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Article: Trocar Site Recurrence after Laparoscopic Cholecystectomy for Unsuspected Isolated Gallbladder Metastasis of Melanoma: A Case Report and Review of the Literature.

Sergeant, Céline / Kerger, Joseph / Drowart, Annie / Sales, François / Langouo, Mireille

2023 Volume 16, Issue 1, Page(s) 1183–1195

Abstract: Cutaneous melanoma can metastasize to almost any organ, including in-transit metastases, lymph nodes, liver, lungs, brain, and bones. Spread to the gastrointestinal tract is less common and generally concerns the small bowel, colon, and stomach. ... ...

Abstract	Cutaneous melanoma can metastasize to almost any organ, including in-transit metastases, lymph nodes, liver, lungs, brain, and bones. Spread to the gastrointestinal tract is less common and generally concerns the small bowel, colon, and stomach. Gallbladder involvement is rarer, and only few cases describe it as the sole site of metastasis upon diagnosis. Melanoma metastases to the gallbladder are usually detected on staging or surveillance imaging, as patients usually show few or no symptoms. In resectable stage IV melanoma patients, complete surgical resection appears to improve the prognosis. However, due to the rarity of isolated gallbladder metastasis of melanoma, there are no guidelines regarding the optimal surgical approach (endoscopic or open cholecystectomy). Here, we report the case of isolated gallbladder melanoma metastasis found after laparoscopic cholecystectomy performed in a 46-year-old female patient with no known history of cancer presenting with acute cholecystitis symptoms. Six weeks after surgery, the patient developed trocar site recurrence. This case highlights the importance of a planned and open surgery for resectable melanoma metastases rather than a laparoscopic approach.
Language	English
Publishing date	2023-10-18
Publishing country	Switzerland
Document type	Case Reports
ZDB-ID	2458961-5
ISSN	1662-6575
ISSN	1662-6575
DOI	10.1159/000534147
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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
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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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Article ; Online: Corrigendum to 'p53 Reactivation by PRIMA-1Met (APR-246) sensitises V600E/KBRAF melanoma to vemurafenib'[Eur J of Cancer 55 (2016) 98-110].

Krayem, Mohammad / Journe, Fabrice / Wiedig, Murielle / Morandini, Renato / Najem, Ahmad / Salès, François / van Kempen, Leon C / Sibille, Catherine / Awada, Ahmad / Marine, Jean-Christophe / Ghanem, Ghanem

European journal of cancer (Oxford, England : 1990)

2022 Volume 175, Page(s) 336–338

Language	English
Publishing date	2022-09-24
Publishing country	England
Document type	Published Erratum
ZDB-ID	82061-1
ISSN	1879-0852 ; 0277-5379 ; 0959-8049 ; 0964-1947
ISSN (online)	1879-0852
ISSN	0277-5379 ; 0959-8049 ; 0964-1947
DOI	10.1016/j.ejca.2022.09.002
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Zs.A 456: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (1.OG) ab Jg. 2022: Lesesaal (EG)
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Article: Tyrosine-Dependent Phenotype Switching Occurs Early in Many Primary Melanoma Cultures Limiting Their Translational Value.

Najem, Ahmad / Wouters, Jasper / Krayem, Mohammad / Rambow, Florian / Sabbah, Malak / Sales, François / Awada, Ahmad / Aerts, Stein / Journe, Fabrice / Marine, Jean-Christophe / Ghanem, Ghanem E

Frontiers in oncology

2021 Volume 11, Page(s) 780654

Abstract: The use of patient-derived primary cell cultures in cancer preclinical assays, including drug screens and genotoxic studies, has increased in recent years. However, their translational value is constrained by several limitations, including variability ... ...

Abstract	The use of patient-derived primary cell cultures in cancer preclinical assays, including drug screens and genotoxic studies, has increased in recent years. However, their translational value is constrained by several limitations, including variability that can be caused by the culture conditions. Here, we show that the medium composition commonly used to propagate primary melanoma cultures has limited their representability of their tumor of origin and their cellular plasticity, and modified their sensitivity to therapy. Indeed, we established and compared cultures from different melanoma patients propagated in parallel in low-tyrosine (Ham's F10) or in high-tyrosine (Ham's F10 supplemented with tyrosine or RPMI1640 or DMEM) media. Tyrosine is the precursor of melanin biosynthesis, a process particularly active in differentiated melanocytes and melanoma cells. Unexpectedly, we found that the high tyrosine concentrations promoted an early phenotypic drift towards either a mesenchymal-like or senescence-like phenotype, and prevented the establishment of cultures of melanoma cells harboring differentiated features, which we show are frequently present in human clinical biopsies. Moreover, the invasive phenotype emerging in these culture conditions appeared irreversible and, as expected, associated with intrinsic resistance to MAPKi. In sharp contrast, differentiated melanoma cell cultures retained their phenotypes upon propagation in low-tyrosine medium, and importantly their phenotypic plasticity, a key hallmark of melanoma cells. Altogether, our findings underline the importance of culturing melanoma cells in low-tyrosine-containing medium in order to preserve their phenotypic identity of origin and cellular plasticity.
Language	English
Publishing date	2021-11-11
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2649216-7
ISSN	2234-943X
ISSN	2234-943X
DOI	10.3389/fonc.2021.780654
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Article ; Online: Acquired resistance to BRAFi reverses senescence-like phenotype in mutant BRAF melanoma.

Krayem, Mohammad / Najem, Ahmad / Journe, Fabrice / Morandini, Renato / Sales, François / Awada, Ahmad / Ghanem, Ghanem E

Oncotarget

2018 Volume 9, Issue 61, Page(s) 31888–31903

Abstract: Targeting MAPK pathway in mutant BRAF melanoma with the specific BRAF inhibitor vemurafenib showed robust initial responses in the majority of patients followed by relapses due to acquired resistance to the drug. ... ...

Abstract	Targeting MAPK pathway in mutant BRAF melanoma with the specific BRAF inhibitor vemurafenib showed robust initial responses in the majority of patients followed by relapses due to acquired resistance to the drug. In
Language	English
Publishing date	2018-08-07
Publishing country	United States
Document type	Journal Article
ZDB-ID	2560162-3
ISSN	1949-2553 ; 1949-2553
ISSN (online)	1949-2553
ISSN	1949-2553
DOI	10.18632/oncotarget.25879
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Article ; Online: P53 and MITF/Bcl-2 identified as key pathways in the acquired resistance of NRAS-mutant melanoma to MEK inhibition.

Najem, Ahmad / Krayem, Mohammad / Salès, François / Hussein, Nader / Badran, Bassam / Robert, Caroline / Awada, Ahmad / Journe, Fabrice / Ghanem, Ghanem E

European journal of cancer (Oxford, England : 1990)

2017 Volume 83, Page(s) 154–165

Abstract: Activating mutations in Neuroblastoma RAS viral oncogene homolog (NRAS) are found in 15-30% of melanomas and are associated with a poor prognosis. Although MAP kinase kinase (MEK) inhibitors used as single agents showed a limited clinical benefit in ... ...

Abstract	Activating mutations in Neuroblastoma RAS viral oncogene homolog (NRAS) are found in 15-30% of melanomas and are associated with a poor prognosis. Although MAP kinase kinase (MEK) inhibitors used as single agents showed a limited clinical benefit in patients with NRAS-mutant melanoma due to their rather cytostatic effect and high toxicity, their combination with other inhibitors of pathways known to cooperate with MEK inhibition may maximise their antitumour activity. Similarly, in a context where p53 is largely inactivated in melanoma, hyperexpression of Microphthalmia associated transcription factor (MITF) and its downstream anti-apoptotic targets may be the cause of the restraint cytotoxic effects of MEK inhibitors. Indeed, drug combinations targeting both mutant BRAF and MITF or one of its important targets Bcl-2 were effective in mutant BRAF melanoma but had no effect on acquired resistance. Therefore, we aimed to further investigate the downstream MITF targets that can explain this anti-apoptotic effect and to evaluate in parallel the effect of p53 reactivation on the promotion of apoptosis under MEK inhibition in a panel of
MeSH term(s)	Apoptosis/drug effects ; Cell Line, Tumor ; Drug Resistance, Neoplasm/genetics ; GTP Phosphohydrolases/genetics ; Humans ; MAP Kinase Kinase Kinases/antagonists & inhibitors ; Melanoma/drug therapy ; Melanoma/genetics ; Membrane Proteins/genetics ; Microphthalmia-Associated Transcription Factor/antagonists & inhibitors ; Molecular Targeted Therapy/methods ; Prognosis ; Protein Kinase Inhibitors/therapeutic use ; Tumor Suppressor Protein p53/physiology ; bcl-2-Associated X Protein/antagonists & inhibitors
Chemical Substances	Membrane Proteins ; Microphthalmia-Associated Transcription Factor ; Protein Kinase Inhibitors ; Tumor Suppressor Protein p53 ; bcl-2-Associated X Protein ; MAP Kinase Kinase Kinases (EC 2.7.11.25) ; GTP Phosphohydrolases (EC 3.6.1.-) ; NRAS protein, human (EC 3.6.1.-)
Language	English
Publishing date	2017-09
Publishing country	England
Document type	Journal Article
ZDB-ID	82061-1
ISSN	1879-0852 ; 0277-5379 ; 0959-8049 ; 0964-1947
ISSN (online)	1879-0852
ISSN	0277-5379 ; 0959-8049 ; 0964-1947
DOI	10.1016/j.ejca.2017.06.033
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Zs.A 456: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (1.OG) ab Jg. 2022: Lesesaal (EG)
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Article: 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

2019 Volume 11, Issue 8

Abstract: Radiotherapy (RT) in patients with melanoma historically showed suboptimal results, because the disease is often radioresistant due to various mechanisms such as scavenging free radicals by thiols, pigmentary machinery, or enhanced DNA repair. However, ... ...

Abstract	Radiotherapy (RT) in patients with melanoma historically showed suboptimal results, because the disease is often radioresistant due to various mechanisms such as scavenging free radicals by thiols, pigmentary machinery, or enhanced DNA repair. However, radiotherapy has been utilized as adjuvant therapy after the complete excision of primary melanoma and lymph nodes to reduce the rate of nodal recurrences in high-risk patients. The resistance of melanoma cells to radiotherapy may also be in relation with the constitutive activation of the MAPK pathway and/or with the inactivation of p53 observed in about 90% of melanomas. In this study, we aimed to assess the potential benefit of adding RT to BRAF-mutated melanoma cells under a combined p53 reactivation and MAPK inhibition in vitro and in a preclinical animal model. We found that the combination of BRAF inhibition (vemurafenib, which completely shuts down the MAPK pathway), together with p53 reactivation (PRIMA-1
Language	English
Publishing date	2019-08-01
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2527080-1
ISSN	2072-6694
ISSN	2072-6694
DOI	10.3390/cancers11081093
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Article ; Online: Prominent role of cyclic adenosine monophosphate signalling pathway in the sensitivity of (WT)BRAF/(WT)NRAS melanoma cells to vemurafenib.

Krayem, Mohammad / Journe, Fabrice / Wiedig, Murielle / Morandini, Renato / Sales, François / Awada, Ahmad / Ghanem, Ghanem

European journal of cancer (Oxford, England : 1990)

2014 Volume 50, Issue 7, Page(s) 1310–1320

Abstract: Vemurafenib improves survival in patients with melanoma bearing the (V600E)BRAF mutation, but it did not show any benefit in clinical trials focusing on wild type tumours while it may well inhibit (WT)BRAF considering the dosage used and the ... ...

Abstract	Vemurafenib improves survival in patients with melanoma bearing the (V600E)BRAF mutation, but it did not show any benefit in clinical trials focusing on wild type tumours while it may well inhibit (WT)BRAF considering the dosage used and the bioavailability of the drug. As tumours may contain a mixture of mutant and wild type BRAF cells and this has been also put forward as a resistance mechanism, we aimed to evaluate the sensitivity/resistance of six, randomly selected, (WT)BRAF/(WT)NRAS lines to vemurafenib and found four sensitive. The sensitivity to the drug was accompanied by a potent inhibition of both phospho-ERK and phospho-AKT, and a significant induction of apoptosis while absent in lines with intrinsic or acquired resistance. Phospho-CRAF expression was low in all sensitive lines and high in resistant ones, and MEK inhibition can effectively potentiate the drug effect. A possible explanation for CRAF modulation is cyclic adenosine monophosphate (cAMP), a mediator of melanocortin receptor 1 (MC1R) signalling, since it can actually inhibit CRAF. Indeed, we measured cAMP and found that all four sensitive lines contained significantly higher constitutive cAMP levels than the resistant ones. Consequently, vemurafenib and cAMP stimulator combination resulted in a substantial synergistic effect in lines with both intrinsic and acquired resistance but only restricted to those where cAMP was effectively increased. The use of a cAMP agonist overcame such restriction. In conclusion, we report that (WT)BRAF/(WT)NRAS melanoma lines with low phospho-CRAF and high cAMP levels may be sensitive to vemurafenib and that CRAF inhibition through cAMP stimulation may overcome the resistance to the drug.
MeSH term(s)	Antineoplastic Agents/pharmacology ; Apoptosis/drug effects ; Cell Line, Tumor ; Cell Proliferation/drug effects ; Cyclic AMP/metabolism ; Cyclic AMP/physiology ; Drug Screening Assays, Antitumor/methods ; GTP Phosphohydrolases/physiology ; Genes, ras ; Humans ; Indoles/pharmacology ; Melanoma/drug therapy ; Melanoma/genetics ; Membrane Proteins/physiology ; Protein Kinase Inhibitors/pharmacology ; Proto-Oncogene Proteins B-raf/antagonists & inhibitors ; Proto-Oncogene Proteins B-raf/genetics ; Signal Transduction/physiology ; Sulfonamides/pharmacology
Chemical Substances	Antineoplastic Agents ; Indoles ; Membrane Proteins ; Protein Kinase Inhibitors ; Sulfonamides ; vemurafenib (207SMY3FQT) ; Cyclic AMP (E0399OZS9N) ; Proto-Oncogene Proteins B-raf (EC 2.7.11.1) ; GTP Phosphohydrolases (EC 3.6.1.-) ; NRAS protein, human (EC 3.6.1.-)
Language	English
Publishing date	2014-05
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	82061-1
ISSN	1879-0852 ; 0277-5379 ; 0959-8049 ; 0964-1947
ISSN (online)	1879-0852
ISSN	0277-5379 ; 0959-8049 ; 0964-1947
DOI	10.1016/j.ejca.2014.01.021
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Zs.A 456: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (1.OG) ab Jg. 2022: Lesesaal (EG)
Zs.MO 583: Show issues

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Article ; Online: Immunohistochemical study of 40 cases of longitudinal melanonychia.

Theunis, Anne / Richert, Bertrand / Sass, Ursula / Lateur, Nadine / Sales, François / André, Josette

The American Journal of dermatopathology

2011 Volume 33, Issue 1, Page(s) 27–34

Abstract: The etiology of longitudinal melanonychia (LM) is difficult to establish by clinical and dermoscopic examinations alone. Microscopic examination of the nail matrix remains crucial. Two groups of LM may be identified: melanocytic activation (melanic ... ...

Abstract	The etiology of longitudinal melanonychia (LM) is difficult to establish by clinical and dermoscopic examinations alone. Microscopic examination of the nail matrix remains crucial. Two groups of LM may be identified: melanocytic activation (melanic pigmentation of the matrix epithelium without any increase in the density of melanocytes) and melanocytic proliferation (lentigo, nevus, or melanoma). The histological examination is challenging, and immunohistochemical investigations can be helpful. The objective of this study was to analyze the immunohistochemical findings with routinely used markers in melanocytic tumors-S-100 protein, HMB-45, and Melan-A-in LM. A series of 40 cases were analyzed: 10 activations, 4 lentigines, 7 nevi, 12 in situ melanomas, and 7 invasive melanomas. The sensitivity of S-100 protein is weak in benign and malignant intraepithelial melanocytes of the nail matrix, and if this marker is performed alone, it may be wrongly reassuring. However, the use of S-100 protein is essential to differentiate invasive melanoma, lacking an intraepithelial component, and particularly desmoplastic melanoma, from epithelial and mesenchymal tumors. HMB-45 and Melan-A are more sensitive than S-100 protein for the evaluation of intraepithelial melanocytic proliferation of the nail apparatus, with HMB-45 being the most intense marker. In the dermal component, HMB-45 and Melan-A were less sensitive than S-100 protein. In conclusion, we recommend that the panel of antibodies used for histological evaluation of LM should include HMB-45 and/or Melan-A and S-100 protein only if an invasive melanoma is suspected.
MeSH term(s)	Adolescent ; Adult ; Aged ; Aged, 80 and over ; Biomarkers/analysis ; Child ; Child, Preschool ; Female ; Humans ; Immunohistochemistry ; MART-1 Antigen/biosynthesis ; Male ; Melanins/metabolism ; Melanocytes/pathology ; Middle Aged ; Nail Diseases/metabolism ; Nail Diseases/pathology ; S100 Proteins/biosynthesis
Chemical Substances	Biomarkers ; MART-1 Antigen ; Melanins ; S100 Proteins
Language	English
Publishing date	2011-02
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	448469-1
ISSN	1533-0311 ; 0193-1091
ISSN (online)	1533-0311
ISSN	0193-1091
DOI	10.1097/DAD.0b013e3181e67c87
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Zs.A 1518: Show issues

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