Results 171 to 180 of about 4,637,538 (347)

Single‐cell transcriptomics redefines focal neuroendocrine differentiation as a distinct prostate cancer pathology

open access: yesMolecular Oncology, EarlyView.
Single‐cell transcriptomics of prostate cancer patient‐derived xenografts reveals distinct features of neuroendocrine (NE) subtypes. Tumours with focal NE differentiation (NED) share transcriptional programmes with adenocarcinoma, differing from large and small cell neuroendocrine prostate cancer (NEPC). Our work defines the molecular landscape of NEPC,
Rosalia Quezada Urban   +12 more
wiley   +1 more source

Characterizing the salivary RNA landscape to identify potential diagnostic, prognostic, and follow‐up biomarkers for breast cancer

open access: yesMolecular Oncology, EarlyView.
This study explores salivary RNA for breast cancer (BC) diagnosis, prognosis, and follow‐up. High‐throughput RNA sequencing identified distinct salivary RNA signatures, including novel transcripts, that differentiate BC from healthy controls, characterize histological and molecular subtypes, and indicate lymph node involvement.
Nicholas Rajan   +9 more
wiley   +1 more source

Microglia limit brain tumor development by restricting tumor cell proliferation and inducing T‐cell immunity

open access: yesMolecular Oncology, EarlyView.
Microglia (BV2) and IL‐4‐treated BMDMs promote astrocytoma clustering and inhibit tumor growth, not shown in other macrophage cells. In vivo, microglial co‐implantation enhances CD8+ T cell infiltration, elevates Granzyme B, lowers circulating MDSCs, and extends survival only in immune‐competent mice, but not in immune‐deficient mice.
Tzu‐Chieh Sun   +5 more
wiley   +1 more source

Adenosine‐to‐inosine editing of miR‐200b‐3p is associated with the progression of high‐grade serous ovarian cancer

open access: yesMolecular Oncology, EarlyView.
A‐to‐I editing of miRNAs, particularly miR‐200b‐3p, contributes to HGSOC progression by enhancing cancer cell proliferation, migration and 3D growth. The edited form is linked to poorer patient survival and the identification of novel molecular targets.
Magdalena Niemira   +14 more
wiley   +1 more source

Investigating the cell of origin and novel molecular targets in Merkel cell carcinoma: a historic misnomer

open access: yesMolecular Oncology, EarlyView.
This study indicates that Merkel cell carcinoma (MCC) does not originate from Merkel cells, and identifies gene, protein & cellular expression of immune‐linked and neuroendocrine markers in primary and metastatic Merkel cell carcinoma (MCC) tumor samples, linked to Merkel cell polyomavirus (MCPyV) status, with enrichment of B‐cell and other immune cell
Richie Jeremian   +10 more
wiley   +1 more source

The influence of ROS1 fusion partners and resistance mechanisms in ROS1‐TKI‐treated non‐small cell lung cancer patients

open access: yesMolecular Oncology, EarlyView.
This real‐world study of ROS1+ NSCLC highlights fusion diversity, treatment outcomes with crizotinib and lorlatinib, and in vitro experiments with resistance mechanisms. G2032R drives strong resistance to ROS1‐targeted TKIs, especially lorlatinib. Fusion partner location does not affect overall survival to crizotinib or lorlatinib. Findings support the
Fenneke Zwierenga   +8 more
wiley   +1 more source

The Essential Norm of Operators on Ap α(Bn)

open access: yes, 2013
In this paper we characterize the compact operators on the weighted Bergman spaces Ap α(Bn) when 1 −1. The main result shows that an operator on Ap α(Bn) is compact if and only if it belongs to the Toeplitz algebra and its Berezin transform vanishes on the boundary of the ...
Mitkovski, Mishko   +2 more
openaire   +1 more source

Emerging role of ARHGAP29 in melanoma cell phenotype switching

open access: yesMolecular Oncology, EarlyView.
This study gives first insights into the role of ARHGAP29 in malignant melanoma. ARHGAP29 was revealed to be connected to tumor cell plasticity, promoting a mesenchymal‐like, invasive phenotype and driving tumor progression. Further, it modulates cell spreading by influencing RhoA/ROCK signaling and affects SMAD2 activity. Rho GTPase‐activating protein
Beatrice Charlotte Tröster   +3 more
wiley   +1 more source

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