Results 161 to 170 of about 1,695,985 (356)

MET and NF2 alterations confer primary and early resistance to first‐line alectinib treatment in ALK‐positive non‐small‐cell lung cancer

open access: yesMolecular Oncology, EarlyView.
Alectinib resistance in ALK+ NSCLC depends on treatment sequence and EML4‐ALK variants. Variant 1 exhibited off‐target resistance after first‐line treatment, while variant 3 and later lines favored on‐target mutations. Early resistance involved off‐target alterations, like MET and NF2, while on‐target mutations emerged with prolonged therapy.
Jie Hu   +11 more
wiley   +1 more source

Global variation in copy number in the human genome

open access: yesNature, 2006
R. Redon   +49 more
semanticscholar   +1 more source

Tonic signaling of the B‐cell antigen‐specific receptor is a common functional hallmark in chronic lymphocytic leukemia cell phosphoproteomes at early disease stages

open access: yesMolecular Oncology, EarlyView.
B‐cell chronic lymphocytic leukemia (B‐CLL) and monoclonal B‐cell lymphocytosis (MBL) show altered proteomes and phosphoproteomes, analyzed using mass spectrometry, protein microarrays, and western blotting. Identifying 2970 proteins and 316 phosphoproteins, including 55 novel phosphopeptides, we reveal BCR and NF‐kβ/STAT3 signaling in disease ...
Paula Díez   +17 more
wiley   +1 more source

Ubiquitination of transcription factors in cancer: unveiling therapeutic potential

open access: yesMolecular Oncology, EarlyView.
In cancer, dysregulated ubiquitination of transcription factors contributes to the uncontrolled growth and survival characteristics of tumors. Tumor suppressors are degraded by aberrant ubiquitination, or oncogenic transcription factors gain stability through ubiquitination, thereby promoting tumorigenesis.
Dongha Kim, Hye Jin Nam, Sung Hee Baek
wiley   +1 more source

Origins and functional impact of copy number variation in the human genome

open access: yesNature, 2010
D. Conrad   +23 more
semanticscholar   +1 more source

Aberrant expression of nuclear prothymosin α contributes to epithelial‐mesenchymal transition in lung cancer

open access: yesMolecular Oncology, EarlyView.
Nuclear prothymosin α inhibits epithelial‐mesenchymal transition (EMT) in lung cancer by increasing Smad7 acetylation and competing with Smad2 for binding to SNAI1, TWIST1, and ZEB1 promoters. In early‐stage cancer, ProT suppresses TGF‐β‐induced EMT, while its loss in the nucleus in late‐stage cancer leads to enhanced EMT and poor prognosis.
Liyun Chen   +12 more
wiley   +1 more source

The Fine-Scale and Complex Architecture of Human Copy-Number Variation [PDF]

open access: bronze, 2008
George H. Perry   +16 more
openalex   +1 more source

Functional impact of global rare copy number variation in autism spectrum disorders

open access: yesNature, 2010
D. Pinto   +176 more
semanticscholar   +1 more source

Home - About - Disclaimer - Privacy