Overview of the Evalita 2018 task on Automatic Misogyny Identification (AMI)

Automatic Misogyny Identification (AMI) is a new shared task proposed for the first time at the Evalita 2018 evaluation campaign. The AMI challenge, based on both Italian and English tweets, is distinguished into two subtasks, i.e. Subtask A on misogyny identification and Subtask B about misogynistic behaviour categorization and target classification. Regarding the Italian language, we have received a total of 13 runs for Subtask A and 11 runs for Subtask B. Concerning the English language, we received 26 submissions for Subtask A and 23 runs for Subtask B. The participating systems have been distinguished according to the language, counting 6 teams for Italian and 10 teams for English. We present here an overview of the AMI shared task, the datasets, the evaluation methodology, the results obtained by the participants and a discussion of the methodology adopted by the teams. Finally, we draw some conclusions and discuss future work.Automatic Misogyny Identification (AMI) è un nuovo shared task proposto per la prima volta nella campagna di valutazione Evalita 2018. La sfida AMI, basata su tweet italiani e inglesi, si distingue in due sottotask ossia Subtask A relativo al riconoscimento della misoginia e Subtask B relativo alla categorizzazione di espressioni misogine e alla classificazione del soggetto target. Per quanto riguarda la lingua italiana, sono stati ricevuti un totale di 13 run per il Subtask A e 11 run per il Subtask B. Per quanto riguarda la lingua inglese, sono stati ricevuti 26 run per il Subtask A e 23 per Subtask B. I sistemi partecipanti sono stati distinti in base alla lingua, raccogliendo un totale di 6 team partecipanti per l’italiano e 10 team per l’inglese. Presentiamo di seguito una sintesi dello shared task AMI, i dataset, la metodologia di valutazione, i risultati ottenuti dai partecipanti e una discussione sulle metodologie adottate dai diversi team. Infine, vengono discusse conclusioni e delineati gli sviluppi futuri

AMI @ EVALITA2020: Automatic Misogyny Identification

Automatic Misogyny Identification (AMI) is a shared task proposed at the Evalita 2020 evaluation campaign. The AMI challenge, based on Italian tweets, is organized into two subtasks: (1) Subtask A about misogyny and aggressiveness identification and (2) Subtask B about the fairness of the model. At the end of the evaluation phase, we received a total of 20 runs for Subtask A and 11 runs for Subtask B, submitted by 8 teams. In this paper, we present an overview of the AMI shared task, the datasets, the evaluation methodology, the results obtained by the participants and a discussion about the methodology adopted by the teams. Finally, we draw some conclusions and discuss future work.Automatic Misogyny Identification (AMI) é uno shared task proposto nella campagna di valutazione Evalita 2020. La challenge AMI, basata su tweet italiani, si distingue in due sub-tasks: (1) subtask A che ha come obiettivo l’identificazione di testi misogini e aggressivi (2) subtask B relativo alla fairness del modello. Al termine della fase di valutazione, sono state ricevute un totale di 20 submissions per il subtask A e 11 per il subtask B, inviate da un totale di 8 team. Presentiamo di seguito una sintesi dello shared task AMI, i dataset, la metodologia di valutazione, i risultati ottenuti dai partecipanti e una discussione sulle metodologie adottate dai diversi team. Infine, vengono discusse le conclusioni e delineati gli sviluppi futuri

Tumor Immune Microenvironment and Genetic Alterations in Mesothelioma

Malignant pleural mesothelioma (MPM) is a rare and fatal disease of the pleural lining. Up to 80% of the MPM cases are linked to asbestos exposure. Even though its use has been banned in the industrialized countries, the cases continue to increase. MPM is a lethal cancer, with very little survival improvements in the last years, mirroring very limited therapeutic advances. Platinum-based chemotherapy in combination with pemetrexed and surgery are the standard of care, but prognosis is still unacceptably poor with median overall survival of approximately 12 months. The genomic landscape of MPM has been widely characterized showing a low mutational burden and the impairment of tumor suppressor genes. Among them, BAP1 and BLM are present as a germline inactivation in a small subset of patients and increases predisposition to tumorigenesis. Other studies have demonstrated a high frequency of mutations in DNA repair genes. Many therapy approaches targeting these alterations have emerged and are under evaluation in the clinic. High-throughput technologies have allowed the detection of more complex molecular events, like chromotripsis and revealed different transcriptional programs for each histological subtype. Transcriptional analysis has also paved the way to the study of tumor-infiltrating cells, thus shedding lights on the crosstalk between tumor cells and the microenvironment. The tumor microenvironment of MPM is indeed crucial for the pathogenesis and outcome of this disease; it is characterized by an inflammatory response to asbestos exposure, involving a variety of chemokines and suppressive immune cells such as M2-like macrophages and regulatory T cells. Another important feature of MPM is the dysregulation of microRNA expression, being frequently linked to cancer development and drug resistance. This review will give a detailed overview of all the above mentioned features of MPM in order to improve the understanding of this disease and the development of new therapeutic strategies

Molecularly defined diffuse leptomeningeal glioneuronal tumor (DLGNT) comprises two subgroups with distinct clinical and genetic features

Diffuse leptomeningeal glioneuronal tumors (DLGNT) represent rare CNS neoplasms which have been included in the 2016 update of the WHO classification. The wide spectrum of histopathological and radiological features can make this enigmatic tumor entity difficult to diagnose. In recent years, large-scale genomic and epigenomic analyses have afforded insight into key genetic alterations occurring in multiple types of brain tumors and provide unbiased, complementary tools to improve diagnostic accuracy. Through genome-wide DNA methylation screening of > 25,000 tumors, we discovered a molecularly distinct class comprising 30 tumors, mostly diagnosed histologically as DLGNTs. Copy-number profiles derived from the methylation arrays revealed unifying characteristics, including loss of chromosomal arm 1p in all cases. Furthermore, this molecular DLGNT class can be subdivided into two subgroups [DLGNT methylation class (MC)-1 and DLGNT methylation class (MC)-2], with all DLGNT-MC-2 additionally displaying a gain of chromosomal arm 1q. Co-deletion of 1p/19q, commonly seen in IDH-mutant oligodendroglioma, was frequently observed in DLGNT, especially in DLGNT-MC-1 cases. Both subgroups also had recurrent genetic alterations leading to an aberrant MAPK/ERK pathway, with KIAA1549:BRAF fusion being the most frequent event. Other alterations included fusions of NTRK1/2/3 and TRIM33:RAF1, adding up to an MAPK/ERK pathway activation identified in 80% of cases. In the DLGNT-MC-1 group, age at diagnosis was significantly lower (median 5 vs 14 years, p < 0.01) and clinical course less aggressive (5-year OS 100, vs 43% in DLGNT-MC-2). Our study proposes an additional molecular layer to the current histopathological classification of DLGNT, of particular use for cases without typical morphological or radiological characteristics, such as diffuse growth and radiologic leptomeningeal dissemination. Recurrent 1p deletion and MAPK/ERK pathway activation represent diagnostic biomarkers and therapeutic targets, respectively—laying the foundation for future clinical trials with, e.g., MEK inhibitors that may improve the clinical outcome of patients with DLGNT

The intracellular detection of MIP-1beta enhances the capacity to detect IFN-gamma mediated HIV-1-specific CD8 T-cell responses in a flow cytometric setting providing a sensitive alternative to the ELISPOT

<p>Abstract</p> <p>Background</p> <p>T-cell mediated immunity likely plays an important role in controlling HIV-1 infection and progression to AIDS. Several candidate vaccines against HIV-1 aim at stimulating cellular immune responses, either alone or together with the induction of neutralizing antibodies, and assays able to measure CD8 and CD4 T-cell responses need to be implemented. At present, the IFN-γ-based ELISPOT assay is considered the gold standard and it is broadly preferred as primary assay for detection of antigen-specific T-cell responses in vaccine trials. However, in spite of its high sensitivity, the measurement of the sole IFN-γ production provides limited information on the quality of the immune response. On the other hand, the introduction of polychromatic flow-cytometry-based assays such as the intracellular cytokine staining (ICS) strongly improved the capacity to detect several markers on a single cell level.</p> <p>Results</p> <p>The cumulative analysis of 275 samples from 31 different HIV-1 infected individuals using an ICS staining procedure optimized by our laboratories revealed that, following antigenic stimulation, IFN-γ producing T-cells were also producing MIP-1β whereas T-cells characterized by the sole production of IFN-γ were rare. Since the analysis of the combination of two functions decreases the background and the measurement of the IFN-γ+ MIP-1β+ T-cells was equivalent to the measurement of the total IFN-γ+ T-cells, we adopted the IFN-γ+ MIP-1β+ data analysis system to evaluate IFN-γ-based, antigen-specific T-cell responses. Comparison of our ICS assay with ELISPOT assays performed in two different experienced laboratories demonstrated that the IFN-γ+ MIP-1β+ data analysis system increased the sensitivity of the ICS up to levels comparable to the sensitivity of the ELISPOT assay.</p> <p>Conclusion</p> <p>The IFN-γ+ MIP-1β+ data evaluation system provides a clear advantage for the detection of low magnitude HIV-1-specific responses. These results are important to guide the choice for suitable highly sensitive immune assays and to build reagent panels able to accurately characterize the phenotype and function of responding T-cells. More importantly, the ICS assay can be used as primary assay to evaluate HIV-1-specific responses without losing sensitivity in comparison to the ELISPOT assay.</p

Tumor Immune Microenvironment and Genetic Alterations in Mesothelioma

Malignant pleural mesothelioma (MPM) is a rare and fatal disease of the pleural lining. Up to 80% of the MPM cases are linked to asbestos exposure. Even though its use has been banned in the industrialized countries, the cases continue to increase. MPM is a lethal cancer, with very little survival improvements in the last years, mirroring very limited therapeutic advances. Platinum-based chemotherapy in combination with pemetrexed and surgery are the standard of care, but prognosis is still unacceptably poor with median overall survival of approximately 12 months. The genomic landscape of MPM has been widely characterized showing a low mutational burden and the impairment of tumor suppressor genes. Among them, BAP1 and BLM are present as a germline inactivation in a small subset of patients and increases predisposition to tumorigenesis. Other studies have demonstrated a high frequency of mutations in DNA repair genes. Many therapy approaches targeting these alterations have emerged and are under evaluation in the clinic. High-throughput technologies have allowed the detection of more complex molecular events, like chromotripsis and revealed different transcriptional programs for each histological subtype. Transcriptional analysis has also paved the way to the study of tumor-infiltrating cells, thus shedding lights on the crosstalk between tumor cells and the microenvironment. The tumor microenvironment of MPM is indeed crucial for the pathogenesis and outcome of this disease; it is characterized by an inflammatory response to asbestos exposure, involving a variety of chemokines and suppressive immune cells such as M2-like macrophages and regulatory T cells. Another important feature of MPM is the dysregulation of microRNA expression, being frequently linked to cancer development and drug resistance. This review will give a detailed overview of all the above mentioned features of MPM in order to improve the understanding of this disease and the development of new therapeutic strategies