title: TLRs: linking inflammation and breast cancer.
abstract: Breast cancer is one of the leading causes of mortality in the females. Intensive efforts have been made to understand the molecular mechanisms of pathogenesis of breast cancer. The physiological conditions that lead to tumorigenesis including breast cancer are not well understood. Toll like receptors (TLRs) are essential components of innate immune system that protect the host against bacterial and viral infection. The emerging evidences suggest that TLRs are activated through pathogen associated molecular patterns (PAMPs) as well as endogenous molecules, which lead to the activation of inflammatory pathways. This leads to increased levels of several pro-inflammatory cytokines and chemokines mounting inflammation. Several evidences support the view that chronic inflammation can lead to cancerous condition. Inflammation aids in tumor progression and metastasis. Association of inflammation with breast cancer is emerging. TLR mediated activation of NF-κB and IRF is an essential link connecting inflammation to cancer. The recent reports provide several evidences, which suggest the important role of TLRs in breast cancer pathogenesis and recurrence. The current review focuses on emerging studies suggesting the strong linkages of TLR mediated regulation of inflammation during breast cancer and its metastasis emphasizing the initiation of the systematic study.
authors.affiliation: Department of Bio-Chemistry, The M.S. University of Baroda, Vadodara 390002, Gujarat, India.
authors.forename: Khyati
authors.initials: K
authors.lastname: Bhatelia
authors.affiliation: Department of Bio-Chemistry, The M.S. University of Baroda, Vadodara 390002, Gujarat, India.
authors.forename: Kritarth
authors.initials: K
authors.lastname: Singh
authors.affiliation: Department of Bio-Chemistry, The M.S. University of Baroda, Vadodara 390002, Gujarat, India. Electronic address: singhraj1975@gmail.com.
authors.forename: Rajesh
authors.initials: R
authors.lastname: Singh
mesh_terms: D000818:Animals; D001943:Breast Neoplasms / Q000209:etiology / Q000235:genetics / Q000378:metabolism* / Q000401:mortality / Q000473:pathology; D018925:Chemokines / Q000235:genetics / Q000378:metabolism; D002908:Chronic Disease; D005260:Female; D006801:Humans; D007249:Inflammation / Q000235:genetics / Q000378:metabolism / Q000401:mortality / Q000473:pathology; D051379:Mice; D016328:NF-kappa B / Q000235:genetics / Q000378:metabolism; D009363:Neoplasm Proteins / Q000235:genetics / Q000378:metabolism*; D051193:Toll-Like Receptors / Q000235:genetics / Q000378:metabolism*
chemical_list: D018925:Chemokines; D016328:NF-kappa B; D009363:Neoplasm Proteins; D051193:Toll-Like Receptors
keywords: Breast cancer; Inflammation; NF-κB; TLRs