Conservation of SAA1-TLR4 signaling in human skeletal muscle identifies a therapeutically actionable tumor–host pathway and demonstrates that host deterioration can be targeted independently of tumor progression.
Findings identify SFRP2 as a key regulator of PDAC progression and support the development of SFRP2-targeted therapies as a novel treatment strategy for pancreatic cancer.
Olivia Sweatt, Lillian Hsu, Lety Reyes Angeles et al.· Cancer Research· 0 citations
An immunosuppressive tumor microenvironment (TME) is a hallmark of pancreatic ductal adenocarcinoma (PDAC), rendering most tumors resistant to immunotherapy approaches. Importantly, “tumor-to-stroma” crosstalk downstream of oncogenic KRAS has emerged as a major driver of immune evasion in PDAC, however the role of re...
Yuwenbin Li, Morgan L. Truitt, Dan Cao et al.· Cancer Research· 0 citations
Pancreatic ductal adenocarcinoma (PDAC) remains highly refractory to chemoimmunotherapy due in large part to its dense, immunosuppressive stroma. Cancer-associated fibroblasts (CAFs), the dominant stromal cell population, promote tumor progression through inflammatory signaling, aligned collagen-rich extracellula...
Camille Acevedo, Sayan Chakraborty, Samara P. Singh et al.· Cancer Research· 0 citations
Pancreatic ductal adenocarcinoma (PDAC) is characterized by a chronically inflamed tumor microenvironment (TME) driven by persistent activation of innate inflammatory signaling. Tumor progression locus 2 (TPL2; MAP3K8) is a serine/threonine kinase downstream of KRAS that activates both MAPK and NF-κB signaling; howev...
Hua-Ping Li, Yu-Tong Geng, Hung-Han Huang et al.· Cancer Research· 0 citations
First-line treatment for gastric cancer (GC) includes PD-1 blockade with chemotherapy, but resistance challenges treatment success. We identify Streptococcus anginosus (SA) as a tumor-resident oncobacterium driving GC progression and immune evasion. SA is enriched in GC patient tumors and drives tumor growth in mice. S...
Xiao-Shan Xie, Yue Wei, Jia-Ying Zheng et al.· Cell Host and Microbe· 0 citations
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