Results 91 to 100 of about 574,116 (318)

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

Genome organization of DNA replication timing and its link to chromatin and transcription [PDF]

open access: yes, 2008
The replication of the genome is a highly organized process. Not every sequence replicates at the same time, instead some genes replicate early, while others replicate later during S phase.
Schwaiger, Michaela
core   +1 more source

A novel method for isolation of histones from serum and its implications in therapeutics and prognosis of solid tumours

open access: yesClinical Epigenetics, 2017
Background Dysregulation in post-translational modifications of histones and their modifiers are now well-recognized as a hallmark of cancer and can be used as biomarkers and potential therapeutic targets for disease progression and prognosis.
Divya Reddy   +3 more
doaj   +1 more source

Structural basis for PRC2 decoding of active histone methylation marks H3K36me2/3

open access: yeseLife, 2020
Repression of genes by Polycomb requires that PRC2 modifies their chromatin by trimethylating lysine 27 on histone H3 (H3K27me3). At transcriptionally active genes, di- and tri-methylated H3K36 inhibit PRC2.
Ksenia Finogenova   +9 more
doaj   +1 more source

Hippo pathway at the crossroads of stemness and therapeutic resistance in breast cancer

open access: yesMolecular Oncology, EarlyView.
Dysregulation of the Hippo pathway drives nuclear accumulation of YAP/TAZ, activating stemness‐related transcriptional programs that sustain breast cancer stemness and fuel therapeutic resistance across subtypes, underscoring Hippo signaling as a targetable vulnerability. Figure created and edited with BioRender.com.
Giulia Schiavoni   +11 more
wiley   +1 more source

Kinetic control of eukaryotic chromatin structure by recursive topological restraints

open access: yes, 2008
Chromatin structure undergoes many changes during the cell cycle and in response to regulatory events. A basic unit of chromatin organization is the nucleosome core particle.
Dominika Borek, Zbyszek Otwinowski
core  

Cell-free system for assembly of transcriptionally repressed chromatin from Drosophila Embryos [PDF]

open access: yes, 1992
We descrtbe a cell·free system, derlved (rom preblastoderm DrosophÜIJ embryos. ror tbe efficient assembly of eloned DNA into chromatin. Tbe cbromatin assembly system ulilizes cndogcDous eure histones aod assembly racton aod yields loog arrays of ...
Earl Wu   +3 more
core  

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

The role of HDAC2 in chromatin remodelling and response to chemotherapy in ovarian cancer [PDF]

open access: yes, 2015
This study was supported by financial support from the University of Edinburgh/China Scholarship Council joint Scholarship Scheme. We are also grateful to support from the Scottish Funding Council.Chromatin undergoes structural changes in response to ...
Mullen, Peter   +8 more
core   +1 more source

E2A selectively regulates TGF‐β–induced apoptosis in KRAS‐mutant non‐small cell lung cancer

open access: yesMolecular Oncology, EarlyView.
Ability to induce apoptosis by TGF‐β is frequently lost in advanced lung adenocarcinoma despite intact TGF‐β signaling. We identify E2A as a mutant KRAS–dependent mediator of resistance to TGF‐β–induced apoptosis. TGF‐β induces E2A via SMAD3 in mutant KRAS cells, and E2A silencing restores apoptosis and enhances radiation response in cell lines ...
Sergei Chuikov   +3 more
wiley   +1 more source

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