A leading Neapolitan cancer researcher is under criminal investigation for fraud, the Italian press is reporting.
Although we have only rough translations of the story, it seems the researcher, Alfredo Fusco, of the National Council of Research’s Institute of Experimental Endocrinology and Oncology, has been accused of manipulating images in published studies and to strengthen the case for grants from the Italian Association for Cancer Research (AIRC).
The case covers eight papers published between 2001 and 2012, according to the media reports. We don’t know the specifics of the eight articles, nor why none appears yet to have been retracted. In our experience, the criminal inquiries usually follow the expose of scientific misconduct, not the other way around.
Fusco’s work is highly cited, with some 50 papers cited at least 100 times, according to Thomson Scientific’s Web of Knowledge.
According to the institute’s website:
The research group coordinated by Professor Alfredo Fusco has identified the CBX7 gene in a screening of a microarray with RNAs extracted from normal human thyroid primary cell culture and six human thyroid carcinoma cell lines of different histotype. The expression of the CBX7 gene is conspicuous in a normal thyroid cell line, but is absent or very low in all the cancerous cell lines. Previous studies demonstrated a deletion of the chromosomal region 22q13.1, where the CBX7 gene is located, in ovary, breast and colon carcinomas, characterized by an aggressive behaviour, suggesting the CBX7 gene as a candidate tumor suppression factor involved in the progression step of carcinogenesis of several neoplasias. In addition, CBX7 is involved in maintaining the transcriptionally repressive state of genes modifying chromatin. The aims of this project are: a) to evaluate the expression of CBX7 in several huan neoplastic diseases and correlate ot with the clonico-pathological status of the patients; b) to define the role of CBX7 in the process of thyroid cell transformation; c) to identify the genes regulated by CBX7; d) to investigate the mechanisms by which the CBX7 protein is possibly involved in the process of carcinogenesis; e) to generate and characterize null mice for the CBX7 gene.
The High Mobility Group A (HMGA) nonhistone chromatin proteins alter chromatin structure and, thereby, regulate the transcription of several genes by either enhancing or suppressing the activity of transcription factors. This protein family is implicated, through different mechanisms, in both benign and malignant neoplasias. Rearrangements of HMGA genes are a feature of most benign human mesenchymal tumors. Conversely, unrearranged HMGA overexpression is a feature of malignant tumors and is also causally related to neoplastic cell transformation. In our project we will investigate the mechanisms by which the HMGA genes contribute to carcinogenesis by identifying genes directly or indirectly regulated by HMGA and the proteins that physically interact with HMGA. The objectives of our project are: a) identification of the HMGA targets: isolation and characterization of the microRNAs (miRNAs) regulated by the HMGA proteins; b) definition of the role of the HMGA1 proteins in cancer progression by the identification and characterization of the interacting proteins; c) analysis of the HMGA-HIPK2-p53 pathway since previous studies of our group have shown that the p53 tumour suppressor activity may be impaired by the interaction of HMGA with p53 and/or the delocalization of HIPK2 induced by HMGA overexpression. Moreover, we will investigate the role of this pathway on the regulation of Bcl2 expression as suggested by our preliminary data and by the presence of AT-rich regions in the Bcl2 promoter region.
Thanks to Fabio Turone for translation help.