Results 101 to 110 of about 1,101,660 (280)
, 2008 The paper shows, how incomplete split-plot designs can be constructed from -designs and how they can be analysed. The incomplete split-plot design can be regarded as both a practical and statistical compromise between traditional split-plot design and ...
Bigongiali, Federica +2 more
core +1 more source
Oncogenic DMTF1β promotes cancer cell motility by regulating autophagy through ULK1 stabilization
Molecular Oncology, EarlyView.In the current study, we demonstrate that the oncogene DMTF1β regulates ULK1 stability by reducing its proteasomal degradation in cancer cells. This stabilization enables ULK1 to induce autophagy, which in turn facilitates cancer cell migration. Consequently, reduced DMTF1β levels lead to decreased autophagy and impaired cancer cell migration.
Jun Xu +13 more
wiley +1 more source
Construction of estimation-equivalent second-order split-split-plot designs
, 2011 In many experimental settings, some experimental factors are very hard to change or very expensive to change, some factors are hard to change, and some factors are easy to change, which usually leads to a split-split-plot design.
RAJA, UZMA +6 more
core +2 more sources
Molecular Oncology, EarlyView.Breast cancer remains a major cause of cancer death in women, frequently developing endocrine therapy resistance. This study demonstrates that upregulated p21‐activated kinase 1 (PAK1) activity drives resistance to tamoxifen and long‐term estrogen deprivation in ER+ breast cancer models.
Luisa Schwarzmüller +10 more
wiley +1 more source
Molecular Oncology, EarlyView.The proposed mechanism of action for the CDK12/13 inhibitor and cyclin K degrader, CT7439. CDK12/13 inhibition interrupts transcription elongation, leading to increased DNA damage that results in cell death. This agent is a potentially novel treatment option for patients with colorectal cancer. Created in BioRender. Cyclin‐dependent kinase (CDK) 12 and
Wylie K. Watlington +10 more
wiley +1 more source
Cancer‐associated mutations in endometriosis reframe a benign disease through molecular oncology
Molecular Oncology, EarlyView.This review aims to comprehensively analyse cancer‐associated somatic mutations (CAMs) present in endometriotic lesions, emphasizing their biological roles, spatial distribution and implications for translational applications in medicine. By contextualizing a benign state within a genomic framework, this analysis seeks to establish its value as a ...
Clarissa Mujacic +15 more
wiley +1 more source
Molecular Oncology, EarlyView.LUNAR is a liver‐specific long noncoding RNA (lncRNA) that is highly expressed in normal liver but becomes epigenetically silenced in hepatocellular carcinoma through promoter hypermethylation. Loss of LUNAR is associated with NOTCH activation, epithelial–mesenchymal transition, and metastasis, whereas restoring LUNAR restrains metastatic progression ...
Se Ha Jang +9 more
wiley +1 more source
CEACAM1 participation in breast cancer progression
Molecular Oncology, EarlyView.In invasive breast cancer (BC), CEACAM1 shifts from an apical to a uniform membranous/cytoplasmic pattern, or is lost, as tumors dedifferentiate, inversely tracking the Ki‐67 proliferative index. In MCF‐7 cells, only CEACAM1‐4L suppresses proliferation, repressing cell cycle and growth factor genes.
Mykola Lyndin +3 more
wiley +1 more source
Paired split-plot designs of multireader multicase studies. [PDF]
J Med Imaging (Bellingham), 2018 Chen W, Gong Q, Gallas BD.
europepmc +1 more source
Pharmacological chromatin remodeling enhances response to estrogen therapy in ER+ breast cancer
Molecular Oncology, EarlyView.Estrogen therapy elicits clinical benefit in ~ 30% of patients with endocrine‐resistant estrogen receptor (ER)‐positive breast cancer. Based on findings that ER transcriptional activation underlies response to estrogen therapy, we tested the effects of epigenetic dysregulation via pharmacological inhibition of histone deacetylases (HDACi).
Anneka L. Johnson Thomas +16 more
wiley +1 more source