Results 71 to 80 of about 74,225 (263)

TNBC-derived Gal3BP/Gal3 complex induces immunosuppression through CD45 receptor

open access: yes, 2023
A preliminary study investigating immunotherapy strategies for aggressive triple negative breast cancer (TNBC) revealed an overexpression of genes involved in the release of extracellular vesicles (EVs).
Julia Lipovetsky   +4 more
core   +1 more source

CHST1 Drives Immunotherapy Resistance in Triple‐Negative Breast Cancer by Orchestrating an Immunosuppressive Microenvironment via the NKRF–CCL20–Macrophage Axis

open access: yesAdvanced Science, EarlyView.
Proposed model of CHST1‐associated immune remodeling in triple‐negative breast cancer. In CHST1‐low tumors, greater nuclear accumulation of NKRF is associated with repression of an NF‐κB‐related CCL20 transcriptional program and an immune‐inflamed microenvironment.
Shu‐Hao Jiang   +6 more
wiley   +1 more source

Inhibition of triple-negative breast cancer growth via delphinidin-mediated suppression of the JAK2/STAT3/PD-L1 pathway

open access: yesFood & Nutrition Research
Background: Breast cancer is a leading cause of cancer-related mortality among women globally, with triple-negative breast cancer (TNBC) being particularly aggressive.
Xiaoping Yu   +7 more
doaj   +1 more source

Recurrent triple-negative breast cancer (TNBC) tissues contain a higher amount of phosphatidylcholine (32:1) than non-recurrent TNBC tissues. [PDF]

open access: yes, 2017
Triple-negative breast cancer (TNBC) is one of the breast cancer subtype that displays a high risk of early recurrence and short overall survival. Improvement of the prognosis of patients with TNBC requires identifying a predictive factor of recurrence ...
Noritaka Masaki   +8 more
core   +1 more source

YTHDC1 Orchestrates Glucose and Glutamate Rewiring to Overcome Lethal Metabolic Stress in Triple‐Negative Breast Cancer

open access: yesAdvanced Science, EarlyView.
Lai et al. find that m6A reader YTHDC1 is specifically overexpressed in triple‐negative breast cancer (TNBC) and orchestrates glucose and glutamine metabolism in an m6A‐dependent manner to confer robust adaptability to lethal metabolic stress. Leveraging YTHDC1 knockdown‐induced metabolic vulnerability, an ATF4 mRNA‐targeted nanotherapy is developed to
Zheng‐Hao Lai   +12 more
wiley   +1 more source

Long‐term prognosis is associated with residual disease after neoadjuvant systemic therapy but not with initial nodal status

open access: yesBJS (British Journal of Surgery), EarlyView., 2020
This long‐term follow‐up study determined survival rates in a Swedish national cohort of 417 patients with breast cancer who all had neoadjuvant systemic therapy (NAST). Sentinel lymph node biopsy (SLNB) was performed before NAST in clinically node‐negative and after NAST in clinically node‐positive patients.
L. Zetterlund   +4 more
wiley   +1 more source

Antiproliferative effects of cetuximab on triple negative breast cancer cell line MDA-MB-231

open access: yesCumhuriyet Science Journal, 2020
In this study, antiproliferative effects of the anti-EGFR monoclonal antibody Cetuximab were evaluated using MDA-MB-231 cell line originated from triple negative breast cancer.
İdil Çetin
doaj   +1 more source

PRR15 deficiency facilitates malignant progression by mediating PI3K/Akt signaling and predicts clinical prognosis in triple-negative rather than non-triple-negative breast cancer

open access: yesCell Death and Disease, 2023
Triple-negative breast cancer (TNBC) is the most aggressive subtype of breast neoplasms with a higher risk of recurrence and metastasis than non-TNBC. Nevertheless, the factors responsible for the differences in the malignant behavior between TNBC and ...
Fengzhu Guo   +14 more
doaj   +1 more source

JAG1 Role in the Extravasation of Metastasized TNBC

open access: yes, 2022
Breast cancer is the second leading cause of cancer death in women. Triple negative breast cancer (TNBC) is an aggressive subclass defined by its lack of hormonal receptors and HER2 amplification.
Vegesna, Bhavya
core  

Cancer‐Associated Fibroblasts Promote Glucose Metabolic Reprogramming and Progression of Triple‐Negative Breast Cancer via Exosomal circFAD104‐Mediated Intercellular Communication

open access: yesAdvanced Science, EarlyView.
CAF‐derived exosomes deliver circFAD104 into TNBC cells, where it acts as a molecular scaffold that bridges the E3 ligase MARCHF8 and PGM1, promoting MARCHF8‐mediated K48‐linked ubiquitination and proteasomal degradation of PGM1. Loss of PGM1 redirects glucose‐phosphate flux from glycogen synthesis toward glycolysis, thereby driving stemness, EMT, and ...
Lei Wang   +16 more
wiley   +1 more source

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