Results 141 to 150 of about 22,423,968 (289)

CEACAM1 participation in breast cancer progression

open access: yesMolecular 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

Adjustable Visual Appearance for Generalizable Novel View Synthesis

open access: yes
We present a generalizable novel view synthesis method which enables modifying the visual appearance of an observed scene so rendered views match a target weather or lighting condition without any scene specific training or access to reference views at the target condition.
Josef Bengtson   +4 more
openaire   +2 more sources

Splatent: Splatting Diffusion Latents for Novel View Synthesis

open access: yesCoRR
CVPR 2026. Project's webpage at https://orhir.github.io/Splatent/
Or Hirschorn   +8 more
openaire   +3 more sources

Pharmacological chromatin remodeling enhances response to estrogen therapy in ER+ breast cancer

open access: yesMolecular 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

PANoptosis in the pathogenesis of myelodysplastic syndromes

open access: yesMolecular Oncology, EarlyView.
PANoptosis, a combination of three types of programmed cell death, is mediated by a large protein complex called a PANoptosome. In healthy bone marrow hematopoietic cells, PANoptosis is restricted by inhibitory signaling. In MDS, bone marrow cells become sensitive to the PANoptotic stimuli due to the aberrant inactivation of inhibitory signaling or ...
Rohit Thalla   +4 more
wiley   +1 more source

Somatostatin receptor 4 (SSTR4) is a tumor suppressor in cutaneous and head & neck squamous cell carcinomas

open access: yesMolecular Oncology, EarlyView.
This study identifies somatostatin receptor 4 (Sstr4) as a critical tumor suppressor against skin and head/neck cancers (HNSCC, cSCC, and BCC). The loss of Sstr4 removes a check on cell growth, causing hyperactivation of the MAPK‐ERK signaling pathway (↑).
Ali Taqvi   +6 more
wiley   +1 more source

ADP‐ribosylation: An emerging regulator of the epigenome

open access: yesMolecular Oncology, EarlyView.
ADP‐ribosylation has emerged as a dynamic epigenetic signaling mechanism that modifies histones and chromatin‐associated proteins. Through coordinated PARylation and MARylation, it integrates with other histone modifications to regulate chromatin structure, transcription factor activity, and gene expression, influencing genome function and disease ...
Cristel V. Camacho   +2 more
wiley   +1 more source

Castration‐resistant prostate cancer cells are addicted to the high activity of cyclin‐dependent kinase 2

open access: yesMolecular Oncology, EarlyView.
We show that emergence of castration‐resistant prostate (CRPC) is associated with significant upregulation of cyclins that positively regulate cyclin‐dependent kinase 2 (CDK2) and concomitant downregulation of CDK4 cyclins. This renders CRPC cells dependent on the high activity of CDK2, and CDK2 inhibitors synergistically sensitize CRPC cells to both ...
Joyeeta Chatterjee   +3 more
wiley   +1 more source

Arginine methylation as a regulatory ratchet in cancer: From substrate selection to malignant‐state stabilization

open access: yesMolecular Oncology, EarlyView.
Arginine methylation can be viewed as a persistence‐prone post‐translational modification regulated by a network of PRMTs. Competitive and compensatory interactions among PRMTs can redistribute methylation across substrate pools shaped by sequence, structural, spatial, and environmental layers, reinforcing RNA‐processing, chromatin, and signaling ...
So Hyun Kwon, Ji Min Lee
wiley   +1 more source

Mechanisms and therapeutic opportunities of the ribotoxic stress response in cancer

open access: yesMolecular Oncology, EarlyView.
Cancer cells' high translational demand creates opportunities to therapeutically target ribosome function. Ribosome stalling and collisions activate ZAKα and the ribotoxic stress response (RSR), which can trigger rapid, p53‐independent apoptosis in cancer.
Anastassiya Kim   +7 more
wiley   +1 more source

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