The COVID-19 pandemic has highlighted long-term health concerns of viral pneumonia, yet its potential impact on cancer development and growth remains poorly understood. Here, we demonstrate that prior infection with SARS-CoV-2 or influenza virus promoted lung tumor progression by reprogramming the local immune landscape. Retrospective clinical analysis revealed that patients hospitalized with COVID-19 exhibited increased lung cancer incidence. Using multiple murine lung cancer models, we show that prior severe respiratory viral infections accelerated tumor growth and reduced survival. Mechanistically, prior viral pneumonia epigenetically remodeled the lung to establish a pro-tumor microenvironment, including the local accumulation of SiglecFhi tumor-associated neutrophils, a transcriptionally reprogrammed, immunosuppressive population whose signature predicted poor prognosis in human lung adenocarcinoma. In parallel, epithelial compartments exhibited altered differentiation trajectories, with persistence of injury-associated alveolar intermediates positioned along tumorigenic lineages. We observe sustained chromatin remodeling at key cytokine loci in immune and structure cells, linking inflammatory memory to persistent immune suppression. Therapeutically, combined inhibition of neutrophil recruitment via CXCR2 and PD-L1 signaling restored CD8⁺ T cell infiltration and suppressed tumor growth. Together, our findings establish a direct causal relationship between viral pneumonia, including COVID-19, and lung tumorigenesis, highlighting the urgent need to monitor survivors for elevated cancer risk and to develop targeted interventions and therapies aimed at preventing potential cancer bursts in COVID-19 convalescents. ![Figure][1]</img> ### Competing Interest Statement The authors have declared no competing interest. NIH Common Fund, https://ror.org/001d55x84, AI147394, AG069264, AI112844, HL170961, AI176171 and AG090337 [1]: pending:yes

The kinase GSK3β drives the metabolism supporting the inflammatory function of pathogenic TH1 cells.

New methylome data from marsupials indicate that genome-wide DNA methylation erasure is restricted to extraembryonic tissues. Ozren Bogdanovic discusses the implications of these findings for understa...

Oncogenic KRAS drives lipid reprogramming in pancreatic ductal adenocarcinoma (PDAC) to promote disease progression, and these changes are manifest in circulation. Using mass spectrometry, we performed lipidomic analyses on plasmas from a cohort of 93 newly-diagnosed resectable PDAC cases, 43 patients with chronic pancreatitis, and 93 age- and sex-matched healthy controls, the results of which revealed pronounced reductions in circulating lysophosphatidylcholines (LysoPC) as a prominent feature associated with PDAC. Using stable-isotope resolved lipidomics, we further found that PDAC cells exhibit a lipid scavenging phenotype characterized by preferential uptake of extracellular unsaturated LysoPCs to sustain pro-growth signals. Restricting bioavailability of extracellular unsaturated LysoPCs shifted the metabolic phenotype of PDAC cells towards enhanced de novo lipogenesis and autophagy, which was accompanied by suppression of AKT signaling activities and increased susceptibility to apoptosis. Using bulk, single-cell, and spatial transcriptomic datasets together with functional experiments, we identified oncogenic KRAS-mediated upregulation of major facilitator superfamily domain-containing protein 2a (MFSD2A) as a key mediator that facilitates extracellular uptake of LysoPCs in PDAC cells. Loss of MFSD2A expression mimicked LysoPC restriction and resulted in inhibition of AKT signaling and increased propensity of PDAC cells to undergo apoptosis in vitro and suppressed tumor growth in vivo. Therapeutic targeting of the KRAS-MFSD2A-LysoPC axis via repurposing of the synthetic alkyl-lysophospholipid edelfosine promoted potent anti-cancer effects in vitro that were mechanistically attributed to reduced extracellular uptake of LysoPCs, and attenuation of AKT signaling. Collectively, our findings describe a previously unrecognized onco-metabolic program of enhanced LysoPC scavenging mediated by MFSD2A that promotes PDAC progression and that is therapeutically targetable via repurposing edelfosine.

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WASHINGTON – Yesterday, U.S. Senator Jeanne Shaheen (D-NH), Ranking Member of the Senate Foreign Relations Committee, and Representative Gregory W....

The study identified Mycobacterium abscessus-induced DNA damage as a driver of senescence through reprogramming of alveolar macrophages. Treatment of navitoclax in chronic infection model reduced bact...