Background: The risk of skin cancer in solid organ transplant recipients (SOTR) is 50 to 100 times as great as in those without a transplant. Multiple factors, including immunosuppression, influence the development of post-transplantation skin cancer. Individuals with cardiac transplant are serially screened for organ rejection and immunosuppressive regimen effectiveness. Gene expression profiling of peripheral blood mononuclear cells has been established as a noninvasive test for monitoring cardiac rejection.
Objective: We examined individuals with cardiac transplant monitored using peripheral gene expression profiling to determine whether the profile of peripheral blood mononuclear cell activity could correlate with the development of post-transplantation skin cancer.
Methods And Materials: Sixty-one patient records were examined for initial endomyocardial biopsy results, gene expression profiling data, immunosuppressive regimens, and post-transplantation skin cancer.
Results: There was no relationship between acute rejection and the development of skin cancer. No relationship between peripheral gene expression profiling and the development of post-transplantation skin cancer was observed. The most common skin cancer in the population was squamous cell carcinoma. SOTR suppressed with azathioprine had a significantly higher incidence of squamous cell carcinoma.
Conclusion: Although gene expression tests have advanced transplant surveillance, they were not associated with post-transplantation skin cancer.
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http://dx.doi.org/10.1111/dsu.12315 | DOI Listing |
Cancer Metab
January 2025
Department of Dermatology, Venereology and Allergology, University Medical Center and Medical Faculty Mannheim, Heidelberg University, Theodor-Kutzer-Ufer 1-3, Mannheim, 68167, Germany.
Background: In malignant melanoma, liver metastases significantly reduce survival, even despite highly effective new therapies. Given the increase in metabolic liver diseases such as metabolic dysfunction-associated steatotic liver disease (MASLD) and metabolic dysfunction-associated steatohepatitis (MASH), this study investigated the impact of liver sinusoidal endothelial cell (LSEC)-specific alterations in MASLD/MASH on hepatic melanoma metastasis.
Methods: Mice were fed a choline-deficient L-amino acid-defined (CDAA) diet for ten weeks to induce MASH-associated liver fibrosis, or a CDAA diet or a high fat diet (HFD) for shorter periods of time to induce early steatosis-associated alterations.
Sci Rep
January 2025
Wallace H. Coulter Department of Biomedical Engineering, Emory University and Georgia Institute of Technology, Atlanta, GA, USA.
The lymphatic system plays complex, often contradictory, roles in many cancers, including melanoma; these roles include contributions to tumor cell metastasis and immunosuppression in the tumor microenvironment as well as generation of antitumor immunity. Advancing our understanding of lymphatic vessel involvement in regulating tumor growth and immune response may provide new therapeutic targets or treatment plans to enhance the efficacy of existing therapies. We utilized a syngeneic murine melanoma model in which we surgically disrupted the lymphatic vessel network draining from the tumor to the tumor-draining lymph node (TDLN) while leaving the TDLN intact.
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January 2025
Department of Dermatology, Asan Medical Center, University of Ulsan College of Medicine, 88, Olympic-ro 43-gil, Songpa-gu, Seoul, 05505, Korea.
There is limited data on the risk of second primary malignancies (SPMs) in Asian melanoma survivors. This study aimed to identify the risk of SPMs in Asian melanoma survivors. Standardized incidence ratios (SIRs) were calculated for overall and specific SPMs.
View Article and Find Full Text PDFCytokine Growth Factor Rev
January 2025
MCW Cancer Center and Genomic Sciences and Precision Medicine Center, Medical College of Wisconsin, Milwaukee, WI, USA; WIN Consortium, Paris, France; University of Nebraska, Lincoln, NE, USA. Electronic address:
IL-17A, referred to as IL-17, is the founding member of a family of pro-inflammatory cytokines, including IL-17B, IL-17C, IL-17D, IL-17E (or IL-25), and IL-17F, which act via receptors IL-17RA to IL-17RE, and elicit potent cellular responses that impact diverse diseases. IL-17's interactions with various cytokines include forming a heterodimer with IL-17F and being stimulated by IL-23's activation of Th17 cells, which can lead to inflammation and autoimmunity. IL-17 is implicated in infectious diseases and inflammatory disorders such as rheumatoid arthritis and psoriasis, promoting neutrophil recruitment and anti-bacterial immunity, but potentially exacerbating fungal and viral infections, revealing its dual role as protective and pathologic.
View Article and Find Full Text PDFOpen Biol
January 2025
Laboratory of Integrative Biology, Institute of Molecular Genetics of the Czech Academy of Sciences, Prague, Czechia.
Epithelia are multicellular sheets that form barriers defining the internal and external environments. The constant stresses acting at this interface require that epithelial sheets are mechanically robust and provide a selective barrier to the hostile exterior. These properties are mediated by cellular junctions which are physically linked with heavily crosslinked cytoskeletal networks.
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