Live Cell Insights Publications Newsletter
Read our summaries of new and notable research articles using the IncuCyte Live Cell Analysis System, including hand-picked publications for applications and research areas like neuroscience, oncology, immunotherapy, and more!
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IncuCyte has reached 2,700 cited publications spanning a wide array of research areas and applications. We’ve experienced over 50% growth in publications in just the last year! Search our publications list to see what exciting research is being published using the IncuCyte® Live-Cell Analysis System.
The pathophysiology of schizophrenia is not well understood, with over 100 genomic regions associated with increased risk and structural abnormalities. Postmortem brain tissue samples from schizophrenia patients (SZ) indicate a reduction in synapse density, while rodent studies suggest a role for the genetic alleles of compliment component 4 (C4). Excessive synaptic pruning by microglia has been proposed for this reduced density, but the ability to replicate this process in vitro has thus far been limited.
In this study, Sellgren et al. developed a high-throughput, validated synaptosome (SYN) system using human induced microglia-like (iMG) cells, and iPSC-derived neurons to study synaptic pruning. Their data revealed an increased uptake of patient-derived synaptic structures from patient-derived (SZ) samples as compared to matched healthy controls, and this process was complement dependent. Similar results were also found in iMG and iPSC-derived neural cocultures. Though compliment plays a role, and the effects could not be attributed only to the associated human C4 risk factors.
Key findings include:
Read the full paper in Nature Neuroscience, February 2019.
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Microglia in the aged brain have impaired homeostatic function, which affects their ability to appropriately phagocytize CNS perturbations such as myelin debris and protein aggregates. The reasons for this impairment, and the resultant effects, are relatively uncharacterized.
This study by Pluvinage et al., from the Wyss-Coray lab at Stanford University, attempted to further characterize the underlying molecular mechanisms that may be responsible for microglial impairment with age, and attempted to restore microglial phagocytosis and observe the resultant effects on age-related brain dysfunction. CRISPR-Cas9 knockout screening was used for the identification of age-related genetic modifiers of microglial phagocytosis in the BV2 cell line. This data was combined with RNA sequencing analysis of hippocampal microglia from young and old mice. The authors then searched for age-upregulated or down-regulated microglial genes that, when subjected to knockout in BV2, resulted in promotion or inhibition of phagocytosis, respectively.
Key findings include:
Read the full paper in Nature, April 2019.
Additional commentary on this finding by Wei and Li Frontiers in Immunology, June 2019.
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The use of recombinant viral vectors in the pre-clinical development of genetic reprogramming of human T cells has been impeded by manufacturing, testing, and cost constraints. Attempts to use non-viral T cell genome targeting of DNA has been hampered by toxicity, especially with larger dsDNA templates.
In this study by Roth et al. from the Marson lab at the University of California, San Francisco, the authors attempted to reprogram human T-cell function using a CRISPR-Cas9 genomic targeting system for primary human T cells, circumventing the use of viral vectors. An efficient system was created for inserting large DNA sequences. This was achieved by performing co-electroporation of human primary T cells with CRISPR-Cas9 RNP complexes as well as long linear dsDNA. The study outlined an efficient method to gene edit human T cells, which remained viable and retained their functionality.
Key findings include:
Read the full paper in Nature, July 2018.
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Efforts toward targeted cancer therapy continue to expand, yet the actual efficacy of this approach has been less than optimal. This is partially due to limited identification of new therapeutic targets. An approach is need to advance and prioritize target identification.
In this paper by Behan, Iorio, and Picco, et al., the authors performed genome-scale CRISPR-Cas9 fitness screens in over 300 cancer cell lines representing 30 types of cancer (over 18,000 genes) in order to prioritize the unbiased discovery of drug candidates. This study presents a valuable framework for early drug discovery that may be used for more specific target identification with the goal of improving cancer therapeutic efficacy.
Key findings include:
Read the full paper in Nature, April 2019.
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Glioblastoma is especially difficult to treat using CAR-T cells directed against a single target. The heterogeneous nature of the tumor antigens, and outgrowth of tumors lacking the target allows for tumor escape from therapy.
In this communication, Choi et al. of the Maus laboratory at Harvard describe their efforts to combine CARs with BiTES, in a complementary manner, into one single T-cell product, CART-EGFRvIII.BiTE-EGFR, for administration as a more effective immune therapy for solid tumors. This construct was developed for the generation of CAR specific for glioblastoma-specific tumor antigen (EGFRvIII), and a bispecific T-Cell engager (BiTE) that is directed against wild-type EGFR (amplified in glioblastoma, not in normal brain) in an attempt to overcome antigen escape, immune suppression, and the exhaustion of T cells. This construct was developed to achieve targeting of multiple antigens and recruitment and activation of bystander T cells.
Key findings include:
Read the full paper in Nature Biotechnology, July 2019.
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The production of reactive oxygen species (ROS) by cancers had previously prompted consumption of antioxidant supplements for cancer prevention. However, recent data indicates that the value of administering antioxidants depends on the cancer and the context. Indeed, ROS have also been found to have anti-tumorigenic roles, preventing tumor progression, which may can be circumvented by antioxidants. In the case of lung cancer, it was previously known that dietary antioxidant supplementation and activation of endogenous antioxidants may actually cause the progression of early lung tumors. However, the potential influence of antioxidants on metastasis of lung cancer was uncharacterized.
In this study by Wiel et al., the authors combined genomic, metabolic, and data mining, with mouse models to study the role of ROS and antioxidants in the development of lung cancer metastasis, focusing on the transcription factor BACH1, which is responsive to oxidative stress.
Key findings include:
Read the full paper in Cell, July 2019.
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