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The Janus kinase (JAK) and signal transducer and activator of transcription (STAT) pathways are evolutionarily conserved transmembrane signaling mechanisms that ensure the ability of normal cellular communication with the external environment. Various cytokines, interferons, growth factors, and other specific molecules can activate JAK-STAT signaling to drive a range of physiological and pathological processes, including proliferation, metabolism, immune response, inflammation, and malignancy. However, the JAK-STAT signaling pathway and related gene mutations are closely associated with aberrant immune activation and cancer progression. Through extensive research into the structure and function of the JAK-STAT pathway, a variety of clinical drugs have emerged and been approved for the treatment of disease, primarily targeting cytokines and their receptors, JAK inhibitors and STAT inhibitors.

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Neuroinflammation is a vital immune response within the central nervous system (CNS), predominantly orchestrated by microglia and astrocytes. It is not merely a byproduct of neurodegeneration but also a pivotal catalyst in this process. These cells are the primary sources of inflammatory factors in neuroinflammation and are implicated in nearly all neurodegenerative diseases, including Alzheimer's and Parkinson's.

Several signaling pathways have been identified as being integral to the genesis of neuroinflammation. To advance our understanding and facilitate drug evaluation in this field, ICE has established a comprehensive neuroinflammation drug evaluation platform. This platform is designed to study the complex interplay of these pathways and to test potential therapeutics aimed at mitigating neuroinflammatory responses.

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Androgen Receptor (AR) belongs to the steroid receptor subfamily of the nuclear receptor superfamily. As a transcription factor, AR is responsible for regulating the physiological effects of androgens, such as testosterone and dihydrotestosterone (DHT), plays a pivotal role in the initiation and advancement of prostate cancer (PCa) and breast cancer (BC), with therapeutic approaches primarily focusing on the modulation of the AR signaling pathway.

We constructed an integrated experimental cascade, including biochemical and cell-based assays to conduct the high throughput hit-to-lead compound screening. Meanwhile, CDX modes are constructed for promisingly conducting in-vivo experiments and biomarker detection. Thus, ICE supports multiple approaches for helping the drug discovery and development of AR to facilitate the treatment of PCa and BC.

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The DNA damage response (DDR) encompasses a series of cellular processes that detect and repair genomic lesions. Targeting DDR pathways and inhibiting DNA repair mechanisms have emerged as promising strategies in cancer therapy, and significant progress has been made in the discovery of DDR-related inhibitors. However, drug resistance has become an increasingly prevalent challenge in this field. To better understand compound potency across various cancer cell lines, we generated drug-sensitive and drug-resistant cell lines by knocking out key DDR genes (e.g., BRCA1/2, XRCC1) and culturing cells under selective pressure from PARP inhibitors. Additionally, together with wild-type (WT) cells commonly used in DDR-related drug discovery, we established a DDR cell panel encompassing 14 distinct cancer types. This panel has been rigorously validated through in vitro proliferation assays and in vivo efficacy studies. Furthermore, sequencing and bioinformatic analyses have been employed to elucidate the mechanisms underlying drug sensitivity and resistance. Our findings demonstrate that this DDR cell panel offers a rapid and comprehensive platform for evaluating DDR inhibitors, thereby facilitating the efficient discovery of novel therapeutics in cancer treatment.