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29. Deutscher Hautkrebskongress

Erstattung der Reisekosten für Study Nurses

2019 fördert die ADO die Teilnahme von StudienassistentInnen/Study Nurses am 29. Deutschen Hautkrebskongress und stellt finanzielle Mittel zur Verfügung.

Die ADO bezuschusst Ausgaben für Reisekosten und Übernachtung mit maximal 400 Euro pro Person. Es können Übernachtungskosten (max. 120 EUR pro Nacht inkl. Frühstück), Teilnahmegebühren und Reisekosten eingereicht werden. Die Auszahlung erfolgt nach dem Kongress gegen Vorlage der Originalbelege entsprechend der Reisekosten-Richtlinien der Deutschen Krebsgesellschaft (abhängig von der Entfernung zum Kongressort).

Antragsberechtigt sind Study Nurses bzw. nichtärztliche Studienassistent-Innen.

Da nur ein begrenztes Budget zur Verfügung steht, beantragen Interessenten bitte den Zuschuss unter Verwendung des Antragsformulars bis zum 15. Juni bei der Geschäftsstelle der ADO. Bitte senden Sie Ihre Antragsunterlagen an ado@conventus.de.

→Antragsformular     →Vergaberichtlinien

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Aktuelle Ausschreibungen der Hiege-Stiftung gegen Hautkrebs - 2019

Gerne machen wir auf die diesjährigen Ausschreibungen der Hiege-Stiftung gegen Hautkrebs aufmerksam. Die Details finden Sie in den beiliegenden PDF-Dokumenten.

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Leitlinien-Update Onkologie

S3-Leitlinie zur aktinischen Keratose und zum Plattenepithelkarzinom der Haut

Das Leitlinien-Update Onkologie der Deutschen Krebsgesellschaft
wendet sich an alle Ärztinnen und Ärzte, die sich über
aktuelle onkologische Leitlinien informieren wollen und dazu
eine kompakte, praxisnahe Fortbildung suchen.

Termine

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NUBs verfügbar

Die aktuellen Vorlagen für die NUBs sind nun verfügbar. 

Herzlichen Dank gilt Herrn Prof. Dr. Michael Weichenthal für die Erstellung.

Hinweis: Für Substanzen, die in mehreren Indikationen zugelassen sind, stellt das Krankenhaus in der Regel einen zusammenfassenden Antrag, so dass die Anträge indikationsübergreifend sind.

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PubMed – Neue Publikationen

Studying the ShcD and ERK interaction under acute oxidative stress conditions in melanoma cells.

Related Articles

Studying the ShcD and ERK interaction under acute oxidative stress conditions in melanoma cells.

Int J Biochem Cell Biol. 2019 May 20;:

Authors: Ahmed SBM, Amer S, Emad M, Rahmani M, Prigent SA

Abstract
The newly identified melanoma-associated adaptor ShcD was found to translocate to the nucleus upon hydrogen peroxide treatment. Therefore, the aim of this study was to identify the ShcD network in melanoma cells under oxidative stress. LC-MS/MS and GFP-trap were performed to study the ShcD phosphorylation status during acute severe oxidative stress. ShcD was found to be phosphorylated at threonine-159 (Thr159) in response to 5 mM H2O2 treatment. The GPS 2.1 phosphorylation prediction program predicted that the Thr159Pro motif, housed in the N-terminus of the ShcD-CH2 domain, is a potential phosphorylation site for MAPKs (ERK, JNK or p38). Co-immunoprecipitation experiments revealed that ShcD mainly interacts with ERK in B16 and MM138 melanoma cells under both hydrogen peroxide-untreated and -treated conditions. Moreover, ShcD interacts with both phosphorylated and un-phosphorylated ERK, although the interaction between ShcD and phospho-ERK was primarily observed after H2O2 treatment. A MEK inhibitor (U0126) enhanced the interaction between ShcD and unphosphorylated ERK under oxidative stress conditions. Furthermore, Thr159 was mutated to either alanine (A) or glutamic acid (E) to study whether the threonine phosphorylation state influences the ShcD/ERK interaction. Introducing the T159E mutation obliterated the ShcD/ERK interaction. To identify the functional impact of the ShcD/ERK interaction on cell survival signalling under oxidative stress conditions, caspase 3/7 assays and 7AAD cell death assays were used. The ShcD/ERK interaction promoted anti-survival signalling upon exposure to hydrogen peroxide, while U0126 treatment reduced death signalling. Our data also showed that the death signalling initiated by the ShcD/ERK interaction was accompanied by p21 phosphorylation. In summary, these data identified ShcD, via its interaction with ERK, as a proapoptotic protein under oxidative stress conditions.

PMID: 31121283 [PubMed - as supplied by publisher]

Dermoscopy of cutaneous melanoma metastases: A color-based pattern classification.

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Dermoscopy of cutaneous melanoma metastases: A color-based pattern classification.

J Dermatol. 2019 May 23;:

Authors: Avilés-Izquierdo JA, Ciudad-Blanco C, Sánchez-Herrero A, Mateos-Mayo A, Nieto-Benito LM, Rodríguez-Lomba E

Abstract
Dermoscopic studies about cutaneous metastases of malignant melanoma (CMMM) are few. Our objective was to analyze the dermoscopic features of CMMM and propose a new dermoscopic pattern classification based on color pigmentation and some specific dermoscopic features. A retrospective evaluation of 150 dermoscopic images of CMMM taken from 40 patients was performed. One hundred CMMM images were individually evaluated by six dermatologists in order to classify them according to four dermoscopic patterns: (i) blue pattern; (ii) pink pattern; (iii) brown pattern; and (iv) mixed pattern. One hundred and fifty dermoscopic images including 50 CMMM and 100 benign lesions were evaluated by five dermatologists to calculate the accuracy of these patterns in the recognition of CMMM. An intra- and interobserver reproducibility agreement study between all different dermoscopic pattern classifications was performed. Seventy-five percent of our cases of CMMM showed a monochromatic pattern. Light brown pigmented halo, peripheral gray spots and polymorphic atypical vessels were the most significant focal dermoscopic structures. The reproducibility of the color-based dermoscopic pattern classification was superior to previous dermoscopic pattern classification. In summary, a dermoscopic pattern classification based on color pigmentation and some specific dermoscopic features may be useful in recognizing early cutaneous melanoma metastasis. Multicentric studies are recommended in order to lower the impact of interobserver variability.

PMID: 31120139 [PubMed - as supplied by publisher]

Stem Cell-Derived Models of Neural Crest Are Essential to Understand Melanoma Progression and Therapy Resistance.

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Stem Cell-Derived Models of Neural Crest Are Essential to Understand Melanoma Progression and Therapy Resistance.

Front Mol Neurosci. 2019;12:111

Authors: Larribère L, Utikal J

Abstract
During development, neural crest (NC) cells are early precursors of several lineages including melanocytes. Along their differentiation from multipotent cells to mature melanocytes, NC cells will go through successive steps which require either proliferative or motile capacities. For example, they will undergo Epithelial to Mesenchymal Transition (EMT) in order the separate from the neural tube and migrate to their final location in the epidermis (Larribere and Utikal, 2013; Skrypek et al., 2017). The differentiated melanocytes are the cells of origin of melanoma tumors which progress through several stages such as radial growth phase, vertical growth phase, metastasis formation, and often resistance to current therapies. Interestingly, depending on the stage of the disease, melanoma tumor cells share phenotypes with NC cells (proliferative, motile, EMT). These phenotypes are tightly controlled by specific signaling pathways and transcription factors (TFs) which tend to be reactivated during the onset of melanoma. In this review, we summarize first the main TFs which control these common phenotypes. Then, we focus on the existing strategies used to generate human NCs. Finally we discuss how identification and regulation of NC-associated genes provide an additional approach to improving current melanoma targeted therapies.

PMID: 31118886 [PubMed]

Baseline platelet counts and derived inflammatory biomarkers: prognostic relevance in metastatic melanoma patients receiving Endostar plus dacarbazine and cisplatin.

Related Articles

Baseline platelet counts and derived inflammatory biomarkers: prognostic relevance in metastatic melanoma patients receiving Endostar plus dacarbazine and cisplatin.

Cancer Manag Res. 2019;11:3681-3690

Authors: Yang L, Xu Y, Luo P, Chen S, Zhu H, Wang C

Abstract
Background: The clinical efficacy and safety of Endostar combined with chemotherapy in the treatment of metastatic malignant melanoma (MM) were analyzed and the indicators capable of predicting the efficacy of the regimen were identified to guide clinical practice. Patients and methods: The clinical data of 55 patients with metastatic MM without gene mutations who were treated with Endostar combined with dacarbazine and cisplatin were retrospectively analyzed. Efficacy was assessed using RECIST 1.1, and adverse events (AEs) were graded according to NCI-CTCAE 4.0. The log-rank test was used to compare the survival curves of patients in different subgroups, and stepwise multivariate Cox regression analysis was used to determine significant prognostic factors. Differences were considered statistically significant at P<0.05. Results: Of the 55 patients, seven showed a partial response, 20 showed stable disease, and 28 showed progressive disease. The median progression-free survival was 17.9 months. AEs were controllable. Univariate analysis identified biotherapy, clinical stage, clinical classification, low baseline platelet count, platelet to albumin ratio (PAR), and platelet to globulin ratio (PGR) as factors affecting drug efficacy. Multivariate Cox regression analysis identified clinical stage and PAR as independent factors predicting the efficacy of the regimen. Conclusions: Endostar combined with chemotherapy showed a curative effect on metastatic MM without gene mutations, and AEs were controllable. The baseline platelet count and derived PAR and PGR values were associated with the efficacy of the regimen. The potential value of efficacy prediction remains to be further verified by prospective random experiments.

PMID: 31118790 [PubMed]

Fibronectin 1 promotes melanoma proliferation and metastasis by inhibiting apoptosis and regulating EMT.

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Fibronectin 1 promotes melanoma proliferation and metastasis by inhibiting apoptosis and regulating EMT.

Onco Targets Ther. 2019;12:3207-3221

Authors: Li B, Shen W, Peng H, Li Y, Chen F, Zheng L, Xu J, Jia L

Abstract
Background and aims: The complex process of cancer metastasis remains the least understood. Tumor cells alter their protein expression profile to survive from the tumor metastasis. Fibronectin 1 (FN1 gene coding protein) is a member of the glycoprotein family that has been shown to play an important role in cancer metastasis. However, its effects on melanoma metastasis are still unclear. Methods: We detected the FN1 expression between metastatic cells and primary cells by using Western blot and RT-qPCR assays. And, we analyzed the expressed feature of FN1 in different tissues and examined the clinical relevance of upregulated FN1 in melanoma progression by bioinformatic analysis. Furthermore, we downregulated the expression of FN1 by small interfering RNA technique to reveal the effect of FN1 on melanoma phenotype and expression of related genes. Finally, we used bioinformatics to reveal the possible mechanism of FN1 regulating melanoma progression. Results: We reported that the expression of FN1 was changed during melanoma metastasis. In this study, we established two metastatic cell lines of melanoma through mouse model, and found that metastatic cells exhibited stronger mesenchyme phenotype and possessed higher FN1 expression level compared to primary cells. Besides, we examined the clinical relevance of upregulated FN1 in tumor progression. Small interfering RNA (siRNA)-mediated downregulation of FN1 suppressed the migration, invasion, adhesion, proliferation capabilities and induced apoptosis of melanoma cells. We detected a diminished EMT-related gene signature including increased expression of E-cadherin and decreased expression of N-cadherin and Vimentin. Downregulation of FN1 also increased Bax/Bcl-2 ratio which might result in apoptosis of melanoma cells. Bioinformatics analysis revealed that FN1 most likely involved in focal adhesion and PI3K-Akt signaling pathway to regulate EMT process and apoptosis. Conclusions: Taken together, these findings demonstrated a role of FN1 in promoting melanoma metastasis by inhibiting apoptosis and regulating EMT.

PMID: 31118673 [PubMed]

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