMet, which regulates response to DNA damage activating proteins and promotes DNA repair. Accordingly, we hypothesized that co-targeting DNA repair (PARP-1) and relevant activated RTKs, c-Met in particular, may radiosensitize wild-type B-Raf Proto-Oncogene, Serine/Threonine Kinase (WTBRAF) melanomas where RTKs are often upregulated. Firstly, we found that PARP-1 is highly expressed in melanoma cell lines. PARP-1 inhibition by Olaparib or its KO mediates melanoma cell sensitivity to radiotherapy (RT). Similarly, specific inhibition of c-Met by Crizotinib or its KO radiosensitizes the melanoma cell lines. Mechanistically, we show that RT causes c-Met nuclear translocation to interact with PARP-1 promoting its activity. This can be reversed by c-Met inhibition. Accordingly, RT associated with the inhibition of both c-Met and PARP-1 resulted in a synergistic effect not only on tumor growth inhibition but also on tumor regrowth control in all animals following the stop of the treatment. We thus show that combining PARP and c-Met inhibition with RT appears a promising therapeutic approach in WTBRAF melanoma.
Language	English
Publishing date	2023-05-04
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2775999-4
ISSN	2296-858X
ISSN	2296-858X
DOI	10.3389/fmed.2023.1149918
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Article: Toad Venom Antiproliferative Activities on Metastatic Melanoma: Bio-Guided Fractionation and Screening of the Compounds of Two Different Venoms

Soumoy, Laura / Wells, Mathilde / Najem, Ahmad / Krayem, Mohammad / Ghanem, Ghanem / Hambye, Stéphanie / Saussez, Sven / Blankert, Bertrand / Journe, Fabrice

Biology. 2020 Aug. 10, v. 9, no. 8

2020

Abstract: Melanoma is the most common cancer in young adults, with a constantly increasing incidence. Metastatic melanoma is a very aggressive cancer with a 5-year survival rate of about 22-25%. This is, in most cases, due to a lack of therapies which are ... ...

Abstract	Melanoma is the most common cancer in young adults, with a constantly increasing incidence. Metastatic melanoma is a very aggressive cancer with a 5-year survival rate of about 22-25%. This is, in most cases, due to a lack of therapies which are effective on the long term. Hence, it is crucial to find new therapeutic agents to increase patient survival. Toad venoms are a rich source of potentially pharmaceutically active compounds and studies have highlighted their possible effect on cancer cells. We focused on the venoms of two different toad species: Bufo bufo and Rhinella marina. We screened the venom crude extracts, the fractions from crude extracts and isolated biomolecules by studying their antiproliferative properties on melanoma cells aiming to determine the compound or the combination of compounds with the highest antiproliferative effect. Our results indicated strong antiproliferative capacities of toad venoms on melanoma cells. We found that these effects were mainly due to bufadienolides that are cardiotonic steroids potentially acting on the Na⁺/K⁺ ATPase pump which is overexpressed in melanoma. Finally, our results indicated that bufalin alone was the most interesting compound among the isolated bufadienolides because it had the highest antiproliferative activity on melanoma cells.
Keywords	Bufo bufo ; Rhinella marina ; active ingredients ; bufadienolides ; extracts ; fractionation ; incidence ; melanoma ; metastasis ; neoplasm cells ; patients ; proton pump ; screening ; survival rate ; therapeutics ; toad venoms ; toads ; young adults
Language	English
Dates of publication	2020-0810
Publishing place	Multidisciplinary Digital Publishing Institute
Document type	Article
Note	NAL-light
ZDB-ID	2661517-4
ISSN	2079-7737
ISSN	2079-7737
DOI	10.3390/biology9080218
Database	NAL-Catalogue (AGRICOLA)

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Article ; Online: Dasatinib Stimulates Its Own Mechanism of Resistance by Activating a CRTC3/MITF/Bcl-2 Pathway in Melanoma with Mutant or Amplified c-Kit.

Sabbah, Malak / Krayem, Mohammad / Najem, Ahmad / Sales, François / Miller, Wilson / Del Rincon, Sonia / Awada, Ahmad / Ghanem, Ghanem E / Journe, Fabrice

Molecular cancer research : MCR

2021 Volume 19, Issue 7, Page(s) 1221–1233

Abstract: Amplification or activating mutations of c-Kit are a frequent oncogenic alteration, which occurs commonly in acral and mucosal melanoma. Among c-Kit inhibitors, dasatinib is the most active due to its ability to bind both active and inactive ... ...

Abstract	Amplification or activating mutations of c-Kit are a frequent oncogenic alteration, which occurs commonly in acral and mucosal melanoma. Among c-Kit inhibitors, dasatinib is the most active due to its ability to bind both active and inactive conformations of the receptor. However, its use as a single agent in melanoma showed limited clinical benefit. We first found that sensitivity to dasatinib is restricted to melanoma cell lines harboring c-Kit alteration but, unexpectedly, we observed lower effect at higher concentrations that can readily be found in patient blood. We then investigated relevant pathway alterations and found complete inhibition of MAPK and PI3K/AKT pathways but an increase in MITF and its downstream target Bcl-2 through CRTC3 pathway, which turn on the CREB regulated transcription of MITF. More importantly, dasatinib upregulates MITF and Bcl-2 through SIK2 inhibition revealed by CRTC3 reduced phosphorylation, CREB transcription activation of MITF, MITF transcription activation of Bcl-2 as well as pigmentation. Furthermore, overexpression of MITF renders melanoma cells resistant to all dasatinib concentrations. Selective Bcl-2 inhibition by ABT-199 or Bcl-2 knockout restores the sensitivity of melanoma cells to dasatinib, validating the involvement of MITF and Bcl-2 axis in the resistance of melanoma to dasatinib. In conclusion, we showed for the first time that dasatinib in melanoma stimulates its proper mechanism of resistance, independently of MAPK and PI3K/AKT pathways reactivation commonly associated to secondary c-Kit mutations, but through CRTC3/MITF/Bcl-2 pathway activation at clinically relevant doses which may explain the weak clinical benefit of dasatinib in patients with melanoma. IMPLICATIONS: Dasatinib stimulates its proper mechanism of resistance through CRTC3/MITF/Bcl-2 pathway, which may explain its modest clinical efficiency in patients with melanoma.
MeSH term(s)	Antineoplastic Agents/pharmacology ; Apoptosis/drug effects ; Apoptosis/genetics ; Cell Line, Tumor ; Cell Proliferation/drug effects ; Cell Proliferation/genetics ; Dasatinib/pharmacology ; Drug Resistance, Neoplasm/drug effects ; Drug Resistance, Neoplasm/genetics ; Gene Amplification ; Gene Expression Regulation, Neoplastic/drug effects ; Humans ; Melanoma/genetics ; Melanoma/metabolism ; Melanoma/pathology ; Microphthalmia-Associated Transcription Factor/genetics ; Microphthalmia-Associated Transcription Factor/metabolism ; Mutation ; Proteins/genetics ; Proteins/metabolism ; Proto-Oncogene Proteins c-bcl-2/genetics ; Proto-Oncogene Proteins c-bcl-2/metabolism ; Proto-Oncogene Proteins c-kit/genetics ; Proto-Oncogene Proteins c-kit/metabolism ; Signal Transduction/drug effects ; Signal Transduction/genetics ; Transcription Factors/genetics ; Transcription Factors/metabolism
Chemical Substances	Antineoplastic Agents ; CRTC3 protein, human ; Microphthalmia-Associated Transcription Factor ; Proteins ; Proto-Oncogene Proteins c-bcl-2 ; Transcription Factors ; Proto-Oncogene Proteins c-kit (EC 2.7.10.1) ; Dasatinib (RBZ1571X5H)
Language	English
Publishing date	2021-03-19
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2098788-2
ISSN	1557-3125 ; 1541-7786
ISSN (online)	1557-3125
ISSN	1541-7786
DOI	10.1158/1541-7786.MCR-20-1040
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