Results 101 to 110 of about 14,586 (245)

Hippo pathway at the crossroads of stemness and therapeutic resistance in breast cancer

Molecular Oncology, EarlyView.
Dysregulation of the Hippo pathway drives nuclear accumulation of YAP/TAZ, activating stemness‐related transcriptional programs that sustain breast cancer stemness and fuel therapeutic resistance across subtypes, underscoring Hippo signaling as a targetable vulnerability. Figure created and edited with BioRender.com.
Giulia Schiavoni, Antonella Palmese, Stefano Scalera, Laura Cipriani, Davide Mascolo, Patrizia Vici, Teresa Arcuri, Lorena Filomeno, Eriseld Krasniqi, Giovanni Blandino, Giulia Bon, Marcello Maugeri‐Saccà   +11 more
wiley   +1 more source

E2A selectively regulates TGF‐β–induced apoptosis in KRAS‐mutant non‐small cell lung cancer

Molecular Oncology, EarlyView.
Ability to induce apoptosis by TGF‐β is frequently lost in advanced lung adenocarcinoma despite intact TGF‐β signaling. We identify E2A as a mutant KRAS–dependent mediator of resistance to TGF‐β–induced apoptosis. TGF‐β induces E2A via SMAD3 in mutant KRAS cells, and E2A silencing restores apoptosis and enhances radiation response in cell lines ...
Sergei Chuikov, Shiva Krishna Katkam, Zhefan Wang, Venkateshwar G. Keshamouni   +3 more
wiley   +1 more source

Cell‐cycle‐specific lesion evolution rather than inhibition of double‐strand‐break repair underpins cisplatin radiosensitization

Molecular Oncology, EarlyView.
We analyze cisplatin–DNA adducts (CDAs) and double‐strand breaks (DSBs) in a cell‐cycle‐dependent manner. We find that CDAs form similarly across all cell cycle phases. DSBs arise only in S‐phase. CDAs might not directly impair DSB repair, but S‐phase DSB lesions evolve in the presence of CDAs and disrupt repair in G2, also causing radiosensitization ...
Ye Qiu, Xixi Lin, Emil Mladenov, Veronika Mladenova, Jürgen Thomale, Ali Sak, Yao Wang, Yunxuan Deng, Eleni Gkika, Martin Stuschke, George Iliakis   +10 more
wiley   +1 more source

Design and methodology of a cluster-randomised controlled trial on cash plus interventions for preventing child wasting in Somalia. [PDF]

J Glob Health
Walton S, Alier KK, Garretson S, Grounds S, Khattak Q, Tripaldi M, Loddo F, Mohamoud SA, Nur MA, Abdiqadir SM, Mitchell E, Mahat MB, Gure M, Jibril DI, Gedi D, Ocircan M, Ismail MO, Farah AA, Mohamed AA, Mohamed AA, Akseer N.   +20 more
europepmc   +1 more source

Hijacking emergency granulopoiesis: Neutrophil ontogeny and reprogramming in cancer

Molecular Oncology, EarlyView.
Neutrophils are highly plastic innate immune cells; their functions in cancer extend beyond the tumour microenvironment. This Review summarises current understanding of neutrophil maturation and heterogeneity and highlights tumour‐induced granulopoiesis as a systemic programme that expands immature, immunosuppressive neutrophils via tumour‐derived ...
Gabriela Marinescu, Yi Feng
wiley   +1 more source

Public health interventions for Non-Communicable Diseases (NCDs) in humanitarian emergencies: an overview of systematic reviews. [PDF]

BMC Public Health
Aoun A, Bou-Karroum L, Chidiac N, Idriss-Wheeler D, El-Jardali F.   +4 more
europepmc   +1 more source

NKCC1: A key regulator of glioblastoma progression

Molecular Oncology, EarlyView.
Glioblastoma (GBM) progression is driven by disrupted chloride cotransporter homeostasis. NKCC1 is highly expressed in stem‐like, astrocytic, and progenitor cells, correlating with earlier recurrence, while overall survival remains unaffected. NKCC1 serves as a prognostic marker and potential therapeutic target, linking chloride transporter imbalance ...
Anja Thomsen, Diana Freitag, Madlen Haase, Christian Senft, Falko Schwarz, Silke Keiner   +5 more
wiley   +1 more source

Humanitarian Intervention

, 2010
openaire   +5 more sources

Starved futures in the Gaza Strip: long-term outcomes of childhood malnutrition as a humanitarian emergency. [PDF]

BMJ Glob Health
Rabayaa M, Rabaya D.
europepmc   +1 more source

Targeting TNBC: core–shell polycationic polyurea dendrimers with inherent anticancer activity

FEBS Open Bio, EarlyView.
Core–shell polycationic PURE dendrimers were tested in TNBC‐derived tumor models. Both formulations selectively targeted TNBC and effectively reduced tumor volume. PUREG4‐OEI48 suppressed tumor growth without detectable toxicity, whereas PUREG4‐OCEI24, despite showing efficacy, induced hepatic toxicity.
Adriana Cruz, Bruna Abreu, Cindy Mendes, Catarina Freitas‐Dias, Filipe Gonçalves, Fernanda Silva, José Ramalho, Saudade André, Vasco D. B. Bonifácio, Jacinta Serpa   +9 more
wiley   +1 more source