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New cell atlas of COVID lungs reveals why SARS-CoV-2 is deadly and different


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NEW YORK, NY (April 29, 2021) A new study is drawing the most detailed picture yet of SARS-CoV-2 infection in the lung, revealing mechanisms that result in lethal COVID-19, and may explain long-term complications and show how COVID-19 differs from other infectious diseases.
Led by researchers at Columbia University Vagelos College of Physicians and Surgeons and Herbert Irving Comprehensive Cancer Center, the study found that in patients who died of the infection, COVID-19 unleashed a detrimental trifecta of runaway inflammation, direct destruction and impaired regeneration of lung cells involved in gas exchange, and accelerated lung scarring.
Though the study looked at lungs from patients who had died of the disease, it provides solid leads as to why survivors of severe COVID may experience long-term respiratory complications due to lung scarring. ....

Cornell University , New York , United States , Mailman School Of Public Health , Columbia University , Arnolds Han , Olivier Elemento , Eli Lilly , Benjamin Izar , Denis Schapiro Harvard , Huachao Huang , Ajay Nair , Aveline Filliol , Yinshan Fang , Robert Schwabe , Olivier Elemento Cornell , Johannesc Melms , Hanina Hibshoosh , Xinzhengv Guo , Louisv Gerstner Jr , Andrea Califano , Jayh Lefkowitch , Georgea Alba , Emmanuel Zorn , Roberte Schwartz , Yiping Wang ,

Big data analysis finds cancer's key vulnerabilities


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NEW YORK, NY (Jan. 11, 2021) Thousands of different genetic mutations have been implicated in cancer, but a new analysis of almost 10,000 patients found that regardless of the cancer s origin, tumors could be stratified in only 112 subtypes and that, within each subtype, the Master Regulator proteins that control the cancer s transcriptional state were virtually identical, independent of the specific genetic mutations of each patient.
The study, published Jan. 11 in
Cell, confirms that Master Regulators provide the molecular logic that integrates the effect of many different and patient-specific mutations to implement the transcriptional state of a specific tumor subtype, thus greatly expanding the fraction of patients who may respond to the same treatment. ....

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