Showing posts with label fadA. Show all posts
Showing posts with label fadA. Show all posts

Saturday, 14 February 2026

Role of Fusobacterium nucleatum and KRAS Genotype in Colorectal Cancer Development | Chapter 9 | An Overview of Disease and Health Research Vol. 9

 

Fusobacterium nucleatum (Fn) and activating mutations in the Kirsten rat sarcoma viral oncogene homolog (KRAS) are increasingly recognised as synergistic drivers of colorectal cancer (CRC). Fn promotes tumorigenesis through several mechanisms, such as virulence factors including FadA and Fap2. KRAS mutations amplify proliferative and inflammatory signalling. This chapter explores how Fn enhances KRAS-driven oncogenic cascades and how KRAS-mutant epithelium fosters bacterial colonisation. We also examine KRAS as a prognostic biomarker and highlight emerging microbiome-targeted strategies. Understanding this microbial–genetic crosstalk provides a foundation for precision prevention and combined therapeutic approaches in CRC.

 

Author(s) Details

Ahmed Dewan
College of Life Sciences, Anhui Agriculture University, Hefei 230036, China.

 

Ivan Tattoli
Department of Translational and Precision Medicine, Sapienza University of Rome, 00185 Rome, Italy.

 

Maria Teresa Mascellino
Department of Public Health and Infectious Diseases, Sapienza University of Rome, 00185 Rome, Italy.

 

Please see the book here :- https://doi.org/10.9734/bpi/aodhr/v9/7037

Wednesday, 3 May 2023

G-Protein Signaling Pathway (GP-SP) and Voriconazole-Resistance (VCZ-R) in Aspergillus species | Chapter 4 | Research Advances in Microbiology and Biotechnology Vol. 5

 The study aims to judge the possible part of G-protein signaling pathway genes in VCZ-R in Aspergillus class. Patients with negotiated immune wholes continue to have a large melancholy from invasive contaminations caused by Aspergillus class. Mortality is still high despite the chance of various azoles, containing isavuconazole (ISZ), posaconazole (POS), voriconazole (VCZ), and itraconazole (ITZ).  Several studies from cancer and relocate centres around the world have proved that azole resistance has arose in clinical and incidental isolates of Aspergillus fumigatus and Aspergillus flavus.   Using wild-type and particular mutant strains of Aspergillus variety, CLSI based susceptibleness and cyp51 gene-particular PCR studies were carried out to analyze the phenotypic changes and changes in the triazole-susceptibleness pattern. It is plausible that various different indicating pathways function in Aspergillus spp. the G-protein signaling pathway has existed shown expected a dominant manager of conidiation in several closely connected Aspergillus spp. Voriconazole inhibits conidiation in A. flavus, probably through its effect on various genes involved in the GP-SP. Our findings indicate that VCZ suppresses conidiation by collect on one of the important G-protein pathway genes, and that distinguishing changes in these genes are probably being the reason for the loss of conidiation and VCZ-R in A. flavus. Testing for cross opposition to additional triazoles, such as POS and ISZ, is more necessary. Our artificial studies comparing the efficiency of azoles using conidia or hyphal masses as inoculums show that hyphae are more opposing to antifungal killing distinguished to conidia.Author(s) Details:


Lulu Farhana,
John D. Dingell VA Medical Center, USA and Wayne State University, Detroit, MI, USA.

Jagdeesh Natesan,
Boston University, Boston, MA, USA.

Suganthini Krishnan,
John D. Dingell VA Medical Center, USA and Wayne State University, Detroit, MI, USA.

Please see the link here: https://stm.bookpi.org/RAMB-V5/article/view/10482