Results 91 to 100 of about 21,276,636 (264)

Mechanisms and therapeutic opportunities of the ribotoxic stress response in cancer

open access: yesMolecular 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   +7 more
wiley   +1 more source

Consensus on Application of Third-generation EGFR-TKI in EGFR Mutated NSCLC 
(2022 Version)

open access: yesChinese Journal of Lung Cancer, 2022
Chinese Society of Clinical Oncology (CSCO) Non-small Cell Lung Cancer Committee   +1 more
doaj   +1 more source

LncRNA MIR503HG Inhibits Non-Small Cell Lung Cancer Cell Proliferation by Inducing Cell Cycle Arrest Through the Downregulation of Cyclin D1

open access: yesCancer Management and Research, 2020
Shufen Xu,* Shengping Zhai,* Tiantian Du,* Zhan Li Respiratory Department, Yantai Yuhuangding Hospital Affiliated to Qingdao University, Yantai City, Shandong Province 264000, People’s Republic of China*These authors contributed equally to this ...
Xu S, Zhai S, Du T, Li Z
doaj  

Regulation of the lncRNA NEAT1 by p53‐ΔNp63 crosstalk modulates the DNA damage response and therapeutic efficacy in HNSCC

open access: yesMolecular Oncology, EarlyView.
In head and neck squamous cell carcinoma (HNSCC) p53 and p63 exert opposite roles on the transcription regulation of the lncRNA NEAT1. Under basal conditions, p53 levels are low and p63 represses NEAT1 expression. Upon genotoxic stress, p53 is rapidly induced, displacing p63 from the NEAT1 promoter leading to NEAT1 transcriptional activation and ...
Sara De Domenico   +5 more
wiley   +1 more source

Mapping of Multiple DNA Gains and Losses in Primary Small Cell Lung Carcinomas by Comparative Genomic Hybridization [PDF]

open access: yes, 1994
Comparative genomic hybridization was applied for a comprehensive screening of under- and overrepresentation of genetic material in 13 autoptic small cell lung cancer specimens.
Speicher, Michael R.   +6 more
core   +1 more source

Impact of adjuvant immunotherapy on prognosis in esophageal squamous cell carcinoma patients following neoadjuvant immunochemotherapy

open access: yesFrontiers in Oncology
IntroductionThe CheckMate-577 trial confirmed that adjuvant nivolumab significantly prolonged disease-free survival (DFS) in patients with esophageal cancer who had residual disease after neoadjuvant chemoradiotherapy (nCRT).
Jiayi Geng   +35 more
doaj   +1 more source

Mortalin overexpression predicts poor prognosis in early stage of non–small cell lung cancer

open access: yesTumor Biology, 2017
Mortalin is a member of the heat shock protein 70 family, which is involved in multiple cellular processes and may play key roles in promoting carcinogenesis.
Jie Sun   +5 more
doaj   +1 more source

Non-Small Cell Lung Cancer: Screening, Diagnosis, and Staging [PDF]

open access: yes, 2012
Lung cancer is the leading cause of cancer deaths worldwide. Tobacco consumption is the primary cause of lung cancer, accounting for more than 85% 90% of all lung cancer deaths.
Rocha, E.   +4 more
core  

Paclitaxel induces NM2‐dependent cellular contraction through GEF‐H1 dissociation from microtubules and RhoA/ROCK activation in cancer cells

open access: yesMolecular Oncology, EarlyView.
Taxanes are widely used chemotherapeutics whose effects on cellular mechanics remain poorly understood. We show that paclitaxel induces rapid cellular contraction by promoting GEF‐H1 dissociation from microtubules and non‐muscle myosin II activation through RhoA/ROCK.
Gloria Asensio‐Juárez   +5 more
wiley   +1 more source

APOBEC3 activity and DNA polymerase‐ε deficiency are associated with distinct IDH1 R132 hotspot mutations

open access: yesMolecular Oncology, EarlyView.
Isocitrate dehydrogenase 1 (IDH1) mutations are highly recurrent in multiple human cancer types, including cholangiocarcinoma and glioma. IDH1 R132C is the most common IDH1 mutation in cholangiocarcinoma and likely arises from APOBEC3A‐ or APOBEC3B‐mediated deamination.
Kelly E. Butler   +3 more
wiley   +1 more source

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