Results 101 to 110 of about 4,504,301 (301)

Extracellular vesicle lipidomics liquid biopsy reveals systemic and tumor microenvironment metabolic reprogramming in ovarian cancer

open access: yesMolecular Oncology, EarlyView.
Extracellular vesicle (EV) lipidomic profiling of plasma and ascites from patients with high‐grade serous ovarian cancer and of ovarian cancer cell lines reveals enrichment of triglycerides (TGs), diacylglycerols (DGs), phosphatidylcholine (PCs), sphingomyelins (SMs), reflecting tumor metabolic reprogramming.
Shikha Rani   +9 more
wiley   +1 more source

Editorial: Recent innovation in breast reconstructive surgery

open access: yesFrontiers in Surgery, 2023
Andrea Lisa   +3 more
doaj   +1 more source

Regulation of the lncRNA NEAT1 by p53‐ΔNp63 crosstalk modulates the DNA damage response and therapeutic efficacy in HNSCC

open access: yesMolecular Oncology, EarlyView.
In head and neck squamous cell carcinoma (HNSCC) p53 and p63 exert opposite roles on the transcription regulation of the lncRNA NEAT1. Under basal conditions, p53 levels are low and p63 represses NEAT1 expression. Upon genotoxic stress, p53 is rapidly induced, displacing p63 from the NEAT1 promoter leading to NEAT1 transcriptional activation and ...
Sara De Domenico   +5 more
wiley   +1 more source

Management of patients with ventriculoperitoneal shunts in breast surgeries

open access: yesJPRAS Open
Ventriculoperitoneal (VP) shunts often pass through the anterior chest involving the breast parenchyma. Operating on patients with VP shunts necessitates extra caution during breast surgeries.
Osama Darras   +5 more
doaj   +1 more source

APOBEC3 activity and DNA polymerase‐ε deficiency are associated with distinct IDH1 R132 hotspot mutations

open access: yesMolecular Oncology, EarlyView.
Isocitrate dehydrogenase 1 (IDH1) mutations are highly recurrent in multiple human cancer types, including cholangiocarcinoma and glioma. IDH1 R132C is the most common IDH1 mutation in cholangiocarcinoma and likely arises from APOBEC3A‐ or APOBEC3B‐mediated deamination.
Kelly E. Butler   +3 more
wiley   +1 more source

Comparison of Vertical and Inverted-T Mammaplasties Using Photographic Measurements

open access: yesPlastic and Reconstructive Surgery, Global Open, 2013
Background: Surgeons have long debated the relative merits of vertical and inverted-T mammaplasties. These debates have centered on surgeons’ opinions. Without measurements, this controversy is unlikely to be resolved.
Eric Swanson, MD
doaj   +1 more source

Influence of stromal–epithelial interactions on breast cancer in vitro and in vivo

open access: yes, 2019
Stromal cell-secreted chemokines including CCL2 have been implicated in the primary tumor microenvironment, as mediators of tumor cell migration, proliferation, and angiogenesis.
Dwyer, Róisín M.   +6 more
core   +1 more source

SPHINX31 acts as a SRPK1 inhibitor targeting the ATR/DNA‐PKcs/CHK1 replicative checkpoint to inhibit cell growth in non‐small cell lung cancer

open access: yesMolecular Oncology, EarlyView.
The kinase SRPK1 directly interacts with the protein TOPBP1 and regulates the pre‐mRNA splicing of WIZ thereby contributing to the activation of the ATR/CHK1 replicative checkpoint in response to replicative stress. This allows cancer cells' genomic stability and survival.
Amani Shreim   +17 more
wiley   +1 more source

Multilevel Breast Reduction: A Retrospective Study of 338 Breast Reduction Surgeries

open access: yesPlastic and Reconstructive Surgery - Global Open, 2019
Background: Aesthetic breast reduction is a common plastic surgery procedure with the potential for considerable improvement of the patient’s quality of life in addition to its aesthetic value. Many different approaches have been described for breast reduction to improve upon previous techniques in terms of scarring, nipple ...
Borenstein, Amiram, Friedman, Or
openaire   +2 more sources

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

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