Association of inflammatory blood markers and pathological complete response in HER2-positive breast cancer: a retrospective single-center cohort study.

Introduction: The association between inflammatory blood markers (IBMs) (monocyte-to-lymphocyte ratio [MLR], neutrophil-to-lymphocyte ratio [NLR], and platelet-to-lymphocyte ratio [PLR]) and breast cancer has been extensively studied. However, the predictive role of IBMs in the neoadjuvant response of human epidermal growth factor receptor 2 (HER2)-positive breast cancer remains unclear.

Methods: This study included 744 patients with HER2 positive breast cancer treated with neoadjuvant therapy.

Identification of sequence polymorphism in the D-loop region of mitochondrial DNA as a risk factor for breast cancer.

Mitochondrial DNA (mtDNA) variations affect the efficiency of the electron transport chain and production of reactive oxygen species, contributing to carcinogenesis. The D-loop region of mtDNA has emerged as a variation hotspot region in human neoplasia; however, the potential contribution of these variations in breast cancer risk prediction remains unknown. We investigated the relationship between germline single nucleotide polymorphisms (SNPs) in the entire D-loop region and breast cancer risk in Chinese women.

MAZ-mediated up-regulation of BCKDK reprograms glucose metabolism and promotes growth by regulating glucose-6-phosphate dehydrogenase stability in triple-negative breast cancer.

Tumour metabolic reprogramming is pivotal for tumour survival and proliferation. Investigating potential molecular mechanisms within the heterogeneous and clinically aggressive triple-negative breast cancer (TNBC) subtype is essential to identifying novel therapeutic targets. Accordingly, we investigated the role of branched-chain α-keto acid dehydrogenase kinase (BCKDK) in promoting tumorigenesis in TNBC.