Oops, you're using an old version of your browser so some of the features on this page may not be displaying properly.

MINIMAL Requirements: Google Chrome 24+Mozilla Firefox 20+Internet Explorer 11Opera 15–18Apple Safari 7SeaMonkey 2.15-2.23

Poster Display session 1

4185 - Modulation of Risk of Cutaneous Melanoma Patients by Variants in STAT3 Gene and Functional Analysis


28 Sep 2019


Poster Display session 1


Basic Science

Tumour Site


Gabriela Gomez


Annals of Oncology (2019) 30 (suppl_5): v1-v24. 10.1093/annonc/mdz238


G.V.B. Gomez1, L.M.O. Monteiro2, R.S. Rocha2, G.J. Lourenço1, C.S.P. Lima1

Author affiliations

  • 1 Department Of Internal Medicine, Faculty Of Medical Sciences, University of Campinas, 13083-888 - São Paulo/BR
  • 2 Department Of Cellular And Molecular Biology, University of São Paulo, 14049-900 - São Paulo/BR


Login to get immediate access to this content.

If you do not have an ESMO account, please create one for free.

Abstract 4185


The JAK/STAT signaling pathway supports the development, progression and metastatic potential of cutaneous melanoma (CM). In normal cells the activation of STAT3 is rapid and transient, but in abnormal melanocytes the activation of the protein occurs in a constitutive manner favoring tumor expansion. STAT3 is coded by the polymorphic gene in humans and thus it is possible that normal individuals show inherited differences in pathway functionality. The aim of the study was to evaluate whether STAT3 c.*1671T>C and STAT3 c.-1937C>G variants influence the risk of CM patients and its functional consequences.


We evaluated 248 MC patients and 274 controls. DNA was analyzed by real-time polymerase chain reaction (PCR) for genotyping. Luciferase assay and gene expression in a genetically modified SK-MEL-28 melanoma cell line to present the STAT3 c.-1937C>G ancestral and variant genotypes were realized in study. Differences between groups were assessed by the Fisher or chi-square test. Comparisons of luciferase and gene expression were performed using t-tests and ANOVA or Mann-Whitney and Kruskal-Wallis tests.


Individuals with STAT3 c.*1671TT and T allele, and STAT3 c.-1937CC genotype had 1.76 (95% CI: 1.08-2.85, P = 0.02), 1.42 (95% CI: 1.03-1.96, P = 0.02) and 1.67 (95% CI: 1.06-2.63, P = 0.02)-fold increased risks of CM than individuals with the other genotypes and allele, respectively. Individuals with TC haplotype of the STAT3 variants were at 1.70 (95% CI: 1.22-2.36, P = 0.001)-fold increased risk of CM than those with other haplotypes. In a genetically modified melanoma cell line to present the distinct genotypes of STAT3 c.-1937C> G, we observed a 30% increase in the promoter activity of the gene and increase of mRNA in cells with the CC genotype compared to those with the GG genotype.


The data present, for the first time, preliminary evidence that inherited abnormalities in the JAK/STAT pathway, related to STAT3 gene, alter the CM risk. These results may contribute to identify individuals at high risk for CM, who deserve special measures for prevention or early diagnosis.

Clinical trial identification

Editorial acknowledgement

Legal entity responsible for the study

The authors.




All authors have declared no conflicts of interest.

This site uses cookies. Some of these cookies are essential, while others help us improve your experience by providing insights into how the site is being used.

For more detailed information on the cookies we use, please check our Privacy Policy.

Customise settings
  • Necessary cookies enable core functionality. The website cannot function properly without these cookies, and you can only disable them by changing your browser preferences.