Results 131 to 140 of about 3,580,419 (303)

Breast cancer chemoprevention : economic and policy considerations. [PDF]

open access: yes
The potential for chemoprevention of breast cancer depends on the benefits being achieved at reasonable cost. This study assesses the economics of chemoprevention of breast cancer with tamoxifen within the context of the ...
Frater, Alison
core   +1 more source

Mutant p53R273H disrupts PDPK1 homodimerization and contributes to PDPK1 activation

open access: yesMolecular Oncology, EarlyView.
How mutant p53R273H drives AKT signaling is unclear. We show that p53R273H, but not wild‐type, directly binds PDPK1 via a mutation‐dependent conformational change. This interaction disrupts inhibitory PDPK1 homodimerization and enhances AKT phosphorylation.
Mei Chee Lim   +11 more
wiley   +1 more source

Lactate mitochondrial oxidation drives stemness potential in metastatic breast cancer

open access: yesNature Communications
Metastatic cancer cells, originating from cancer stem cells with metastatic capacity, utilize nutrient flexibility to navigate the challenges of the metastatic cascade.
Jia-Jia Zhang   +16 more
doaj   +1 more source

Hydrostatic pressure activates HIF‐1α via β‐catenin to promote stemness in breast cancer cells

open access: yesFEBS Open Bio, EarlyView.
To mimic the elevated intestinal fluid pressure in breast cancers, we loaded human breast cancer cells (MCF‐7, MDA‐MB‐453, and BT‐474) to 50 mmHg hydrostatic pressure. Hydrostatic pressure exposure upregulated HIF‐1α and induced stemness in MCF‐7 and BT‐474 cells.
Da Zhai   +8 more
wiley   +1 more source

Aquaporin‐3 and aquaporin‐5 impact the development of pancreatic ductal adenocarcinoma spheroids

open access: yesFEBS Open Bio, EarlyView.
Schematic representation of the role of aquaporin‐3 (AQP3) and aquaporin‐5 (AQP5) in pancreatic ductal adenocarcinoma (PDAC). Both proteins are upregulated in PDAC and are associated with tumor progression and metastatic potential. Silencing AQP3 or AQP5 in PDAC spheroids results in decreased diameter, area, and overall growth, underscoring their key ...
Catarina Pimpão   +3 more
wiley   +1 more source

Pertuzumab in Metastatic Breast Cancer [PDF]

open access: yesJournal of the Advanced Practitioner in Oncology, 2012
Rachana, Patel, Jill S, Bates
openaire   +2 more sources

Loss of AMBRA1 activates MAPK and angiogenesis signaling pathways in melanoma cells

open access: yesFEBS Open Bio, EarlyView.
Loss of AMBRA1 in melanoma cells activates multiple oncogenic pathways associated with tumor progression. Transcriptomic and protein network analyses revealed that AMBRA1 depletion enhances MAPK/ERK signaling, angiogenesis, TGF‐β/EMT signaling, and Wnt/axon guidance pathways.
Milad Ibrahim   +4 more
wiley   +1 more source

Exercise boost after surgery improves survival in model of metastatic breast cancer

open access: yesFrontiers in Immunology
IntroductionDespite advances in breast cancer diagnosis and treatment of the primary tumor, metastatic breast cancer tumors remain largely incurable, and their growth is responsible for the majority of breast cancer-related deaths.
Rikke Stagaard   +13 more
doaj   +1 more source

From energy provision to protein synthesis: Tunnelling nanotubes as mediators of intercellular metabolic cooperation in cancer

open access: yesFEBS Open Bio, EarlyView.
The cytoskeleton‐mediated transport of mitochondria via tunnelling nanotubes restores respiration, increases ATP production, rescues cells from apoptosis, activates the AKT/mTOR signalling pathway, promotes cell migration and invasiveness, contributes to cancer progression and treatment resistance.
Stanislava Martínková, Jan Trnka
wiley   +1 more source

GGNBP2 suppresses triple-negative breast cancer aggressiveness through inhibition of IL-6/STAT3 signaling activation

open access: yes, 2018
Background Triple-negative breast cancer (TNBC) is the most aggressive subtype of breast cancer, lacking effective targeted therapies, and whose underlying mechanisms are still unclear.
Liu, Jingjing   +7 more
core   +1 more source

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