Results 111 to 120 of about 92,418,164 (308)

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

Catalog: Boston University School of Medicine, School of Public Health [PDF]

open access: yes, 1991
Viewbook/course catalog of the Boston University School of Public ...
Boston University School of Public Health
core  

Unique circulating miRNAome signatures captured with distinct molecular states in Lynch syndrome and sporadic colorectal cancer

open access: yesMolecular Oncology, EarlyView.
Circulating microRNA profiles distinguish nonmalignant Lynch syndrome from cancer‐associated Lynch syndrome, sporadic colorectal cancer, and healthy controls. Age‐stratified analysis reveals disease‐specific regulatory states, and a six‐miRNA panel shows concordant separation in an independent colorectal tissue cohort.
Ramadhani Salum Chambuso   +5 more
wiley   +1 more source

Catalog: Boston University School of Medicine, School of Public Health [PDF]

open access: yes, 1990
Viewbook/course catalog of the Boston University School of Public Health.Program descriptions, application ...
Boston University School of Public Health
core  

SPHINX31 acts as a SRPK1 inhibitor targeting the ATR/DNA‐PKcs/CHK1 replicative checkpoint to inhibit cell growth in non‐small cell lung cancer

open access: yesMolecular Oncology, EarlyView.
The kinase SRPK1 directly interacts with the protein TOPBP1 and regulates the pre‐mRNA splicing of WIZ thereby contributing to the activation of the ATR/CHK1 replicative checkpoint in response to replicative stress. This allows cancer cells' genomic stability and survival.
Amani Shreim   +17 more
wiley   +1 more source

Catalog: Boston University School of Medicine, School of Public Health [PDF]

open access: yes, 1985
Viewbook/course catalog of the Boston University School of Public Health.Program description, application ...
Boston University School of Public Health
core  

Targeting the EpCAM‐AXL axis to overcome drug resistance in lung cancer

open access: yesMolecular Oncology, EarlyView.
Lung cancer cells often evade therapy by hijacking signaling pathways. We reveal that cleaved EpCAM (sEpCAM) stabilizes the oncogenic protein AXL, driving NF‐κB and STAT3‐mediated chemoresistance. This EpCAM‐AXL axis identifies a high‐risk patient subset with poor prognosis.
Alexa Guerrero‐Alba   +5 more
wiley   +1 more source

Catalog: Boston University School of Medicine, School of Public Health [PDF]

open access: yes, 1989
Viewbook/course catalog of the Boston University School of Public Health.Program descriptions, application ...
Boston University School of Public Health
core  

Reprogramming tumor cells with LCOR mRNA nanotherapy to enhance immunotherapy

open access: yesMolecular Oncology, EarlyView.
LCOR (Ligand‐dependent corepressor) mRNA encapsulated in polymeric nanoparticles restores LCOR activity in tumor cells, constraining aggressive tumor cell states and increasing tumor immunogenicity. This reprogramming makes tumor cells more vulnerable to T‐cell attack and enhances their response to immune‐checkpoint immunotherapy.
Gabriel Serra‐Mir   +9 more
wiley   +1 more source

News: BUSPH Dean's report [PDF]

open access: yes, 2000
Report from the Dean of the Boston University School of Public ...
Boston University School of Public Health
core   +1 more source

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