Detection of fraudulent campaigns on donation-based crowdfunding platforms using a combination of machine

In today’s world where acts of kindness are seldom and rare, there are still many people who are able and willing to help their fellow human beings. One such way of doing that is donating to a crowdfunding campaign. People in need of financial assistance describe their stories on a crowdfunding platform and generous people donate to these campaigns. Even in such a noble cause, there are malicious actors who post fake campaigns and misuse the donations made to the campaign. In this study, we propose a fraud detection method to classify a campaign as genuine or fake. We have collected the details of non-fraudulent campaigns from ww.GoFundMe.com and we are collecting details of fraudulent campaigns from www.GoFraudMe.com. We propose a combination of machine learning classifier and a rule-based classifier to classify a campaign as genuine or fake. We have based our rule-based classifier on theories in deception which uses cognitive load, certainty, emotion, and distancing strategy depicted in a text. We then aggregate the results of these two classifiers to label a campaign as genuine or fake. Fraudulent campaigns add up to $30M and hence their detection has significant practical use

Growth hormone upregulates melanocyte-inducing transcription factor expression and activity via JAK2-STAT5 and SRC signaling in GH receptor-positive human melanoma

© 2019 by the authors. Licensee MDPI, Basel, Switzerland. Growth hormone (GH) facilitates therapy resistance in the cancers of breast, colon, endometrium, and melanoma. The GH-stimulated pathways responsible for this resistance were identified as suppression of apoptosis, induction of epithelial-to-mesenchymal transition (EMT), and upregulated drug efflux by increased expression of ATP-binding cassette containing multidrug efflux pumps (ABC-transporters). In extremely drug-resistant melanoma, ABC-transporters have also been reported to mediate drug sequestration in intracellular melanosomes, thereby reducing drug efficacy. Melanocyte-inducing transcription factor (MITF) is the master regulator of melanocyte and melanoma cell fate as well as the melanosomal machinery. MITF targets such as the oncogene MET, as well as MITF-mediated processes such as resistance to radiation therapy, are both known to be upregulated by GH. Therefore, we chose to query the direct effects of GH on MITF expression and activity towards conferring chemoresistance in melanoma. Here, we demonstrate that GH significantly upregulates MITF as well as the MITF target genes following treatment with multiple anticancer drug treatments such as chemotherapy, BRAF-inhibitors, as well as tyrosine-kinase inhibitors. GH action also upregulated MITF-regulated processes such as melanogenesis and tyrosinase activity. Significant elevation in MITF and MITF target gene expression was also observed in mouse B16F10 melanoma cells and xenografts in bovine GH transgenic (bGH) mice compared to wild-type littermates. Through pathway inhibitor analysis we identified that both the JAK2-STAT5 and SRC activities were critical for the observed effects. Additionally, a retrospective analysis of gene expression data from GTEx, NCI60, CCLE, and TCGA databases corroborated our observed correlation of MITF function and GH action. Therefore, we present in vitro, in vivo, and in silico evidence which strongly implicates the GH–GHR axis in inducing chemoresistance in human melanoma by driving MITF-regulated and ABC-transporter-mediated drug clearance pathways