Results 181 to 190 of about 287,154 (333)
Recent Advances in Immunotherapy for Breast Cancer: A Review
Qian-Er Wen,1 Liang Li,1 Rui-Qi Feng,1 De-Hui Li,2 Chang Qiao,1 Xiao-Song Xu,3 Yan-Jing Zhang2 1Graduate School, Hebei University of Chinese Medicine, Shijiazhuang, Hebei Province, People’s Republic of China; 2Oncology Department II, The First Affiliated
Wen QE +6 more
doaj
64P Comprehensive genomic analysis of primary triple negative breast cancer prior to neoadjuvant chemotherapy [PDF]
Monika Drobnienė +5 more
openalex +1 more source
CDK4/6 inhibition promotes CD8+ T cell expansion through tumor‐macrophage crosstalk by activating HIF‐1α and enhancing MIF‐CD44/CD74 signaling. This reprograms TAMs to boost MHC‐I antigen presentation, and CDK4/6 inhibitor‐trained M1 TAM supernatant therapy synergizes with low‐dose PD‐1 blockade to restore antitumor immunity.
Lin He +17 more
wiley +1 more source
Snord17, through interaction with Thoc3, promotes nuclear export and translation of Yy2 mRNA in Snord17+/+ ISCs. The Yy2 protein subsequently binds the Tead4 promoter to promote its transcription, activating Hippo signaling, which is essential for ISC maintenance.
Peikang Zhang +10 more
wiley +1 more source
HOXB7 overexpression leads triple-negative breast cancer cells to a less aggressive phenotype [PDF]
Simone Aparecida de Bessa Garcia +3 more
openalex +1 more source
Chemotherapy‐induced efferocytosis drives ovarian cancer stem cell enrichment. By engulfing apoptotic cancer cells, macrophages upregulate ODC1 and produce putrescine, which elevates osteopontin (OPN) expression. Secreted OPN then activates the CD44 receptor on cancer cells, promoting stemness and chemoresistance.
Wenhan Li +19 more
wiley +1 more source
A home-based lifestyle intervention program reduces the tumorigenic potential of triple-negative breast cancer cells [PDF]
Giulia Baldelli +13 more
openalex +1 more source
This study provides the first evidence that PM2.5 impairs iWAT browning via PTG‐mediated glycogen metabolism disruption, which is initiated by ADRB3 inhibition and subsequently triggers VEGFB upregulation. It thereby delineates the ADRB3‐PTG‐VEGFB axis as central to PM2.5‐induced metabolic dysfunction and identifies adipose glycogen metabolism as a ...
Limin Wang +12 more
wiley +1 more source

