Results 131 to 140 of about 9,740,536 (302)

Inhibition of cyclin‐dependent kinases 12/13 using CT7439 as a treatment for colorectal cancer with CDK12 upregulation

Molecular Oncology, EarlyView.
The proposed mechanism of action for the CDK12/13 inhibitor and cyclin K degrader, CT7439. CDK12/13 inhibition interrupts transcription elongation, leading to increased DNA damage that results in cell death. This agent is a potentially novel treatment option for patients with colorectal cancer. Created in BioRender. Cyclin‐dependent kinase (CDK) 12 and
Wylie K. Watlington, Divya L. Dayanidhi, Mohammad Zokaasadi, John B. Mantyh, Pelumi D. Olawuni, Gabrielle Rupprecht, Jeremy M. Force, Shannon McCall, Ashwani K. Bahl, David S. Hsu, Jason A. Somarelli   +10 more
wiley   +1 more source

The clinical impact of copy number variants in inherited bone marrow failure syndromes

, 2017
Inherited bone marrow failure syndromes comprise a genetically heterogeneous group of diseases with hematopoietic failure and a wide array of physical malformations. Copy number variants were reported in some inherited bone marrow failure syndromes.
Robert J. Klaassen, Yves D. Pastore, Lawrence Jardine, Joseé Brossard, Bozana Zlateska, Tom Enbar, Liat Kofler, Yigal Dror, Geoff D. E. Cuvelier, Santhosh Dhanraj, Nicolas Waespe, Jeffrey H. Lipton, Roona Sinha, John K. Wu, Lisa Goodyear, Hongbing Li, Conrad V. Fernandez, Stephen W. Scherer, Elena Tsangaris, Mariana Silva, MacGregor Steele, Mark J. Belletrutti, Mary Shago, Sharon Abish, Manju Wahala, Michaela Cada, Bruno Michon, Vicky R. Breakey, Lillian Sung   +28 more
core   +1 more source

In vitro and in silico modelling of ROS1‐positive non‐small cell lung cancer reveals fusion‐dependent tyrosine kinase inhibitor responses

Molecular Oncology, EarlyView.
Drug resistance limits treatment success in a subset of lung cancers driven by ROS1 gene alterations. Using patient‐derived cells and computer simulations, we studied three key mutations and how they affect five targeted drugs. The mutations reduced drug effectiveness in different ways by altering protein structure and behavior.
Farhan Ul Haq, Marc Terrones, Felicia Rodrigues Fortes, Anne Schepers, Alessia Denis, Christophe Deben, Ken Op de Beeck, Guy Van Camp, Geert Vandeweyer   +8 more
wiley   +1 more source

Expression Profiling and Population Structure Analysis of Copy Number Variants (CNVs) in Autism Spectrum Disorder (ASD): 1st Triennium Post Doc Fellowship Report

, 2013
Fellowship: SFRH/BPD/74739/2010Autism Spectrum Disorder (ASD) is a common complex behavioral disorder with significant clinical heterogeneity and unclear etiology.
Pires Carreira da Conceição, Inês Susana
core  

CNVDeep: deep association of copy number variants with neurocognitive disorders

BMC Bioinformatics
Background Copy number variants (CNVs) have become increasingly instrumental in understanding the etiology of all diseases and phenotypes, including Neurocognitive Disorders (NDs).
Zahra Rahaie, Hamid R. Rabiee, Hamid Alinejad-Rokny   +2 more
doaj   +1 more source

An interaction-based model for neuropsychiatric features of copy-number variants.

PLoS Genetics, 2019
Variably expressive copy-number variants (CNVs) are characterized by extensive phenotypic heterogeneity of neuropsychiatric phenotypes. Approaches to identify single causative genes for these phenotypes within each CNV have not been successful.
Matthew Jensen, Santhosh Girirajan
doaj   +1 more source

Epigenetic silencing of the liver‐specific lncRNA LUNAR promotes liver cancer progression via NOTCH activation

Molecular Oncology, EarlyView.
LUNAR is a liver‐specific long noncoding RNA (lncRNA) that is highly expressed in normal liver but becomes epigenetically silenced in hepatocellular carcinoma through promoter hypermethylation. Loss of LUNAR is associated with NOTCH activation, epithelial–mesenchymal transition, and metastasis, whereas restoring LUNAR restrains metastatic progression ...
Se Ha Jang, Hyung Seok Kim, Geum Ok Baek, Moon Gyeong Yoon, Su In Lee, Jee‐Yeong Jeong, Ji Eun Han, Soon Sun Kim, Jae Youn Cheong, Jung Woo Eun   +9 more
wiley   +1 more source

CEACAM1 participation in breast cancer progression

Molecular Oncology, EarlyView.
In invasive breast cancer (BC), CEACAM1 shifts from an apical to a uniform membranous/cytoplasmic pattern, or is lost, as tumors dedifferentiate, inversely tracking the Ki‐67 proliferative index. In MCF‐7 cells, only CEACAM1‐4L suppresses proliferation, repressing cell cycle and growth factor genes.
Mykola Lyndin, Irina Kube‐Golovin, Anatolii Romaniuk, Gunther Wennemuth   +3 more
wiley   +1 more source

Strategies for genome-wide association analysis: gene-centric approach, network-based analysis and copy number variants: 1st Triennium Post Doc Fellowship report

, 2013
Fellowship: SFRH/BPD/ 64281/2009Genome-wide association studies (GWAS) have successfully identified numerous genetic risk factors for many common phenotypes, such as diabetes, Crohn's disease or height (http://www.genome.gov/gwastudies/).
Tavares Correia, Catarina Alexandra
core  

Pharmacological chromatin remodeling enhances response to estrogen therapy in ER+ breast cancer

Molecular Oncology, EarlyView.
Estrogen therapy elicits clinical benefit in ~ 30% of patients with endocrine‐resistant estrogen receptor (ER)‐positive breast cancer. Based on findings that ER transcriptional activation underlies response to estrogen therapy, we tested the effects of epigenetic dysregulation via pharmacological inhibition of histone deacetylases (HDACi).
Anneka L. Johnson Thomas, Barbara Karakyriakou, Patricia C. Muskus, Alyssa M. Roberts, Justin Rendleman, Alexa Warren, Hanxu Lu, Kimberly A. Birmingham, Malone K. Friedman, Abigail E. Goen, Huijuan Yang, Owen M. Wilkins, Fred W. Kolling, Eugene Demidenko, Julie M. Jorns, Brock C. Christensen, Todd W. Miller   +16 more
wiley   +1 more source