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Insulin-Like Growth Factor II mRNA-Binding Protein 3 Expression Correlates with Poor Prognosis in Acral Lentiginous Melanoma.

ABSTRACT: Insulin-like growth factor-II mRNA-binding protein 3 (IMP-3) is an RNA-binding protein expressed in multiple cancers, including melanomas. However, the expression of IMP-3 has not been investigated in acral lentiginous melanoma (ALM). This study sought to elucidate its prognostic value in ALMs. IMP-3 expression was studied in 93 patients diagnosed with ALM via immunohistochemistry. Univariate and multivariate analyses for survival were performed, according to clinical and histologic parameters, using the Cox proportional hazard model. Survival curves were graphed using the Kaplan-Meier method. IMP-3 was over-expressed in 70 out of 93 tumors (75.3%). IMP-3 expression correlated with thick and high-stage tumor and predicted poorer overall, melanoma-specific, recurrence-free and distant metastasis-free survivals (P = 0.002, 0.006, 0.008 and 0.012, respectively). Further analysis showed that patients with tumor thickness ? 4.0 mm and positive IMP-3 expression had a significantly worse melanoma-specific survival than those without IMP-3 expression (P = 0.048). IMP-3 (hazard ratio 3.67, 95% confidence intervals 1.35-9.97, P = 0.011) was confirmed to be an independent prognostic factor for melanoma-specific survival in multivariate survival analysis. Positive IMP-3 expression was an important prognostic factor for ALMs.

SUBMITTER: Sheen YS

PROVIDER: S-EPMC4721868 | biostudies-literature | 2016

REPOSITORIES: biostudies-literature

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Poor Lymphocyte Infiltration to Primary Tumors in Acral Lentiginous Melanoma and Mucosal Melanoma Compared to Cutaneous Melanoma.

Project description:Recent clinical trials have demonstrated the efficacy of immune checkpoint inhibitors (ICIs) for treating melanoma. However, these previous studies comprised mainly Caucasian populations, in which cutaneous melanoma (CM) is the major clinical type. In contrast, Asian populations have a distinct profile of melanoma and show much higher frequencies of acral lentiginous melanoma (ALM) and mucosal melanoma (MCM). Compared with CM, ALM and MCM show poorer response to ICIs, but the mechanisms have not been fully understood. To evaluate the immune status in each melanoma subtype, we examined the number of total tumor-infiltrating lymphocytes (TILs), CD4+ TILs, CD8+ TILs, and tumor-infiltrating FoxP3+ regulatory T cells (Tregs) to evaluate the immune status in each melanoma subtype using data from 137 patients with melanoma. Total TIL numbers in ALM and MCM were significantly lower than that in CM. CD4+ TIL number in MCM was also lower than CM although CD4+ TIL number in ALM was comparable with CM. In contrast, CD8+ TIL numbers in both ALM and MCM were significantly lower than that in CM. Although number of tumor-infiltrating Tregs was comparable among the 3 subtypes, the proportion of tumor-infiltrating Tregs in CD4+ T cells in MCM was significantly higher than in CM and ALM. Multivariate regression analysis revealed that ALM and MCM were significantly associated with a lower total TIL number, but only MCM was significantly associated with a lower CD4+ TIL number. Multivariate regression analysis also revealed that both ALM and MCM were significantly associated with a lower CD8+ TIL number. Our results suggest that both ALM and MCM are independent factors of lower total TIL number, which may be associated with poorer responses to ICIs in ALM and MCM.

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| S-EPMC8342238 | biostudies-literature

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Genetic alterations in RAS-regulated pathway in acral lentiginous melanoma.

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Acral lentiginous melanoma-Population, treatment, and survival using the NCDB from 2004 to 2015.

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Project description:Background:AURKA kinase is an essential serine/threonine kinase for mitosis and chromosome stability. The aberrant amplification and overexpression of AURKA are commonly observed in various types of cancer, including cutaneous melanoma. However, the status and the clinical significance of AURKA copy number (CN) in acral melanoma (AM) have not been fully elucidated. Methods: Four hundred and seventy-two AM samples were included in the study. AURKA CN was examined using the QuantiGenePlex DNA Assay. We analysed the relationship of AURKA CN to clinicopathological characteristics and survival of patients with AM. Results: In this study, AURKA copy gain (set as more than 2.0 copies) was detected in 24.6% (116/472) of the samples. We did not observe any obvious correlation between clinicopathological characteristics and AURKA copy gain of the patients. However, patients with AURKA copy gain had a significantly shorter overall survival time (OS) and progression-free survival time (PFS) than those with normal AURKA CN (OS: P = 0.022; PFS: P < 0.001). Furthermore, multivariate Cox regression analysis showed that AURKA copy gain was an independent poor prognostic factor for patients with AM undergoing adjuvant interferon therapy. Conclusions: This study suggested that AURKA copy gain is an adverse prognostic factor for AM. Furthermore, AURKA copy gain may be a useful biomarker to predict the outcome of interferon therapy in patients with AM.

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| S-EPMC6956422 | biostudies-literature

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