Results 101 to 110 of about 69,701 (316)

To Be or not to Be? A Critical Appraisal of the Welfare of Children Conceived through New Reproductive Technologies [PDF]

open access: yes, 2008
Over three million children are believed to have been born worldwide - and over 200,000 annually - as a result of “new reproductive technologies” (NRTs).
Blyth, Eric
core   +1 more source

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

open access: yesMolecular 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   +3 more
wiley   +1 more source

2014 Assisted Reproductive Technology National Summary Report [PDF]

open access: yes
The data for this national report come from the 458 fertility clinics in operation in 2014 that provided and verified data on the outcomes of all ART cycles started in their clinics. Of the 208,604 ART cycles performed in 2014 at these reporting clinics,

core  

Assisted fertilization

open access: yes, 2023
Assisted reproduction has recently entered the field of interest of researchers and physicians and has become an open topic of research. Considering the 1.5 million babies born with assisted reproductive techniques today, we can also understand why this ...
Yapıcı, Tunahan, Aghayeva, Aynura
core  

CD47 promotes mitogen‐activated protein kinase and epithelial‐to‐mesenchymal transition molecular programs to drive prometastatic phenotypes in non‐small cell lung cancer

open access: yesMolecular Oncology, EarlyView.
Beyond its role in immune evasion, this study identified that CD47 drives tumor‐intrinsic signaling in non‐small cell lung cancer (NSCLC). Transcriptomic profiling and functional studies revealed that CD47 regulates cell adhesion, migration, and metastasis through an ERK–EMT signaling axis.
Asa P.Y. Lau   +8 more
wiley   +1 more source

Circulating tumor cell viability during and after radiotherapy mirrors treatment response in cancer patients

open access: yesMolecular Oncology, EarlyView.
Radiotherapy (RT) response depends on the DNA repair capacity of tumor and host cells. We show that circulating tumor cell (CTC) counts and apoptosis rates before and after RT predict treatment response and outcome, which can be accessed via easily accessible liquid biopsy approaches. Created in BioRender. Wikman, H.
Yvonne Goy   +10 more
wiley   +1 more source

2011 Assisted Reproductive Technology National Summary Report [PDF]

open access: yes
The data for this national report come from the 451 fertility clinics in operation in 2011 that provided and verified data on the outcomes of all ART cycles started in their clinics.

core  

Stimulator of interferon genes agonist augmented antitumor immunity of osimertinib in Egfr‐mutated lung cancer

open access: yesMolecular Oncology, EarlyView.
Combining osimertinib with the STING agonist ADU‐S100 activates innate and adaptive immunity to overcome the non‐inflamed microenvironment of Egfr‐mutant lung cancer. This combination increases NK and CD8+ T‐cell infiltration, associated with activation of the STING‐IRF3 pathway and local immunogenic cell death.
Jun Nishimura   +19 more
wiley   +1 more source

2018 Assisted Reproductive Technology National Summary Report [PDF]

open access: yes
The data for this national report come from the 456 US fertility clinics in operation in 2018 that provided and verified data on the outcomes of all ART cycles started in their clinics.

core  

Loss of IGF‐1R impairs DNA‐PKcs recruitment to chromatin leading to defective end‐joining

open access: yesMolecular Oncology, EarlyView.
IGF‐1R promotes radioresistance by facilitating DNA‐PKcs recruitment to chromatin, enabling non‐homologous end‐joining (NHEJ) repair of double‐strand breaks. Inhibition or loss of IGF‐1R disrupts this recruitment to damage sites, driving compensatory reliance on microhomology‐mediated end‐joining (MMEJ) repair.
Matthew O. Ellis   +3 more
wiley   +1 more source

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