Results 91 to 100 of about 19,933,051 (310)

Intrapatient tumour heterogeneity and clonal evolution in an autopsy study of metastatic salivary gland cancer

Molecular Oncology, EarlyView.
Tumour heterogeneity and clonal evolution of metastatic salivary gland cancer were evaluated in two patients with adenoid carcinoma and one patient with myoepithelial carcinoma. Radiology‐guided autopsy enabled multi‐region sampling (total samples n = 149), followed by whole‐genome sequencing and phylogenetic reconstruction (17 tumour samples, 4–7 per ...
Gerben Lassche, Niels J. van Ruitenbeek, Charlotte Adang, Luke O'Gorman, Pui Yuen Lee, Willemijn M. Klein, Adriana C. H. van Engen‐van Grunsven, Jack A. Schalken, Sander Bervoets, Gerald W. Verhaegh, Carla M. L. van Herpen   +10 more
wiley   +1 more source

LINC01963 promotes pancreatic ductal adenocarcinoma proliferation via METTL3/IGF2BP2 axis-mediated m⁶A modification of c-Myc

Journal of Experimental & Clinical Cancer Research
Background C-Myc overexpression is an important molecular hallmark of pancreatic ductal adenocarcinoma (PDAC), but directly targeting c-Myc is extremely challenging.
Qixian Liu, Ruiyu Li, Bohan Liu, Hangqi Liu, Xuqing Shi, Xianglin Yin, Xinping Ju, Sichong Zhang, Jun Wang, Yuhan Zhang, Xiaoding Liu, Dongmei Li, Longyun Chen, Yamei Niu, Huanwen Wu, Zhiyong Liang   +15 more
doaj   +1 more source

Domain-specific c-Myc ubiquitylation controls c-Myc transcriptional and apoptotic activity [PDF]

Proceedings of the National Academy of Sciences, 2012
The oncogenic transcription factor c-Myc causes transformation and tumorigenesis, but it can also induce apoptotic cell death. Although tumor suppressors are necessary for c-Myc to induce apoptosis, the pathways and mechanisms are unclear.
Qin, Zhang, Erick, Spears, David N, Boone, Zhaoliang, Li, Mark A, Gregory, Stephen R, Hann   +5 more
openaire   +2 more sources

Transcription profiling of lung adenocarcinomas of c-myc-transgenic mice: Identification of the c-myc regulatory gene network-0

, 2011
C: LightCycler). Fold changes are shown on the y-axis. Significant changes of gene expression are indicated either with a diamond for array analysis or with an asterisk for real time PCR.Copyright information:Taken from "Transcription profiling of lung ...
Susanne Reymann (56981), Jürgen Borlak (47026)   +1 more
core   +1 more source

Mechanisms and therapeutic opportunities of the ribotoxic stress response in cancer

Molecular 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, Maryam Aslam, Elouise Torruella, Alphons Sony, Asif Rahman, Simira Smith, Columba de la Parra, Moira Sauane   +7 more
wiley   +1 more source

c-Myc Inhibition Induces an Additive Effect with Cyclophosphamide in Acute Lymphoblastic Leukemia [PDF]

ImmunoAnalysis
Background: Cellular-myelocytomatosis (c-Myc), an oncoprotein and a transcription factor, is involved in several essential cellular processes. The c-Myc expression level is highly regulated in normal cells.
Mohammad Sadeghi, Maryam Panahi, Zahra Kheyrizadeh, Leili Aghebati-Maleki, Ali Akbar Movasaghpour Akbari, Abbas Ali Hosseinpour Feizi, Sima Shahmohammadi Farid, Sanam Dolati, Farhad Jadidi-Niaragh   +8 more
doaj   +1 more source

Nucleophosmin interacts directly with c-Myc and controls c-Myc-induced hyperproliferation and transformation [PDF]

Proceedings of the National Academy of Sciences, 2008
The transcription factor c-Myc is essential for cellular proliferation and is one of the most frequently activated oncogenes, but the molecular mechanism mediating its critical role in transformation is unclear. Like c-Myc, multifunctional nucleophosmin (NPM) is tightly regulated during proliferation and is overexpressed in several different types of ...
Zhaoliang, Li, David, Boone, Stephen R, Hann   +2 more
openaire   +2 more sources

Brief inactivation of c-Myc is not sufficient for sustained regression of c-Myc-induced tumours of pancreatic islets and skin epidermis-2

, 2011
Copyright information:Taken from "Brief inactivation of c-Myc is not sufficient for sustained regression of c-Myc-induced tumours of pancreatic islets and skin epidermis"BMC Biology 2004;2():26-26.Published online 21 Dec 2004PMCID:PMC544575.Copyright ...
Sevasti Zervou (71022), Stella Pelengaris (71018), Linda Cheung (71020), Michael Khan (71023), Sylvie Abouna (71019), Vasiliki Ifandi (71021)   +5 more
core   +1 more source

Obesity under the moonlight of c-MYC

, 2023
The moonlighting protein c-Myc is a master regulator of multiple biological processes including cell proliferation, differentiation, angiogenesis, apoptosis and metabolism.
Nevzorova, Yulia, Cubero Palero, Francisco Javier   +1 more
core   +1 more source

Profiling neoadjuvant therapy response in rectal cancer using meta‐analysis of publicly available transcriptomic RNA‐seq datasets

Molecular Oncology, EarlyView.
This study integrates publicly available transcriptomic datasets to identify molecular signatures associated with response to neoadjuvant chemoradiotherapy in locally advanced rectal cancer. By analyzing a combination of multiple cohorts with bioinformatics approaches, we reveal biological pathways and immune‐related features that may improve ...
Aleksandra Stanojevic, Rafael Stroggilos, Mladen Marinkovic, Ana Djuric, Suzana Stojanovic‐Rundic, Radmila Jankovic, Sergi Castellvi‐Bel, Remond J.A. Fijneman, Antonia Vlahou, Jerome Zoidakis, Milena Cavic   +10 more
wiley   +1 more source