Results 51 to 60 of about 1,331,530 (241)

Developmental programmes drive cellular plasticity, disease progression and therapy resistance in lung adenocarcinoma

open access: yesMolecular Oncology, EarlyView.
This study shows that lung adenocarcinomas exploit developmental branching morphogenesis to acquire a therapy resistant basal‐like tumour cell state. This process was found to be regulated by combined TP53 loss‐of‐function and type‐I interferon signalling, identifying a novel axis for biomarker and therapeutic target discovery.
Kamila J Bienkowska   +13 more
wiley   +1 more source

Loss of proton‐sensing TDAG8 increases tumor progression in mouse models of colon cancer

open access: yesMolecular Oncology, EarlyView.
Loss of the pH‐sensing receptor TDAG8 accelerates colorectal cancer progression in mice. Animals lacking TDAG8 expression had increased tumor growth, DNA damage, and recruitment of tumor‐associated immune cells, including macrophages, neutrophils, and monocytes.
Ermanno Malagola   +11 more
wiley   +1 more source

Cancer‐associated mutations in endometriosis reframe a benign disease through molecular oncology

open access: yesMolecular 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

Interview with Jimmy Limit: "Recent Advancements"

open access: yes, 2014
Jimmy Limit\u27s "Recent Advancements" (18 Jan-4 May 2014) at Rodman Hall, St. Catharines, Ontario.
Limit, Jimmy
core   +1 more source

Refined cyclic renormalization group in Russian doll model

open access: yesSciPost Physics
Focusing on Bethe-Ansatz integrable models, robust to both time-reversal symmetry breaking and disorder, we consider the Russian Doll Model (RDM) for finite system sizes and energy levels.
Vedant Motamarri, Ivan M. Khaymovich, Alexander Gorsky
doaj   +1 more source

Translating whole‐genome doubling into precision medicine in cancer

open access: yesMolecular Oncology, EarlyView.
Whole‐genome doubling creates a WGD‐positive tumor state characterized by persistent chromosomal instability, karyotypic diversification, and cellular stress. These same biological pressures drive aggressive tumor evolution while exposing therapeutic vulnerabilities, providing a rationale for WGD‐informed precision medicine. Whole‐genome doubling (WGD)
Sejung Lee, Junghyeok Lim, Jinhyuk Bhin
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

Efficient control of fluxonium qubits via nonadiabatic transitions

open access: yesPhysical Review Research
The fluxonium qubit is a promising platform for quantum operations due to its large anharmonicity and long coherence time. However, conventional resonant driving methods often require long operation times and complex implementation.
I-Yun Hsiao   +2 more
doaj   +1 more source

Pitch in esophageal speech

open access: yesSouth African Journal of Communication Disorders, 1975
Most reports on pitch in esophageal speech emphasize that it is low-pitched with a measured fundamental frequency rarely higher than 100 cps. Our investigations show, however, that much esophageal 'phonation' lacks periodicity and, therefore, a ...
L. W. Lanham, W. A. Kerr
doaj   +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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