RESUMO
Fusobacterium nucleatum (F. nucleatum) is a Gram-negative anaerobic bacterium that plays a key role in the development of oral inflammation, such as periodontitis and gingivitis. In the last 10 years, F. nucleatum has been identified as a prevalent bacterium associated with colorectal adenocarcinoma and has also been linked to cancer progression, metastasis and poor disease outcome. While the role of F. nucleatum in colon carcinogenesis has been intensively studied, its role in gastric carcinogenesis is still poorly understood. Although Helicobacter pylori infection has historically been recognized as the strongest risk factor for the development of gastric cancer (GC), with recent advances in DNA sequencing technology, other members of the gastric microbial community, and F. nucleatum in particular, have received increasing attention. In this review, we summarize the existing knowledge on the involvement of F. nucleatum in gastric carcinogenesis and address the potential translational and clinical significance of F. nucleatum in GC.
Assuntos
Carcinogênese , Infecções por Fusobacterium , Fusobacterium nucleatum , Neoplasias Gástricas , Humanos , Neoplasias Gástricas/microbiologia , Neoplasias Gástricas/patologia , Fusobacterium nucleatum/patogenicidade , Infecções por Fusobacterium/microbiologia , Infecções por Fusobacterium/complicações , Infecções por Helicobacter/microbiologia , Infecções por Helicobacter/complicações , Helicobacter pylori/patogenicidade , Helicobacter pylori/genética , Fatores de Risco , Microbioma Gastrointestinal , Animais , Mucosa Gástrica/microbiologia , Mucosa Gástrica/patologia , Estômago/microbiologia , Estômago/patologia , Adenocarcinoma/microbiologia , Adenocarcinoma/patologiaRESUMO
Clear cell renal cell carcinoma is the most common and deadly type of cancer affecting the kidney, and is characterized histologically by large intracellular lipid deposits. These deposits are thought to result from lipid metabolic reprogramming occurring in tumor cells, but the exact mechanisms and implications of these metabolic alterations are incompletely understood. Obesity is an independent risk factor for clear cell renal cell carcinoma, and is also associated with lipid accumulation in noncancerous epithelial cells of the proximal tubule, where clear cell renal cell carcinoma originates. This article explores the potential link between obesity-associated renal lipid metabolic disturbances and lipid metabolic reprogramming in clear cell renal cell carcinoma, and discusses potential implications for future research.