Results 41 to 50 of about 320,341 (266)

Recurrent DNA break clusters drive replication-stress-induced copy number variants and genome diversification

open access: yesNature Communications
Copy number variants (CNVs) are strongly implicated in neurological and psychiatric disorders and brain cancer, yet the process by which replication stress generates CNVs—and why some recur while others remain rare—remains poorly understood.
Lorenzo Corazzi   +17 more
doaj   +1 more source

Transient receptor potential vanilloid type 4 (TRPV4) promotes tumorigenesis via NFAT4 activation in nasopharyngeal carcinoma

open access: yesFrontiers in Molecular Biosciences, 2022
Transient receptor potential vanilloid type 4 (TRPV4) can function as an oncogene or tumor suppressor depending on the tumor types. However, little is known regarding the effect of TRPV4 in nasopharyngeal carcinoma (NPC), a highly prevalent malignancy in
Peng Zhang   +10 more
doaj   +1 more source

From mice to humans—divergent strategies for intestinal homeostasis and regeneration

open access: yesFEBS Letters, EarlyView.
Recent advances such as organoid genome editing, xenotransplantation, imaging, and whole‐genome sequencing have enabled direct studies of human intestinal stem cells (ISCs). These studies reveal species‐specific features, including slower ISC proliferation, distinct injury responses, slower somatic mutation accumulation in humans, and an inverse ...
Keiko Ishikawa   +2 more
wiley   +1 more source

PVT1 Signaling Is a Mediator of Cancer Progression

open access: yesFrontiers in Oncology, 2019
There is increasing evidence that PVT1 has oncogenic properties and regulates proliferation and growth of many cancers. Themolecular mechanisms of action of PVT1 are mediated, in part, by microRNAs (miRNAs).
Camille Derderian   +4 more
doaj   +1 more source

Multistep tumorigenesis and the microenvironment [PDF]

open access: yesBreast Cancer Research, 2004
Early-stage cancers have long been considered to be less aggressive than late-stage cancers because it is assumed that they have accumulated fewer of the mutations that are required for full metastatic potential. For breast cancer, recent gene expression profiling data have challenged this paradigm by identifying early-stage cancers with similar gene ...
Pepper, Schedin, Anthony, Elias
openaire   +2 more sources

The role of miR‐335‐5p in the redifferentiation of BRAF p.V600E thyroid cancers

open access: yesMolecular Oncology, EarlyView.
The BRAF p.V600E mutation promotes thyroid cancer dedifferentiation and radioiodine resistance. Using a network approach, we identified miR‐335‐5p as a key regulator of BRAF‐mutated thyroid tumors. Restoring miR‐335‐5p increased thyroid‐specific gene expression and iodine uptake in cells and organoids.
Valeria Pecce   +11 more
wiley   +1 more source

Metabolic reprogramming: a bridge between aging and tumorigenesis

open access: yesMolecular Oncology, 2022
Aging is the most robust risk factor for cancer development, with more than 60% of cancers occurring in those aged 60 and above. However, how aging and tumorigenesis are intertwined is poorly understood and a matter of significant debate.
Stanislav Drapela   +2 more
doaj   +1 more source

AMP‐activated protein kinase β1 or β2 deletion enhances colon cancer cell growth and tumorigenesis

open access: yesActa Biochimica et Biophysica Sinica, 2022
Abnormal metabolism is a major hallmark of cancer and has been validated as a therapeutic target. Adenine monophosphate‐activated protein kinase (AMPK), an αβγ heterotrimer, performs essential functions in cancer progression due to its central role in ...
Shi Fuli   +8 more
doaj   +1 more source

Somatic mutational landscape in von Hippel–Lindau familial hemangioblastoma

open access: yesMolecular Oncology, EarlyView.
The causes of central nervous system (CNS) hemangioblastoma in Von Hippel–Lindau (vHL) disease are unclear. We used Whole Exome Sequencing (WES) on familial hemangioblastoma to investigate events that underlie tumor development. Our findings suggest that VHL loss creates a permissive environment for tumor formation, while additional alterations ...
Maja Dembic   +5 more
wiley   +1 more source

CCDC80 suppresses high‐grade serous ovarian cancer migration via negative regulation of B7‐H3

open access: yesMolecular Oncology, EarlyView.
PAX8 is a lineage‐specific master regulator of transcription in high‐grade serous ovarian cancer (HGSC) progression. We show for the first time that PAX8 facilitates proliferation and metastasis by repressing the cell autonomous tumor suppressor CCDC80 and inducing B7‐H3 expression.
Aya Saleh   +12 more
wiley   +1 more source

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