Consumer-facing technology fraud: Economics, attack methods and potential solutions

The emerging use of modern technologies has not only benefited society but also attracted fraudsters and criminals to misuse the technology for financial benefits. Fraud over the Internet has increased dramatically, resulting in an annual loss of billions of dollars to customers and service providers worldwide. Much of such fraud directly impacts individuals, both in the case of browser-based and mobile-based Internet services, as well as when using traditional telephony services, either through landline phones or mobiles. It is important that users of the technology should be both informed of fraud, as well as protected from frauds through fraud detection and prevention systems. In this paper, we present the anatomy of frauds for different consumer-facing technologies from three broad perspectives - we discuss Internet, mobile and traditional telecommunication, from the perspectives of losses through frauds over the technology, fraud attack mechanisms and systems used for detecting and preventing frauds. The paper also provides recommendations for securing emerging technologies from fraud and attacks.N/

Genomic hallmarks and therapeutic implications of G0 cell cycle arrest in cancer

BACKGROUND: Therapy resistance in cancer is often driven by a subpopulation of cells that are temporarily arrested in a non-proliferative G0 state, which is difficult to capture and whose mutational drivers remain largely unknown. RESULTS: We develop methodology to robustly identify this state from transcriptomic signals and characterise its prevalence and genomic constraints in solid primary tumours. We show that G0 arrest preferentially emerges in the context of more stable, less mutated genomes which maintain TP53 integrity and lack the hallmarks of DNA damage repair deficiency, while presenting increased APOBEC mutagenesis. We employ machine learning to uncover novel genomic dependencies of this process and validate the role of the centrosomal gene CEP89 as a modulator of proliferation and G0 arrest capacity. Lastly, we demonstrate that G0 arrest underlies unfavourable responses to various therapies exploiting cell cycle, kinase signalling and epigenetic mechanisms in single-cell data. CONCLUSIONS: We propose a G0 arrest transcriptional signature that is linked with therapeutic resistance and can be used to further study and clinically track this state

Data Study Group Final Report: Roche

Data Study Groups are week-long events at The Alan Turing Institute bringing together some of the country’s top talent from data science, artificial intelligence, and wider fields, to analyse real-world data science challenges. Roche: Personalised lung cancer treatment modelling using electronic health records and genomics Cancer immunotherapy (CIT) is a promising new type of cancer treatment that uses the patient’s own immune system to fight cancer cells. CIT drugs work to stop the cancer cells from turning off the immune system’s T-cells by inhibiting the PD-L1 produced by the tumour cells (PD-L1 is a protein that binds to PD-1 receptors on T-cells and prevents the immune system from attacking the cancer cells). CIT is currently being used to treat patients with non-small cell lung cancer (NSCLC) for whom chemotherapy or other drugs have failed. CIT is also be-ing used as part of the first-line treatment in patients with advanced NSCLC (aNSCLC - stage III and higher). Theoretically, patients with high PD-L1 ex-pression levels are more likely to respond well to CIT; however, in practice, patient outcomes vary considerably. In this data study group, we investigated different approaches for predicting survival time for patients treated with CIT as first line of treatment, using both electronic health records and tumour genomic data. We also investigated the causal effects of CIT vs other oncology treatments, and studied treatment heterogeneity. The results contribute to identifying patients who are most likely to benefit from CIT

Genomic hallmarks and therapeutic implications of G0 cell cycle arrest in cancer

BackgroundTherapy resistance in cancer is often driven by a subpopulation of cells that are temporarily arrested in a non-proliferative G0 state, which is difficult to capture and whose mutational drivers remain largely unknown.ResultsWe develop methodology to robustly identify this state from transcriptomic signals and characterise its prevalence and genomic constraints in solid primary tumours. We show that G0 arrest preferentially emerges in the context of more stable, less mutated genomes which maintain TP53 integrity and lack the hallmarks of DNA damage repair deficiency, while presenting increased APOBEC mutagenesis. We employ machine learning to uncover novel genomic dependencies of this process and validate the role of the centrosomal gene CEP89 as a modulator of proliferation and G0 arrest capacity. Lastly, we demonstrate that G0 arrest underlies unfavourable responses to various therapies exploiting cell cycle, kinase signalling and epigenetic mechanisms in single-cell data.ConclusionsWe propose a G0 arrest transcriptional signature that is linked with therapeutic resistance and can be used to further study and clinically track this state