HSP-70, C-myc and HLA-DR were examined in patients with cutaneous malignant melanoma metastatic to lymph nodes. Lymph-nodal fine-needle aspiration biopsies (FNABs) were analyzed and the results were correlated to other variables, such as the gender of the patients, Clark level and Breslow thickness of the primary tumor. Thirty cases of metastatic melanoma in lymph nodes from 30 patients with cutaneous malignant melanoma were studied. All patients (100%) had microscopic regional nodal metastasis and a recurrence of the lesion during the first two years. The HSP-70, C-myc and HLA-DR expressions were investigated immunocytologically, using the APAAP (alkaline phosphatase) method on the FNAB samples. The immunocytochemical expressions of HSP-70 protein, C-myc oncogene, and HLA-DR antigen were found in 18 cases (60%), in 14 cases (43.3%) and in 12 cases (40%), respectively. Clark levels were significantly associated with HSP-70 protein (< 0.01), C-myc oncogene expression (< 0.05) and HLA-DR antigen (< 0.01) expression. The HLA-DR antigen was also found to be related (< 0.05) to higher Breslow thickness (> 1.5 mm). The clinical course of malignant cutaneous melanoma is related to the expression of these indices, which seem to play a significant role in the metastasis and prognosis of this aggressive tumor. The immunocytochemical expression of HSP-70 in the malignant melanoma tumor could be of particular value in the identification of patients with poor prognosis.
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J Dermatol Sci
January 2025
Department of Biochemistry, Institute of Biomedical & Health Sciences, Hiroshima University, Hiroshima, Japan; Department of Frontier Science and Interdisciplinary Research, Faculty of Medicine, Kanazawa University, Ishikawa, Japan. Electronic address:
Background: Melanocytes protect the body from ultraviolet radiation by synthesizing melanin. Tyrosinase, a key enzyme in melanin production, accumulates in the endoplasmic reticulum (ER) during melanin synthesis, potentially causing ER stress. However, regulating ER function for melanin synthesis has been less studied than controlling Tyrosinase activity.
View Article and Find Full Text PDFInt J Biol Macromol
January 2025
College of Life Science, Yangtze University, Jingzhou, China. Electronic address:
Tyrosinase is a rate-limiting enzyme for melanogenesis and abnormal melanin production can be controlled by utilizing tyrosinase inhibitory substances. To develop potent and safe inhibitors of tyrosinase, complex tannins a narrowly distributed plant polyphenols were prepared from the fruit peel of Euryale ferox (EPTs) and then structurally characterized, as well as investigated for their inhibitory effects and the involved mechanisms against tyrosinase activity and melanogenesis. The structures of EPTs were established to consist of 63.
View Article and Find Full Text PDFCell Syst
January 2025
Rutgers Cancer Institute, Rutgers, the State University of New Jersey, New Brunswick, NJ, USA. Electronic address:
Treatment resistance poses a significant challenge in the care of cancer patients. Hirsch et al. applied computational and genomic approaches, examining gene expression dynamics from a mouse model of melanoma at single-cell resolution to reveal that semi-heritable non-genetic alterations in tumor cell populations confer adaptive resistance to treatment.
View Article and Find Full Text PDFJ Cachexia Sarcopenia Muscle
February 2025
Center for Health Information Partnerships, Northwestern University Feinberg School of Medicine, Chicago, Illinois, USA.
Background: Cancer-associated cachexia can inhibit immune checkpoint inhibitor (ICI) therapy efficacy. Cachexia's effect on ICI therapy has not been studied in large cohorts of cancer patients aside from lung cancer. We studied associations between real-world routinely collected clinical cachexia markers and disability-free, hospitalization-free and overall survival of cancer patients.
View Article and Find Full Text PDFJ Clin Invest
January 2025
State Key Laboratory of Oncology in South China, Guangdong Provincial Clinical Research Center for Cancer, Sun Yat-sen University Cancer Center, Guangzhou, China.
Stimulator of interferon genes (STING) agonists have been developed and tested in clinical trials for their antitumor activity. However, the specific cell population(s) responsible for such STING activation-induced antitumor immunity have not been completely understood. In this study, we demonstrated that endothelial STING expression was critical for STING agonist-induced antitumor activity.
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