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Journal articles on the topic 'Melanoma, TDG'

Author: Grafiati

Published: 14 March 2023

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1

Hafner-Marx, Angela, and Wolfram Breuer. "Primäres malignes Melanom im Gehirn eines 7 Monate alten Schafs (Ovis aries f. domestica)." Tierärztliche Praxis Ausgabe G: Großtiere / Nutztiere 45, no. 02 (2017): 108–11. http://dx.doi.org/10.15653/tpg-160585.

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ZusammenfassungVorgestellt wird ein bislang nicht beschriebener Fall eines malignen Melanoms im Gehirn eines Schafs. Ein wegen Ataxie euthanasiertes, erst 7 Monate altes, weibliches Schaf wurde pathologisch-anatomisch und histopathologisch untersucht. Sowohl das Gehirn als auch das Schädeldach waren von einem malignen Melanom infiltriert. Metastasen fanden sich in Leber und Nieren. Auch histomorphologisch zeigte das Melanom die Charakteristika einer malignen Neoplasie. Die kongenitale Ansammlung von Melanozyten in der Hirnhaut des Schafs (kongenitale Melanose) ist eine regelmäßig beobachtete Pigmentanomalie, die sich im vorliegenden Fall als Ausgangspunkt des Melanoms anbietet. Das geringe Alter des vorgestellten Tieres legt diesen Zusammenhang nahe. In Fällen von diagnostisch unklaren Erkrankungen sollte auch bei landwirtschaftlichen Nutztieren einschließlich des Schafs ein neoplastisches Geschehen differenzialdiagnostisch in Betracht gezogen werden.

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2

Voigt, Katja, Almuth Falkenau, Nadja Herbach, Melanie Feist, and Theresa Tschoner. "Intraokuläres Melanom bei einer 10 Jahre alten Lamastute (Lama glama)." Tierärztliche Praxis Ausgabe G: Großtiere / Nutztiere 46, no. 05 (October 2018): 334–39. http://dx.doi.org/10.15653/tpg-180093.

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ZusammenfassungEine 10-jährige Lamastute wurde mit einer chronisch wuchernden Masse des linken Auges vorgestellt. Das Tier zeigte einen linksseitigen Exophthalmus, die Nickhaut war gerötet. Die Hornhaut war von einer gelblich-rötlichen, undurchsichtigen Gewebsmasse bedeckt und wies ulzerative Veränderungen auf. Die tieferen Strukturen des Auges ließen sich nicht beurteilen. Das rechte Auge stellte sich unauffällig dar. Das linke Auge wurde unter Allgemeinanästhesie entfernt. Die histopathologische Untersuchung des Exstirpats ergab ein okuläres amelanotisches Melanom. Kornea, Sklera, Glaskörper und Linse waren nicht mehr zu identifizieren. Vierzehn Monate später wurde das Lama mit einer Umfangsvermehrung im Bereich der linken Orbita und Blindheit auf dem rechten Auge eingeliefert und aufgrund des schlechten Allgemeinzustands eingeschläfert. Bei der pathologisch-anatomischen und histopathologischen Untersuchung wurde ein Rezidiv des amelanotischen Melanoms mit Metastasierung in die regionären Lymphknoten unter Mitbeteiligung des Nervus opticus festgestellt, was die Blindheit des rechten Auges erklärte.

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3

THARPE, Ansley S., Kenneth J. VEGA, and Bruce W. TROTMAN. "Primary anorectal melanoma." Turkish Journal of Gastroenterology 23, no. 6 (December 1, 2012): 820–21. http://dx.doi.org/10.4318/tjg.2012.0498.

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4

Lecouturier, Jan, Helen Bosomworth, Marie Labus, Rob A. Ellis, and Penny E. Lovat. "Health professional and patient views of a novel prognostic test for melanoma: A theoretically informed qualitative study." PLOS ONE 17, no. 4 (April 4, 2022): e0265048. http://dx.doi.org/10.1371/journal.pone.0265048.

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Objectives Cutaneous melanoma rates are steadily increasing. Up to 20% of patients diagnosed with AJCC Stage I/II melanomas will develop metastatic disease. To date there are no consistently reliable means to accurately identify truly high versus low-risk patient subpopulations. There is hence an urgent need for more accurate prediction of prognosis to determine appropriate clinical management. Validation of a novel prognostic test based on the immunohistochemical expression of two protein biomarkers in the epidermal microenvironment of primary melanomas was undertaken; loss of these biomarkers had previously been shown to be associated with a higher risk of recurrence or metastasis. A parallel qualitative study exploring secondary care health professional and patient views of the test was undertaken and this paper reports the perceived barriers and enablers to its implementation into the melanoma care pathway. Methods Qualitative methods were employed drawing upon the Theoretical Domains Framework (TDF) in the exploration and analysis. An inductive-deductive analysis was performed, with all data coded using a thematic then TDF framework. Findings 20 dermatologists, plastic surgeons, cancer nurse specialists, oncologists and histopathologists participated. Nine TDF domains were relevant to all health professional groups and the ‘Skills’ and ‘Beliefs about Capabilities’ domains were relevant only to histopathologists. ‘Optimism’ and ‘Beliefs about consequences’ were strong enablers particularly for clinicians. ‘Environmental context and resources’ (impact on pathology services) and ‘Knowledge’ (the need for robust evidence about the test reliability) were the main perceived barriers. 19 patients and one carer were interviewed. For the patients eight domains were relevant. (‘Knowledge’, ‘Emotions’, ‘Beliefs about consequences’, ‘Social Role and identity’, ‘Behavioural regulation’, ‘Memory, attention and decision processes’, ‘Reinforcement’ and ‘Skills’). The consequences of the implementation of the test were reassurance about future risk, changes to the follow-up pathway on which there were mixed views, and the need to ensure they maintained self-surveillance (Beliefs about consequences). The test was acceptable to all patient interviewees but the resultant changes to management would need to be supported by mechanisms for fast-track back into the clinic, further information on self-surveillance and clear management plans at the time the result is conveyed (Behavioural regulation). Conclusions Health professionals and patients perceived positive consequences—for patients and for health services—of adopting the test. However, its implementation would require exploration of the resource implications for pathology services, psychological support for patients with a high-risk test result and mechanisms to reassure and support patients should the test lead to reduced frequency or duration of follow-up. Exploring implementation at an early stage with health professionals presented challenges related to the provision of specific details of the test and its validation.

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5

Titov, K. S., D. L. Rotin, A. M. Kazakov, O. U. Micheeva, I. M. Telezhnikova, and D. A. Ryabchikov. "Expression rate of ALK tyrosine kinase and TAG-72 oncoprotein in primary skin melanoma." Russian Journal of Biotherapy 17, no. 3 (November 25, 2018): 50–54. http://dx.doi.org/10.17650/1726-9784-2018-17-3-50-54.

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Objective.Determine the frequency of occurrence of tyrosine kinase expression of the mutated ALK and TAG-72 gene among patients with primary melanoma of the skin, to identify their association with a number of histological parameters, and to assess the diagnostic value of the determination of ALK and TAG-72.Materials and methods.Paraffin blocks with surgical material from 40 patients with primary skin melanoma. For routine histological examination, the material was fixed with 10 % neutral formalin for 24 h, poured into paraffin, sections were prepared with a thickness of 4–5 μm, stained with hematoxylin and eosin. IHC study with monoclonal antibodies D57.3 to ALK was performed on an immunostender – Ventana, with antibodies B72.3 to TAG-72 – on Thermo Fischer. As a detection system used: Envision – for TAG-72 and Ventana – for ALK.Results.ALK mutation was detected in 7 (12 %), TAG-72 – 4 (10 %) cases. Evaluation of the correlation force between the presence of ALK and TAG-72 showed a direct average coupling strength (correlation coefficient was 0.31). A direct correlation of the mean force between the presence of TAG-72 oncoprotein, ALK mutation and ulceration in the patient was found – the correlation coefficient was 0.53 and 0.68, respectively. There was a statistically significant association between the presence of ALK and lymphoid infiltration, which in most cases (57 %) was pronounced (p <0.05).Conclusion.Comparing the positive sign of the expression of ALK – 17.5 % and TAG-72 – 10 %, and the positive of their simultaneous detection – 7.5 %, it can be concluded that further studies to determine their diagnostic value are promising. The presence of severe lymphoid infiltration in ALK-positive patients claims a diagnostic value in primary skin melanoma.

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Duffy, David, Rick Sturm, Gu Zhu, and Stuart MacGregor. "Gene Discovery Using Twins." Twin Research and Human Genetics 23, no. 2 (April 2020): 90–93. http://dx.doi.org/10.1017/thg.2020.38.

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AbstractOne of Nick’s key early achievements at QIMR was to establish a twin study on melanoma risk factors. The Brisbane Twin Nevus Study (BTNS) had an initial focus on nevus (mole) count in adolescents but, reflecting Nick’s broad interests, expanded in scope enormously over the decades. In the skin cancer arena, BTNS was essential to genetic discoveries in melanoma, eye color and pigmentation. Later studies amassed data on thousands of phenotypes, ranging from molecular phenotypes such as gene expression to studies where gene mapping findings in adolescents turned out to have translational potential in late-onset diseases. Nick’s twin data have formed the basis for an enormous range of discoveries, with Nick and his colleagues continuing to capitalize on these data.

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Karakök Güngör, Hilayda, and Bengü Nisa Akay. "Current Treatment Modalities in Advanced Melanoma." Turkish Journal of Dermatology / Türk Dermatoloji Dergisi 10, no. 4 (December 1, 2016): 137–44. http://dx.doi.org/10.4274/tdd.3103.

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8

Arican, Ozer, and Irem Erturk. "A Case of Melanoma Associated Leukoderma." Turkish Journal of Dermatology / Türk Dermatoloji Dergisi 4, no. 2 (June 1, 2010): 52–54. http://dx.doi.org/10.5152/tdd.2010.05.

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9

Malindi, Zaria, Stefan Barth, and Heidi Abrahamse. "The Potential of Antibody Technology and Silver Nanoparticles for Enhancing Photodynamic Therapy for Melanoma." Biomedicines 10, no. 9 (September 1, 2022): 2158. http://dx.doi.org/10.3390/biomedicines10092158.

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Melanoma is highly aggressive and is known to be efficient at resisting drug-induced apoptotic signals. Resection is currently the gold standard for melanoma management, but it only offers local control of the early stage of the disease. Metastatic melanoma is prone to recurrence, and has a poor prognosis and treatment response. Thus, the need for advanced theranostic alternatives is evident. Photodynamic therapy has been increasingly studied for melanoma treatment; however, it relies on passive drug accumulation, leading to off-target effects. Nanoparticles enhance drug biodistribution, uptake and intra-tumoural concentration and can be functionalised with monoclonal antibodies that offer selective biorecognition. Antibody–drug conjugates reduce passive drug accumulation and off-target effects. Nonetheless, one limitation of monoclonal antibodies and antibody–drug conjugates is their lack of versatility, given cancer’s heterogeneity. Monoclonal antibodies suffer several additional limitations that make recombinant antibody fragments more desirable. SNAP-tag is a modified version of the human DNA-repair enzyme, O6-alkylguanine-DNA alkyltransferase. It reacts in an autocatalytic and covalent manner with benzylguanine-modified substrates, providing a simple protein labelling system. SNAP-tag can be genetically fused with antibody fragments, creating fusion proteins that can be easily labelled with benzylguanine-modified payloads for site-directed delivery. This review aims to highlight the benefits and limitations of the abovementioned approaches and to outline how their combination could enhance photodynamic therapy for melanoma.

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Foureau, David, Kendall Carpenter, Asim Amin, Fei Guo, Richard White, and Jonathan Salo. "Myeloid-conditioning using Toll-like receptor agonists to restore immune potency against melanoma. (TUM4P.926)." Journal of Immunology 192, no. 1_Supplement (May 1, 2014): 138.27. http://dx.doi.org/10.4049/jimmunol.192.supp.138.27.

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Abstract Suppressor cells of myeloid origin contribute to the immune imbalance observed in advanced melanoma. Toll-Like Receptor (TLR) signaling regulates myeloid differentiation and maturation. This study sought to determine the distribution of myeloid suppressor cell subsets in B16F10 melanoma-bearing mice, and modulate their immunosuppressive phenotype by employing a regimen of intracellular TLR agonist(s). Tolerogenic dendritic cells (tDC) and granulocytic myeloid-derived suppressor cells (gMDSC) are primarily observed in the periphery (spleen, PBMC, draining lymph node) of B16F10-bearing mice whereas M2 macrophages (M2) are noted to be intratumoral. Toll-Like Receptor-expression analysis by quantitative PCR showed TLR9 was ubiquitously expressed on tDC, gMDSC and M2, while TLR3 was restricted to tDC and M2. Myeloid conditioning regimens employing TLR3 and 9 agonists were tested in vitro on bone marrow-derived tDC (CD11c+, MHCII+, IL-10+) and M2 (F4/80+, CD206+, Arg1+). Combinations of TLR3+9 agonists or Type A+B TLR9 agonists decreased IL-10/Arg1 mRNA expression while triggered IL-12 expression. In vivo, subcutaneous injection of type A+B TLR9 agonists reduced circulating tDC and gMDSC prevalence by 67% and 82% respectively, intratumoral M2 dropped by 35%. In conclusion, we demonstrate combining type A+B TLR9 agonists promoted immune potency by reducing prevalence of peripheral tDC and gMDSC, as well as tumoral M2 in vivo, and triggering IL-12 production by tDC and M2 in vitro.

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11

YENIOVA, Ozgur, Akif ALTINBAS, Osman ERSOY, Musa AYDINLI, and Yusuf BAYRAKTAR. "Metastatic liver malignant melanoma of unknown origin." Turkish Journal of Gastroenterology 23, no. 4 (August 1, 2012): 420–21. http://dx.doi.org/10.4318/tjg.2012.0375.

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12

Aoude, Lauren G., Michael Gartside, Peter Johansson, Jane M. Palmer, Judith Symmons, Nicholas G. Martin, Grant W. Montgomery, and Nicholas K. Hayward. "Prevalence of Germline BAP1, CDKN2A, and CDK4 Mutations in an Australian Population-Based Sample of Cutaneous Melanoma Cases." Twin Research and Human Genetics 18, no. 2 (March 19, 2015): 126–33. http://dx.doi.org/10.1017/thg.2015.12.

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Mutations in Cyclin-Dependent Kinase Inhibitor 2A (CDKN2A) and Cyclin-Dependent Kinase 4 (CDK4) contribute to susceptibility in approximately 40% of high-density cutaneous melanoma (CMM) families and about 2% of unselected CMM cases. BRCA-1 associated protein-1 (BAP1) has been more recently shown to predispose to CMM and uveal melanoma (UMM) in some families; however, its contribution to CMM development in the general population is unreported. We sought to determine the contribution of these genes to CMM susceptibility in a population-based sample of cases from Australia. We genotyped 1,109 probands from Queensland families and found that approximately 1.31% harbored mutations in CDKN2A, including some with novel missense mutations (p.R22W, p.G35R and p.I49F). BAP1 missense variants occurred in 0.63% of cases but no CDK4 variants were observed in the sample. This is the first estimate of the contribution of BAP1 and CDK4 to a population-based sample of CMM and supports the previously reported estimate of CDKN2A germline mutation prevalence.

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Baykal, Can, and Algün Polat Ekinci. "Malign Melanoma: Risk Factors and Major Clinical Findings." Turkish Journal of Dermatology / Türk Dermatoloji Dergisi 9, no. 1 (March 5, 2015): 1–7. http://dx.doi.org/10.4274/tdd.2671.

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14

SERIN, Gurdeniz, Basak DOGANAVSARGIL, Cemil CALISKAN, Taner AKALIN, Murat SEZAK, and Muge TUNCYUREK. "Colonic malignant melanoma, primary or metastatic? Case report." Turkish Journal of Gastroenterology 21, no. 1 (March 1, 2010): 45–49. http://dx.doi.org/10.4318/tjg.2010.0048.

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15

Platt, Sarah, Ewan Wilson, Joya Pawade, Axel Walther, and Claire Newton. "Review of gynaecological malignant melanomas." Obstetrician & Gynaecologist 22, no. 3 (July 2020): 199–207. http://dx.doi.org/10.1111/tog.12666.

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16

Wiraja, Christian, David C. Yeo, and Chenjie Xu. "Framework Nucleic Acids: A Paradigm Shift in Transdermal Drug Delivery." SLAS TECHNOLOGY: Translating Life Sciences Innovation 24, no. 5 (May 23, 2019): 531–32. http://dx.doi.org/10.1177/2472630319848679.

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Transdermal drug delivery (TDD) provides a direct drug administration route bypassing gastrointestinal and liver metabolism. Until now, topical nanocarriers responsible for efficient TDD are predominantly polymeric or lipid based. The size-dependent skin penetration ability of framework nucleic acids (FNAs) has recently been reported, along with their efficacy in delivering doxorubicin for skin melanoma therapy. This commentary is to highlight the paradigm shift of nucleic acid delivery from being a cargo moiety to serving as a drug carrier instead. Further development directions to maximize the potential of FNAs for TDD are also discussed.

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Başak, Pınar, and Rainer Hofmann-Wellenhof. "Atipik Dermatofibroma Benzeri Dermoskopik Bulgular Gösteren Bir Melanoma Olgusu." Turkish Journal of Dermatology / Türk Dermatoloji Dergisi 8, no. 2 (June 5, 2014): 121–22. http://dx.doi.org/10.4274/tdd.1879.

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18

Cubukcu, Erdem, Omer Fatih Olmez, Kanat Ozkan, Murat Pekgoz, Nesrin Ugras, Adem Deligonul, and Osman Manavoglu. "Malignant melanoma of the stomach in an elderly patient." Turkish Journal of Gastroenterology 25, no. 1 (April 22, 2015): 295–96. http://dx.doi.org/10.5152/tjg.2014.3845.

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19

Fang, Shenying, Jiachun Lu, Xinke Zhou, Yuling Wang, Merrick I. Ross, Jeffrey E. Gershenwald, Janice N. Cormier, et al. "Functional annotation of melanoma risk loci identifies novel susceptibility genes." Carcinogenesis 41, no. 4 (October 21, 2019): 452–57. http://dx.doi.org/10.1093/carcin/bgz173.

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Abstract Genome-wide association study (GWAS)-identified single-nucleotide polymorphisms (SNPs) are tag SNPs located in both transcribed and non-coding regulatory DNA regions, rather than representing causal or functional variants for disease. To identify functional variants or genes for melanoma susceptibility, we used functional mapping and annotation (FUMA) to perform functional annotation of the summary statistics of 2541 significant melanoma risk SNPs (P < 5 × 10−8) identified by GWAS. The original GWAS melanoma study included 15 990 cases and 26 409 controls, representing the largest international meta-analysis of melanoma susceptibility. We prioritized 330 unique genes, including those in immune cytokine signaling pathways, from 19 loci through positional, expression quantitative trait locus, and chromatin interaction mapping. In comparison, only 38 melanoma-related genes were identified in the original meta-analysis. In addition to the well-known melanoma susceptibility genes confirmed in the meta-analysis (MC1R, CDKN2A, TERT, OCA2 and ARNT/SETDB1), we also identified additional novel genes using FUMA to map SNPs to genes. Through chromatin interaction mapping, we prioritized IFNA7, IFNA10, IFNA16, IFNA17, IFNA14, IFNA6, IFNA21, IFNA4, IFNE and IFNA5; these 10 most significant genes are all involved in immune system and cytokine signaling pathways. In the gene analysis, we identified 72 genes with a P < 2.5 × 10−6. The genes associated with melanoma risk were DEF8 (P = 1.09 × 10−57), DBNDD1 (P = 2.19 × 10−42), SPATA33 (P = 3.54 × 10−38) and MC1R (P = 1.04 × 10−36). In summary, this study identifies novel putative melanoma susceptibility genes and provides a guide for further experimental validation of functional variants and disease-related genes.

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Çiloğlu, Sinem, Alpay Duran, Ahmet Yiğit, Hasan Büyükdoğan, and Ekrem Keskin. "Non-Melanoma Skin Cancers of Pinna: Retrospective Assesment of 51 Cases." Turkish Journal of Dermatology / Türk Dermatoloji Dergisi 9, no. 4 (December 5, 2015): 177–80. http://dx.doi.org/10.4274/tdd.2584.

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21

DOGAN, Mutlu, Suleyman OZDEMIR, Ethem GECIM, Esra ERDEN, and Fikri ICLI. "Intestinal malignant melanoma presenting with small bowel invagination: A case report." Turkish Journal of Gastroenterology 21, no. 4 (December 1, 2010): 439–42. http://dx.doi.org/10.4318/tjg.2010.0133.

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22

Davila, Eduardo, Degui Geng, Ratika Srivastava, Adam Riker, and Svetomir Markovic. "Amplifying TLR-MyD88 signals within tumor-specific T-cells enhances antitumor activity to low concentrations of subdominant tumor-antigens (101.35)." Journal of Immunology 184, no. 1_Supplement (April 1, 2010): 101.35. http://dx.doi.org/10.4049/jimmunol.184.supp.101.35.

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Abstract There is a dire need to understand the cellular signals that can potentiate T-cell responses to weakly immunogenic tumor antigens (TAg) and to tumors expressing suboptimal levels of these antigens. We examined the anti-tumor activity and survival of TLR2-MyD88-stimulated tumor-specific CD8 T-cells derived from melanoma patients and TAg-specific T-cell receptor transgenic pmel mice. TLR2 engagement on pmel CD8 T-cells, but not on TLR2-/-pmel or MyD88-/-pmel T-cells, reduced the activation threshold to a subdominant TAg, resulting in increased production of effector molecules and cytotoxicity. Wild-type or MyD88-/- mice treated with pmel T-cells and TLR2 ligand, but not TLR2-/-pmel or MyD88-/-pmel T-cells, showed significant tumor regression of an established melanoma tumor. Over-expressing TLR2 in pmel T-cells eradicated established tumors and four-times fewer cells were needed to generate anti-tumor responses. The enhanced anti-tumor activity was associated with improved survival and increased effector function of TLR2-MyD88-stimulated T-cells. Activating TLR-MyD88 signals in patient-derived T-cells reduced the activation threshold to several weakly immunogenic TAgs, resulting in increased cytokine production, expansion and cytotoxicity. These data highlight the physiological importance of activating TLR-MyD88 signals within tumor-reactive T-lymphocytes for enhancing their longevity and augmenting effector function against suboptimal levels of weakly-immunogenic antigens.

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23

Suzuki, Kaori, Keiko Akimoto, Nobutaka Fujisawa, Shigeru Koyama, Akisa Tsunemi, Michio Tanaka, Yusuke Sekino, et al. "A metastatic melanoma of the small intestine diagnosed by single-balloon enteroscopy." Turkish Journal of Gastroenterology 25, no. 1 (April 22, 2015): 262–63. http://dx.doi.org/10.5152/tjg.2014.4113.

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24

GLIGORIJEVIC, Jasmina, Vesna ZIVKOVIC, Biljana DJORDJEVIC, and Irena DIMOV. "Primary gallbladder melanoma in dysplastic nevus syndrome: Report of case and literature review." Turkish Journal of Gastroenterology 22, no. 6 (December 1, 2011): 626–30. http://dx.doi.org/10.4318/tjg.2011.0278.

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25

Manga, P., J. D. Goldberg, I. Belitskaya-Levy, I. Lobach, D. Polsky, A. Pavlick, R. Shapiro, R. Berman, I. Osman, and H. Ostrer. "Developing genetic markers for melanoma risk assessment." Journal of Clinical Oncology 27, no. 15_suppl (May 20, 2009): 9046. http://dx.doi.org/10.1200/jco.2009.27.15_suppl.9046.

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9046 Background: Risk assessment for melanoma is currently based on phenotype, family and exposure history. This approach is subject to recall bias and excludes at-risk groups such as those with darker skin pigmentation. Poorly stratified risk pools also result in unnecessary dermatologist visits and biopsies for those at lower risk. Use of genetic markers may improve risk assessment; however few susceptibility markers have been developed to date. There have been a number of reports of association between melanoma and genetic markers though few have been replicated or validated. In addition, these studies frequently utilized specific coding region variants as markers and failed to test the entire gene. We have therefore assembled a case-control cohort in which to search for potential biomarkers for melanoma risk by interrogating genes using recently developed tools for genetic analysis. A pilot study was performed to test the utility of our cohort. Methods: A cohort of 326 individuals diagnosed with melanoma and treated at the New York University Langone Medical Center and 400 controls obtained from the New York Cancer project was assembled. Candidate genes were selected based on involvement in determining melanoma predisposition factors (skin pigmentation and DNA repair capability) and previous studies showing association. Three genes, ERCC1, ERCC4 (DNA repair) and MATP (skin pigmentation) were selected. Tag Single Nucleotide Polymorphisms (tSNPs) were selected using Haploview (Hapmap.org) and DNA genotyped (Sequenom Inc, San Diego, CA). Odds ratios and confidence intervals were computed for each SNP. Results: An association was found between SNP rs11615 at the ERCC1 locus and melanoma (Odds ratio = 1.718, 95% Confidence interval: 1.259 - 2.343 for TT vs TC/CC). Conclusions: A tSNP approach is thus useful in identifying associations in our melanoma case-control cohort. Sequence variation at the ERCC1 locus contributes to melanoma risk and the gene will now be screened for clinically useful susceptibility biomarkers. Additional DNA repair and pigmentation genes will also be interrogated using this approach. Genes found to be associated with melanoma will be screened by high- density SNP analysis to identify the most appropriate biomarker/s for use in risk assessment. No significant financial relationships to disclose.

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Geng, Degui, Ratika Srivastava, Chaoyang Li, and Eduardo Davila. "Tumor-targeted T cells secreting TLR5 ligand effectively treat melanoma-bearing mice (127.34)." Journal of Immunology 188, no. 1_Supplement (May 1, 2012): 127.34. http://dx.doi.org/10.4049/jimmunol.188.supp.127.34.

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Abstract T-cell-based therapies can kill tumor cells expressing immunodominant tumor antigens (TAg). However, this process allows the escape and metastases of tumor cells expressing low levels of TAg or expressing subdominant TAgs. Our preliminary data and published reports indicate that stimulating TLR2 or TLR5 directly on tumor-reactive T-cells reduces the activation threshold to poorly immunogenic TAgs. Genetically engineering T-cells expressing the MART-1 TCR and producing the TLR5 ligand flagellin (Fg) will generate potent and long-lived antitumor activity by costimulating T-cells and antigen-presenting cells at the tumor site. Human T-cells engineered to express the MART-1 TCR-Fg showed significantly greater proliferation, survival, and cytolytic activity than MART-1 T-cells. TLR5-stimulated T-cells responded to 10-to-50 times lower levels of TCR stimulation. TLR5 stimulation also augmented the production of various cytokines including IL-2, GM-CSF, IFN and TNF. Unexpectedly, we found that TLR5 stimulation on melanoma tumors induced the production of cytokines and chemokines which further promoted the recruitment of CD4 and CD8 T-cells, and NK cells. We are currently examining the therapeutic efficacy of using TCR-Fg T cells to treat NOD-scid IL2Rgammanull (NSG) mice bearing melanoma tumors.

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Akar, Tarik. "An interesting case of anal melanoma caused liver metastases due to misdiagnosed as hemorrhoids." Turkish Journal of Gastroenterology 29, no. 5 (August 31, 2018): 619–20. http://dx.doi.org/10.5152/tjg.2018.18201.

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28

Das, H. S., C. Panda, and S. Padhi. "Endoscopic diagnosis of a case of malignant melanoma." Tropical Gastroenterology 33, no. 4 (December 1, 2012): 296–97. http://dx.doi.org/10.7869/tg.2012.78.

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ONAK KANDEMIR, Nilufer, Burak BAHADIR, Sibel BEKTAS, Figen BARUT, Gamze YURDAKAN, Banu DOGAN GUN, Huseyin ENGIN, Selim AYDEMIR, and Sukru Oguz OZDAMAR. "Malignant melanoma associated with congenital melanocytic nevus and diagnosed with intestinal metastases: Two case reports." Turkish Journal of Gastroenterology 22, no. 1 (February 1, 2011): 77–82. http://dx.doi.org/10.4318/tjg.2011.0161.

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30

Silva, Catarina Oliveira, Jesús Molpeceres, Belén Batanero, Ana Sofia Fernandes, Nuno Saraiva, João Guilherme Costa, Patrícia Rijo, Isabel Vitória Figueiredo, Pedro Faísca, and Catarina Pinto Reis. "Functionalized diterpene parvifloron D-loaded hybrid nanoparticles for targeted delivery in melanoma therapy." Therapeutic Delivery 7, no. 8 (August 2016): 521–44. http://dx.doi.org/10.4155/tde-2016-0027.

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Gülseren, Duygu, Gonca Elçin, Tülin Akan, Nilgün Karabıçak, and Gül Erkin. "A case of Candida parapsilosis Which is Similar to Subungual Malignant Melanoma Clinically and Similar to Glomus Tumor Radiologically." Turkish Journal of Dermatology / Türk Dermatoloji Dergisi 12, no. 1 (April 2, 2018): 65–67. http://dx.doi.org/10.4274/tdd.3003.

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Kayaş, Yavuz, Ferhan Sağın, Yasemin Akçay, Gizem Kocabaş Yenipazar, Elif Azarsız, Eser Sözmen, Fezal Özdemir, and Işıl Karaarslan. "Serum Amyloid A and Lipoprotein Associated Phospholipase A2 Levels in Patients with Malign Melanoma: Correlations with Clinical Assessment and Stage." Turkish Journal of Dermatology 12, no. 3 (August 31, 2018): 135–42. http://dx.doi.org/10.4274/tdd.3643.

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Cozen, Wendy, Amie E. Hwang, Myles G. Cockburn, Ann S. Hamilton, John Zadnick, and Thomas M. Mack. "The USC Adult Twin Cohorts: International Twin Study and California Twin Program." Twin Research and Human Genetics 16, no. 1 (December 7, 2012): 366–70. http://dx.doi.org/10.1017/thg.2012.134.

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The study of twin subjects permits the documentation of crude heritability and may promote the identification of specific causal alleles. We believe that at the current time, the chief research advantage of twins as subjects, especially monozygotic twins, is that the commonality of their genetic and cultural identity simplifies the interpretation of biological associations. In order to study genetic and environmental determinants of cancer and chronic diseases, we developed two twin registries, maintained at the University of Southern California: The International Twin Study (ITS) and the California Twin Program (CTP). The ITS is a volunteer registry of twins with cancer and chronic disease consisting of 17,245 twin pairs affected by cancer and chronic disease, respectively, ascertained by advertising in periodicals from 1980–1991. The CTP is a population-based registry of California-born twin pairs ascertained by linking the California birth records to the State Department of Motor Vehicles. Over 51,000 individual California twins representing 36,965 pairs completed and returned 16-page questionnaires. Cancer diagnoses in the California twins are updated by regular linkage to the California Cancer Registry. Over 5,000 cancer patients are represented in the CTP. Twins from both registries have participated extensively in studies of breast cancer, melanoma, lymphoma, multiple sclerosis, systemic lupus erythematosus, diabetes mellitus type 1, mammographic density, smoking, and other traits and conditions.

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Elsner, Prof Dr med P., and Dr med Steven Goetze. "22. Dermatoonkologischer Tag: Adjuvante Therapie des Malignen Melanoms – 3. November 2018, Jena." Dermatologie in Beruf und Umwelt 66, no. 10 (October 1, 2018): 194–97. http://dx.doi.org/10.5414/dbx00332.

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Siudak, Krystyna, Lena Stallenberger, Christiane Herden, and Julia Vienenkötter. "Renal neoplasia in horses – a retrospective study." Tierärztliche Praxis Ausgabe G: Großtiere / Nutztiere 45, no. 05 (2017): 290–95. http://dx.doi.org/10.15653/tpg-161091.

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SummaryObjective: Being confronted with a case series of renal neoplasia in several horses which was in striking divergence to literature data, we recognized the need of a retrospective study to assess the presence of renal neoplasms in horses. Material and methods: Anamnestic animal data, necropsy findings and results of histological and immuno histochemical examinations from 2010 through 2015 were collected and evaluated regarding renal neoplasia. Results: Data from postmortem examinations of 1069 horses revealed 20 horses with renal tumors constituting a prevalence of 1.87 %. Primary renal neoplasms built the majority of cases (n = 15; 75 % of total renal neoplasms) and comprised nine renal carcinomas, four renal adenomas, one renal neuroendocrine tumor and a single nephroblastoma. Among the five secondary renal neoplasms lymphosarcoma was most common (3/5). Remaining metastatic tumors comprised one melanoma and one hemangiosarcoma. No breed or sex predilections were noticeable. Except for the case of nephroblastoma in a stillborn foal, all horses presenting with renal tumors were more than 10 years of age, often older than 20 years. Anamnestic data and clinical symptoms were inconclusive and not assigned to renal disease in most cases. Merely one horse with renal carcinoma presented with renal insufficiency and two horses showed signs of shock due to severe bleeding after tumor capsule rupture in renal carcinoma. Conclusion and clinical relevance: Renal tumors occur more often than anticipated, especially in older horses. Contradictorily to the literature, primary renal tumors significantly outnumbered secondary neoplasms in this study.

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Yasumoto, K., K. Yokoyama, K. Shibata, Y. Tomita, and S. Shibahara. "Microphthalmia-associated transcription factor as a regulator for melanocyte-specific transcription of the human tyrosinase gene." Molecular and Cellular Biology 14, no. 12 (December 1994): 8058–70. http://dx.doi.org/10.1128/mcb.14.12.8058-8070.1994.

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Tyrosinase is a rate-limiting enzyme in melanin biosynthesis and is specifically expressed in differentiated melanocytes. We have identified the enhancer element in the 5'-flanking region of the human tyrosinase gene that is responsible for its pigment cell-specific transcription and have termed it tyrosinase distal element (TDE) (positions -1861 to -1842). Transient expression assays showed that TDE confers efficient expression of a firefly luciferase reporter gene linked to the tyrosinase gene promoter in MeWo pigmented melanoma cells but not in HeLa cells, which do not express tyrosinase. TDE was specifically bound by nuclear proteins of MeWo and HeLa cells, the binding properties of which were indistinguishable in gel mobility shift assays. TDE contains the CATGTG motif in its center, and mutation analysis indicates that the CA dinucleotides of this motif are crucial for protein binding and pigment cell-specific enhancer function. The CATGTG motif is consistent with the consensus sequence recognized by a large family of transcription factors with a basic helix-loop-helix structure, which prompted us to examine the possible involvement of a ubiquitous transcription factor, USF, and a novel factor, microphthalmia-associated transcription factor (MITF), recently cloned as the human homolog of the mouse microphthalmia (mi) gene product. The mi phenotype is associated with a mutant mi locus and characterized by small eyes and loss of melanin pigments. Both USF and MITF are predicted to contain a basic helix-loop-helix structure and a leucine zipper structure. We provide evidence that USF binds to TDE, whereas we were unable to detect the DNA-binding activity of MITF. Transient coexpression assays showed that MITF specifically transactivates the promoter activity of the tyrosinase gene through the CATGTG motif of TDE but not the promoter of the ubiquitously expressed heme oxygenase gene, while USF is able to activate both promoters. These results indicate that MITF is a cell-type-specific factor that is capable of activating transcription of the tyrosinase gene.

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Yasumoto, K., K. Yokoyama, K. Shibata, Y. Tomita, and S. Shibahara. "Microphthalmia-associated transcription factor as a regulator for melanocyte-specific transcription of the human tyrosinase gene." Molecular and Cellular Biology 14, no. 12 (December 1994): 8058–70. http://dx.doi.org/10.1128/mcb.14.12.8058.

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Tyrosinase is a rate-limiting enzyme in melanin biosynthesis and is specifically expressed in differentiated melanocytes. We have identified the enhancer element in the 5'-flanking region of the human tyrosinase gene that is responsible for its pigment cell-specific transcription and have termed it tyrosinase distal element (TDE) (positions -1861 to -1842). Transient expression assays showed that TDE confers efficient expression of a firefly luciferase reporter gene linked to the tyrosinase gene promoter in MeWo pigmented melanoma cells but not in HeLa cells, which do not express tyrosinase. TDE was specifically bound by nuclear proteins of MeWo and HeLa cells, the binding properties of which were indistinguishable in gel mobility shift assays. TDE contains the CATGTG motif in its center, and mutation analysis indicates that the CA dinucleotides of this motif are crucial for protein binding and pigment cell-specific enhancer function. The CATGTG motif is consistent with the consensus sequence recognized by a large family of transcription factors with a basic helix-loop-helix structure, which prompted us to examine the possible involvement of a ubiquitous transcription factor, USF, and a novel factor, microphthalmia-associated transcription factor (MITF), recently cloned as the human homolog of the mouse microphthalmia (mi) gene product. The mi phenotype is associated with a mutant mi locus and characterized by small eyes and loss of melanin pigments. Both USF and MITF are predicted to contain a basic helix-loop-helix structure and a leucine zipper structure. We provide evidence that USF binds to TDE, whereas we were unable to detect the DNA-binding activity of MITF. Transient coexpression assays showed that MITF specifically transactivates the promoter activity of the tyrosinase gene through the CATGTG motif of TDE but not the promoter of the ubiquitously expressed heme oxygenase gene, while USF is able to activate both promoters. These results indicate that MITF is a cell-type-specific factor that is capable of activating transcription of the tyrosinase gene.

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Ferrari de Andrade, Lucas, Rong En Tay, Deng Pan, Adrienne M. Luoma, Yoshinaga Ito, Soumya Badrinath, Daphne Tsoucas, et al. "Antibody-mediated inhibition of MICA and MICB shedding promotes NK cell–driven tumor immunity." Science 359, no. 6383 (March 29, 2018): 1537–42. http://dx.doi.org/10.1126/science.aao0505.

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MICA and MICB are expressed by many human cancers as a result of cellular stress, and can tag cells for elimination by cytotoxic lymphocytes through natural killer group 2D (NKG2D) receptor activation. However, tumors evade this immune recognition pathway through proteolytic shedding of MICA and MICB proteins. We rationally designed antibodies targeting the MICA α3 domain, the site of proteolytic shedding, and found that these antibodies prevented loss of cell surface MICA and MICB by human cancer cells. These antibodies inhibited tumor growth in multiple fully immunocompetent mouse models and reduced human melanoma metastases in a humanized mouse model. Antitumor immunity was mediated mainly by natural killer (NK) cells through activation of NKG2D and CD16 Fc receptors. This approach prevents the loss of important immunostimulatory ligands by human cancers and reactivates antitumor immunity.

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Price, Joseph A., J. Michael C. McGee, Marion R. Patten, and Diane Snyder. "Effects of the adjuvant MPL+TDM on tumor challenge in the B 16 mouse melanoma model." International Journal of Immunopharmacology 18, no. 2 (February 1996): 163–65. http://dx.doi.org/10.1016/0192-0561(96)00003-3.

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Campesato, Luis Felipe, Sadna Budhu, Jeremy Tchaicha, Abhinav Jaiswal, Mathieu Gigoux, Stephane Pourpe, Cailian Liu, et al. "Blockade of IDO/TDO downstream effectors restricts cancer immune suppression." Journal of Immunology 202, no. 1_Supplement (May 1, 2019): 137.3. http://dx.doi.org/10.4049/jimmunol.202.supp.137.3.

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Abstract Immune checkpoint blockade (ICB) results in clinical benefit for a subset of cancer patients, yet multiple mechanisms of resistance can impair optimal response. The catabolism of tryptophan into metabolites known as kynurenines (Kyn) by the expression of enzymes such as IDO or TDO is a frequent phenomenon that plays a suppressive role in tumor immunity. Recently it was shown that Kyn acts as agonist of the aryl hydrocarbon receptor (AHR). Here we sought to characterize the mechanisms of immune suppression associated with the AHR pathway and to evaluate its potential as therapeutic target. RNAseq analysis of human cancers revealed a correlation between the expressions of AHR-related genes with markers associated with immunotherapy resistance (PD-1, FOXP3, CD206). By using IDO or TDO-overexpressing variants of a melanoma cell model (B16-F10), we found that myeloid cells, such as tumor-associated macrophages (TAMs) and dendritic cells (DCs), present up-regulation of the AHR. IDO-expressing tumors (B16-IDO) show higher myeloid cell infiltration, which present a tolerogenic phenotype. Tumor-antigen specific CD8T cells present reduced expression of activation markers and proliferation rate when primed by Kyn-treated BMDCs. Treatment of B16-IDO-bearing mice with an AHR-specific antagonist (CH-223191) leads to an increase of MHC II in TAMs, of activation markers in CD8 T cells and reduced frequency of T-regs. AHR inhibition delays progression of tumors with an active IDO/TDO/Kyn pathway (B16-IDO and B16-TDO), and efficacy is further improved when ICB is used in combination. In summary, our findings demonstrate that targeting the Kyn pathway through AHR inhibition could overcome key suppressive mechanisms and sensitize tumors to ICB.

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Wucherpfennig, Kai W. "Immune-Tumor Interactions in Resistance to Cancer Immunotherapy." Blood 134, Supplement_1 (November 13, 2019): SCI—45—SCI—45. http://dx.doi.org/10.1182/blood-2019-121065.

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MICA and MICB (MICA/B) are expressed by many human cancers due to cellular stress and tag cells for elimination by cytotoxic lymphocytes through NKG2D receptor activation. However, tumors evade this immune recognition pathway through proteolytic shedding of MICA/B proteins. We rationally designed antibodies targeting the MICA α3 domain, the site of proteolytic shedding, and found that these antibodies prevented loss of cell surface MICA/B by human cancer cells. These antibodies inhibited tumor growth in multiple fully immunocompetent mouse models and also reduced human melanoma metastases in a humanized mouse model. Anti-tumor immunity was mediated mainly by NK cells through activation of NKG2D and CD16 Fc receptors. This novel approach prevents the loss of important immunostimulatory ligands by human cancers and reactivates antitumor immunity. Disclosures Wucherpfennig: BMS: Research Funding; Novartis: Research Funding; TCR2: Consultancy; Tscan: Consultancy.

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Adeshakin, Adeleye Oluwatosin, Dehong Yan, Funmilayo O. Adeshakin, Mengqi Zhang, Lukman O. Afolabi, and Xiaochun Wan. "Blockade of diacylglycerol transferase 1 reprograms lipid accumulation in myeloid-derived suppressor cells and suppressed tumor progression." Journal of Immunology 206, no. 1_Supplement (May 1, 2021): 101.16. http://dx.doi.org/10.4049/jimmunol.206.supp.101.16.

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Abstract Immunotherapy, a way of restoring immune response and anti-cancer immunity, has revolutionized cancer therapy. However, immunosuppressive cells such as myeloid-derived suppressor cells (MDSC) still represent a significant impediment to immunotherapy, contributing to therapy failure and poor clinical responses. We previously reported that uptake of polyunsaturated fatty acid (PUFA) by MDSCs led to lipid accumulation via upregulation of fatty acid transport protein 2 (FATP2) to induce ROS-mediated immunosuppressive function thereby impairing T-cells activation to demonstrate their anti-tumor effect. Here lipidomics analysis revealed the exact lipid species accumulated in MDSCs from tumor-bearing tissues to be phospholipids and triglycerides (TAG). Interestingly, we observed significantly increased expression of a key enzyme involved in TAG synthesis - diacylglycerol transferase 1 (DGAT1), in MDSCs of Lewis lung carcinoma (LLC) and melanoma (B16F10)-bearing mice. Inhibiting DGAT1 reduced neutral lipid accumulation in MDSCs. Also, DGAT1 blockade downregulated MDSCs immunosuppressive genes and decreased MDSCs immunosuppressive function. Remarkably, blockade of DGAT1 expression reduced MDSCs and macrophages, thus abrogated tumor growth. Altogether, our study identified an unreported lipid metabolic target in MDSCs that promises a novel therapeutic option in clinical settings to enhance cancer immunotherapy. This work was supported by the National Key R&D Program of China (2019YFA0906100), National Natural Science Foundation of China (Grants 82071772, 81501356 and 81373112), Key-Area R&D Program of Guangdong Province (2019B020201014).

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Ramarathinam, Sri H., Pouya Faridi, Angela Peng, Pacman Szeto, Nicholas C. Wong, Andreas Behren, Mark Shackleton, and Anthony W. Purcell. "Abstract 1373: PeptidePCR: Direct identification of cancer vaccine targets from scant clinical samples." Cancer Research 82, no. 12_Supplement (June 15, 2022): 1373. http://dx.doi.org/10.1158/1538-7445.am2022-1373.

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Abstract Background: Peptides presented by Human Leukocyte antigen (HLA) class I and II molecules form an important component of the adaptive immune response against tumors. Identifying HLA-bound peptides is therefore crucial to understand the specificity of T cell responses in cancer. Due to sample limitations, it is often difficult or impossible to confirm epitope presentation in clinical biopsy material. To develop truly personal medicine, target epitopes need to be directly identified or validated in patient tumors at the peptide antigen level. Methodology: We have developed a microscale HLA immunoprecipitation protocol which when combined with a tandem mass tag (TMT)-based barcoding approach was able to identify HLA-bound peptides. HLA-complexes were affinity purified from either cultured cells, patient-derived xenograft or melanoma biopsies and the peptide cargo was tagged using TMT barcodes and analyzed using high-resolution mass spectrometry. Like primers in PCR, the carrier peptides and multiplexing of samples amplifies the signal enabling sensitive detection. Results: By using this strategy, we identified HLA-bound peptides from as few as ~1000 cultured cells. We demonstrate the clinical utility of this approach by confirming the presentation of around 1000 peptides from a challenging melanoma biopsy (~1-20mg in total), including 11 well-known T-cell response-inducing epitopes and other potential epitopes derived from Melanoma-associated antigens and neoantigens. Conclusion: This strategy will be useful for studying peptidome subsets in other clinical samples where the amount of tissue available via sampling is limiting, including biopsies taken for autoimmune diseases and infections, or to sample rare cell types in tissue/cell samples, such as different antigen-presenting cell subsets. The approach can directly isolate antigens that are already presented by HLA molecules, thereby increasing the precision of personalized approaches to cancer treatment with less than 1-week turnaround times. Citation Format: Sri H. Ramarathinam, Pouya Faridi, Angela Peng, Pacman Szeto, Nicholas C. Wong, Andreas Behren, Mark Shackleton, Anthony W. Purcell. PeptidePCR: Direct identification of cancer vaccine targets from scant clinical samples [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2022; 2022 Apr 8-13. Philadelphia (PA): AACR; Cancer Res 2022;82(12_Suppl):Abstract nr 1373.

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Nguyen-Dinh, K. V., D. Vanel, J. Lumbroso, C. Robert, and R. Sigal. "TDM, IRM et TEP-FDG. Conference de consensus de 2005 : indications et resultats dans le melanome." Journal de Radiologie 87, no. 10 (October 2006): 1218. http://dx.doi.org/10.1016/s0221-0363(06)86772-7.

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Astrof, Sophie, Denise Crowley, Elizabeth L. George, Tomohiko Fukuda, Kiyotoshi Sekiguchi, Douglas Hanahan, and Richard O. Hynes. "Direct Test of Potential Roles of EIIIA and EIIIB Alternatively Spliced Segments of Fibronectin in Physiological and Tumor Angiogenesis." Molecular and Cellular Biology 24, no. 19 (October 1, 2004): 8662–70. http://dx.doi.org/10.1128/mcb.24.19.8662-8670.2004.

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ABSTRACT Fibronectin splice variants containing the EIIIA and/or EIIIB exons are prominently expressed in the vasculature of a variety of human tumors but not in normal adult tissues. To understand the functions of these splice variants in physiological and tumor angiogenesis, we used EIIIB-null and EIIIA-null strains of mice to examine neovascularization of mouse retinas, pancreatic tumors in Rip-Tag transgenic mice, and transplanted melanomas. Contrary to expectations, physiological and tumor angiogenesis was not significantly affected by the absence of either EIIIA or EIIIB splice variants. Tumor growth was also not affected. In addition, the expression levels of smooth muscle alpha actin, believed to be modulated by EIIIA-containing fibronectins, were not affected either. Our experiments show that despite their tight regulation during angiogenesis, the presence of EIIIA or EIIIB splice variants individually is not essential for neovascularization.

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Maschke, Jan. "Metastasiertes Melanom: Nach der Studie ist vor der Studie." Kompass Dermatologie 9, no. 3 (2021): 129–31. http://dx.doi.org/10.1159/000517940.

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Die IMspire150 Studie wurde als Phase III Zulassungsstudie konzipiert und sollte prüfen, ob es bei behandlungsnaiven erwachsenen Patienten mit BRAF-V600-mutierten metastasierten Melanomen (nicht resezierbares klinisches Stadium IIIC-IV, AJCC 2009) einen Unterschied macht, wenn die Erstlinientherapie allein mit der Kombination des BRAF-Inhibitors Vemurafenib (Vem) und dem MEK-Inhibitor Cobimetinib (Cobi) erfolgt oder um den PDL-1 Antikörper Atezolizumab ergänzt wird. Patienten mit unbehandelten oder fortschreitenden Melanom-Hirnmetastasen, anderen aktiven Tumorerkrankungen und schwerwiegenden Autoimmunerkrankungen in der Vorgeschichte wurden ausgeschlossen. Die Randomisierung erfolgte 1:1. Der LDH Wert wurde zur Stratifizierung verwendet, Nebenwirkungen wurden gemäß CTCAE 4.0 Kriterien erfasst und als primärer statistischer Endpunkt der Studie wurde das vom Studienarzt bewertete progressionsfreie Überleben (progression-free survival, PFS) gewählt. Die Zwischenanalyse des Gesamtüberlebens der Patienten erfolgte gemäß Protokoll zum Zeitpunkt der Primäranalyse des PFS. Sekundäre Endpunkte waren das PFS, bewertet durch ein unabhängiges Komitee, das objektive Ansprechen, die Dauer des Tumoransprechens, das Gesamtüberleben und die Zeit bis zur Verschlechterung des Gesamtbefindens bzw. der Organfunktionen der Patienten. In den 112 Studienzentren wurden 514 Patienten eingeschlossen (n = 256 Vem/Cobi+Atezolizumab; n = 258 Vem/Cobi); 79% aller Patienten wurden in Europa rekrutiert. In beiden Studienarmen waren ca. 77% der Patienten jünger als 65, hatten einen unauffälligen Allgemeinstatus (ECOG = 0), ca. 94% waren jeweils im Stadium IV (hiervon ca. 60% Stadium M1c) und je 33% hatten einen erhöhten LDH Wert. Zunächst erhielten alle Patienten in beiden Gruppen 2 x tgl. 960mg Vem (2 x tgl. jeweils 4 Tabletten mit 240mg Vem) plus 1 x tgl. 60mg Cobi (1 x tgl. 3 Tabletten mit 20mg Cobi) per os für 21 Tage. Dann wurde Vem bei den Patienten, die in den Atezolizumab-Arm randomisiert worden waren, auf 2 x tgl. 720mg reduziert (3 × 240mg Vem plus je eine Placebotablette), im anderen Arm bei 2 x tgl. 960mg belassen. Cobi wurde zulassungsgemäß in der letzten Woche der 28 Tage dauernden Behandlungszyklen pausiert. In der Atezolizumab-Gruppe erhielten die Patienten an Tag 1 und 15 jeweils 840mg Atezolizumab i.v., in der anderen Gruppe eine Placeboinfusion. Dosismodifikationen und –unterbrechungen waren für Vem und Cobi erlaubt, für Atezolizumab waren allein Behandlungsunterbrechungen erlaubt.

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Sugathan, Vinu, Latha K. Abraham, Sunitha Thomas, V. P. Paily, and Susan John. "Hymenal tag; a clue to the diagnosis of vaginal polyp: A case report of primary vaginal melanoma mimicking an undifferentiated pleomorphic sarcoma." Indian Journal of Pathology and Oncology 7, no. 4 (November 15, 2020): 665–68. http://dx.doi.org/10.18231/j.ijpo.2020.131.

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Hopkins, Ashley M., Ganessan Kichenadasse, Chris S. Karapetis, Andrew Rowland, and Michael J. Sorich. "Early tumor shrinkage identifies long-term disease control and survival in patients with lung cancer treated with atezolizumab." Journal for ImmunoTherapy of Cancer 8, no. 1 (June 2020): e000500. http://dx.doi.org/10.1136/jitc-2019-000500.

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BackgroundPreliminary evidence indicates that early tumor shrinkage (ETS) following immune checkpoint inhibitor (ICI) initiation may be associated with survival outcomes in patients with advanced melanoma. ETS has not been explored as a biomarker of survival outcomes or patient-reported outcomes in patients with advanced non-small cell lung cancer (NSCLC) treated with ICIs.MethodsThe study pooled data from patients with NSCLC in the randomized trials OAK and POPLAR (atezolizumab vs docetaxel; n=1464), and single-arm atezolizumab trials BIRCH and FIR (n=797). The association between ETS (≥10% decrease in pretreatment sum-of-longest diameters of target-lesions at 6 weeks) and overall survival (OS), progression-free survival (PFS), time to deterioration (TDD) in health-related quality-of-life (HRQoL) and physical function (PF) was assessed using Cox proportional hazard analysis.ResultsETS occurred in 20% of atezolizumab-treated patients with NSCLC within OAK and POPLAR and was associated with highly favorable OS (HR 0.33, p<0.001), PFS (HR 0.31, p<0.001), TDD in HRQoL (HR 0.73, p=0.01) and PF (HR 0.52, p<0.001). The results were replicated in the BIRCH and FIR data. Atezolizumab-treated patients achieving ETS had markedly improved OS compared with docetaxel-treated patients achieving ETS (24-month OS 55% vs 32%); PFS was also markedly improved (24-month PFS 31% vs 4%). In contrast, for patients not achieving ETS, atezolizumab-treatment was associated with more modest OS (24-month OS 23% vs 20%) and PFS (24-month PFS 3% vs 1%) improvement compared with docetaxel. Overall, the effect size for ETS within the atezolizumab-treated patients was significantly greater than that in the docetaxel-treated patients (P(interaction)=0.002 for OS and P(interaction)<0.001 for PFS).ConclusionsETS is an easily measurable biomarker, predictive of highly favorable survival and patient-reported outcomes with atezolizumab treatment for advanced NSCLC. Further, ETS identifies patients with significantly greater treatment benefit for ICI therapy.

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Kooshyar, Mohammad Mehdi, Mohammadreza Nassiri, Aliasghar Aslaminezad, and Morteza Betaraf. "Feasibility study of SNPs detection associated with breast cancer by genome-wide association virtual studies." Journal of Clinical Oncology 31, no. 15_suppl (May 20, 2013): e22167-e22167. http://dx.doi.org/10.1200/jco.2013.31.15_suppl.e22167.

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e22167 Background: Available genomic data and genome-wide association virtual studies (GWAS), provide possibility of genetic markers detection known to be associated with the complex diseases. Genome-wide association studies, involving direct testing of genetic polymorphisms in large series of disease cases versus controls, provide a powerful approach to identify lower penetrance alleles that cannot be detected by genetic linkage studies. Methods: By utilizing genotyping platforms that can type hundreds of thousands of SNPs simultaneously, it is possible to conduct association studies using sets of SNPs that tag most known common variants in the genome, and hence scan associations without prior knowledge of function or position. GWAS have been conducted in five of the most common cancer types: breast, prostate, colorectal, lung and melanoma. GWAS of breast cancer was performed by simulation of 7 known SNPs on chromosomes 2, 5, 6, 8, 10, 11 and 16 for 10,000 women. Results: The strongest associations were found for rs2981582 in the FGFR2 gene. SNPs: rs889312 ° rs2180341 and rs3817198 were associated with breast cancer in benferroni significant level. However, SNPs: rs 13387042 ° rs2180341 and rs13281615 on chromosomes 2, 6 and 8 were not associated with breast. Conclusions: Results of this research show that the detection of SNPs associated with disease is easily possible through employing virtual systems based on real data of Hap Map project by using R software.

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Wąchalska, Magda, Michał Rychłowski, Kinga Grabowska, Kinga Kowal, Magdalena Narajczyk, Krystyna Bieńkowska-Szewczyk, and Andrea D. Lipińska. "Palmitoylated mNeonGreen Protein as a Tool for Visualization and Uptake Studies of Extracellular Vesicles." Membranes 10, no. 12 (November 27, 2020): 373. http://dx.doi.org/10.3390/membranes10120373.

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Extracellular vesicles (EVs) are membranous nanoparticles released by cells as vital mediators of intercellular communication. As such, EVs have become an attractive target for pathogens and cancer cells, which can take control over their cargo composition, as well as their trafficking, shaping the pathogenesis. Despite almost four decades of research on EVs, the number of specific and efficient EV labeling methods is limited, and there is still no universal method for the visualization of their transport in living cells. Lipophilic dyes that non-specifically intercalate into the EVs membranes may diffuse to other membranes, leading to the misinterpretation of the results. Here, we propose a palmitoylated fluorescent mNeonGreen (palmNG) protein as an alternative to chemical dyes for EVs visualization. The Branchiostoma lanceolatum-derived mNeonGreen is a brighter, more stable, and less sensitive to laser-induced bleaching alternative to green fluorescent protein (GFP), which makes it a more potent tag in a variety of fluorescence-based techniques. A palmNG-expressing stable human melanoma cell line was generated using retrovirus gene transfer and cell sorting. This protein partially localizes to cellular membranes, and can be detected inside size-exclusion (SEC)-purified EVs. With the use of flow cytometry and fluorescent confocal microscopy, we performed qualitative and quantitative analyses of palmNG-EVs uptake in recipient human hepatoma cells, in comparison to PKH67-labeled vesicles. Our findings confirm that membrane-embedded mNeonGreen can be successfully applied as a tool in EVs transfer and uptake studies.

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